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CardioNerds (Dr. Dan Ambinder and guest host, Dr. Pooja Prasad) join Dr. Donny Mattia from Phoenix Children's pediatric cardiology fellowship, Dr. Sri Nayak from the Mayo Clinic – Arizona adult cardiology fellowship, and Dr. Harrison VanDolah from the University of Arizona College of Medicine - Phoenix Med/Peds program for a sunrise hike of Piestewa Peak, followed by some coffee at Berdena's in Old Town Scottsdale (before the bachelorette parties arrive), then finally a stroll through the Phoenix Desert Botanical Gardens to discuss a thought-provoking case series full of clinical cardiology pearls. Expert commentary is provided by Dr. Tabitha Moe. Episode audio was edited by Dan Ambinder. They discuss the following case: Cardiology is consulted by the OB team for a 27-year-old female G1, now P1, who has just delivered a healthy baby boy at 34 weeks gestation after going into premature labor. She is experiencing shortness of breath and is found to have a significant past cardiac history, including atrial fibrillation and preexcitation, now with a pacemaker and intracardiac defibrillator. We review the differential diagnosis for peripartum cardiomyopathy (PPCM) and then combine findings from her infant son, who is seen by our pediatric cardiology colleagues and is found to have severe hypertrophic cardiomyopathy (HCM). Genetic testing for both ultimately reveals a LAMP2 mutation consistent with Danon Disease. The case discussion focuses on the differential diagnosis for PPCM, HCM, pearls on Danon Disease and other HCM “phenocopies,” and the importance of good history. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media Pearls Peripartum cardiomyopathy is a diagnosis of exclusion – we must exclude other possible etiologies of heart failure! Be on the lookout for features of non-sarcomeric HCM – as Dr. Michelle Kittleson said in Episode 166, “LVH plus” states. HCM with preexcitation, heart block, strong family history, or extracardiac symptoms such as peripheral neuropathy, myopathy, or cognitive impairment should be evaluated for infiltrative/inherited cardiomyopathies! As an X-linked dominant disorder, Danon disease will present differently in males vs females, with males having much more severe and earlier onset disease with extracardiac features. Making the diagnosis for genetic disorders such as Danon disease is important for getting the rest of family members tested as well as the opportunity for specialized treatments such as gene therapy Up to 5% of Danon disease cases may be due to copy number variants, which may be missed in genetic testing that does not do targeted deletion/duplication analysis!). Notes What is the differential diagnosis for peripartum cardiomyopathy? Peripartum cardiomyopathy is a diagnosis of exclusion – we must exclude other possible etiologies of heart failure! First, ensure that you are not missing an acute life-threatening etiology of acute decompensated heart failure – pulmonary embolism, amniotic fluid embolism, ACS, and SCAD should all be ruled out. Second, a careful history can identify underlying heart disease or risk factors for the development of heart failure, such as substance use, high-risk behaviors that put one at risk for HIV infection, and family history that suggests an inheritable cardiomyopathy. Lastly, a careful review of echocardiographic imaging may also identify underlying etiologies that warrant a change in management. Diagnosis of peripartum cardiomyopathy is important to consider as within 7 days of onset, patients may be eligible for treatment with bromocriptine – consider referring ...
N Engl J Med 2020;382:1395-407 - ISCHEMIAN Engl J Med 2020;382:1608-16 - ISCHEMIA-CKDBackground: The COURAGE trial, published in 2007, represented a major reversal in cardiovascular medicine. In patients with stable CAD an initial strategy of revascularization plus medical therapy did not reduce the chance of dying or having a heart attack compared to an initial strategy of medical therapy alone. Prior to these results, patients with stable CAD were routinely managed with an initial invasive approach and the field of cardiology was intensely focused on finding coronary blockages and “fixing” them in symptomatic and asymptomatic patients alike. Thus, it's not surprising that following results from COURAGE, the practice continued to be vigorously defended and applied routinely in the management of patients with stable CAD.The first major attempt to reverse the results of COURAGE came from the FAME 2 trial, published in 2012, which tested the hypothesis that patients with stable CAD and an abnormal fractional flow reserve (FFR) in the cath lab would do better with an initial invasive strategy compared to medical therapy alone. The trial was stopped early for efficacy but the positive results were driven entirely by revascularization during follow up - not death or heart attack. The trial was criticized for being stopped inappropriately without providing an answer to whether an early invasive strategy improved hard endpoints compared to initial medical therapy alone. The concepts of “faith healing” and “subtraction anxiety” are useful for understanding the results and limitations of the FAME 2 trial.The ISCHEMIA trial which began enrolling patients in 2012 sought to overcome limitations of COURAGE and FAME. The investigative aim of the study was to test the hypothesis that in patients with stable CAD and moderate to severe ischemia on provocative testing, an initial invasive strategy reduced a composite of major cardiac events compared to initial medical therapy alone. The ISCHEMIA-CKD trial was performed in conjunction with the ISCHEMIA Research Group to address an important knowledge gap in managing patients with CAD. Patients with advanced chronic kidney disease (CKD) experience a higher rate of cardiac events than their counterparts without CKD; however, they are also at a higher risk of procedural complications. The standard of care at the time was generally to manage a patient with stable CAD and CKD like any other patient with CAD despite the fact that such patients were historically excluded from participation in clinical trials and thus, there was really no data from clinical trials to guide decision making.The ISCHEMIA-CKD investigators sought to test the hypothesis that in patients with advanced CKD and stable CAD and moderate to severe ischemia on stress testing, an initial invasive strategy reduced death or MI compared to initial medical therapy alone.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber.Patients: For the ISCHEMIA trial, eligible patients had to be at least 21 years of age or older with at least moderate ischemia on a qualifying stress test based on the following criteria:* Nuclear perfusion with SPECT or PET with >/= 10% ischemic myocardium* Echocardiography with >/= 3/16 segments with stress-induced severe hypokinesis or akinesis* Cardiac MRI with >/= 10% ischemic myocardium on perfusion imaging and/or >/= 3/16 segments with stress-induced severe hypokinesis or akinesis on wall motion assessment* Exercise treadmill test without imaging that met all 4 following criteria* clinical history of typical angina or typical angina during the stress test* absence of resting ST depression > 1.0 mm or confounders that render exercise EKG non-interpretable (LBBB, LVH with repolarization, pacemaker, etc.)* exercise-induced horizontal or downsloping ST depression >/= 1.5 mm in 2 leads or >/= 2.0 mm in any lead or ST elevation >/= 1.0 mm in a non-infarct territory* either of the following:* workload at which ST segment criteria are met is NOT to exceed completion of stage 2 of a standard Bruce protocol or 7 METS if a non-Bruce protocol is used* ST segment criteria are met at
CardioNerds cofounder Dr. Amit Goyal and cardiology fellows from the Cleveland Clinic (Drs. Alejandro Duran Crane, Gary Parizher, and Simrat Kaur) discuss the following case: A 61-year-old man presented with symptoms of heart failure and left ventricular hypertrophy. He was given a diagnosis of obstructive hypertrophic cardiomyopathy. He eventually underwent septal myectomy, mitral valve replacement, aortic aneurysm repair, and aortic valve replacement with findings of Fabry's disease on surgical pathology. The case discussion focuses on the differential diagnosis for LVH and covers Fabry disease as an HCM mimic. Expert commentary was provided by Dr. Angelika Ewrin. The episode audio was edited by student Dr. Diane Masket. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - An Unusual Cause of Hypertrophic Cardiomyopathy – Cleveland Clinic Pearls - An Unusual Cause of Hypertrophic Cardiomyopathy – Cleveland Clinic Left ventricular hypertrophy is a cardiac manifestation of several different systemic and cardiac processes, and its etiology should be clarified to avoid missed diagnosis and treatment opportunities. Fabry disease is a rare, X-linked inherited disease that can present cardiac and extra-cardiac manifestations, the former of which include hypertrophic cardiomyopathy, conduction defects, coronary artery disease, conduction abnormalities, arrhythmias, and heart failure. The diagnosis of Fabry disease includes measurement of alpha-galactosidase enzyme activity as well as genetic testing to evaluate for pathogenic variants or variants of unknown significance in the GLA gene. Family members of patients diagnosed with Fabry disease should be screened based on the inheritance pattern. Multimodality imaging can be helpful in the diagnosis of Fabry disease. Echocardiography can show left ventricular hypertrophy (LVH), reduced global strain, aortic and mitral valve thickening, and aortic root dilation with associated mild to moderate aortic regurgitation. Cardiac MRI can show hypertrophy of papillary muscles, mid-wall late gadolinium enhancement and low-native T1 signal. The treatment of Fabry disease involves a multi-disciplinary approach with geneticists, nephrologists, cardiologists, nephrologists, and primary care doctors. Enzyme replacement therapy can delay the progression of cardiac disease. Show Notes - An Unusual Cause of Hypertrophic Cardiomyopathy – Cleveland Clinic What are the causes of left ventricular hypertrophy? LVH is extremely common. It is present in 15-20% of the general population, and is more common in Black individuals, the elderly, obese or hypertensive individuals, with most cases being secondary to hypertension and aortic valve stenosis. In general terms, it is helpful to divide the causes of LVH into three main groups: high afterload states, obstruction to LV ejection, and intrinsic myocardial problems. Increased afterload states include both primary and secondary hypertension and renal artery stenosis. Mechanical obstruction includes aortic stenosis, subaortic stenosis, and coarctation of the aorta. Lastly, several intrinsic problems of the myocardium can cause LV hypertrophy, such as athletic heart with physiological LVH, hypertrophic cardiomyopathy with or without outflow obstruction, and infiltrative or storage diseases such as cardiac amyloidosis, Fabry's disease, or Danon disease, among others. How does Fabry disease present? Fabry disease is present in all races and is an X-linked lysosomal storage disorder caused by pathogenic variants in the GLA gene that result in reduced alpha-galactosidase enzyme activity,
Recognizing the Longstanding Concerns in ECG Interpretation Proficiency Guest: Mary-Tiffany A. Oduah, M.D. Host: Anthony H. Kashou, M.D. In this episode, we delve into the significance and accuracy of diagnosing left ventricular hypertrophy (LVH) using ECG, emphasizing the potential variances across racial and ethnic groups. We explore the underlying reasons for these disparities, the implications of a universal LVH diagnostic criterion, and the need for possible race-specific thresholds in cardiological diagnoses. Topics Discussed Diagnosing Left Ventricular Hypertrophy (LVH) using ECG Variances in specificity and sensitivity for LVH criteria Connect with Mayo Clinic's Cardiovascular Continuing Medical Education online at https://cveducation.mayo.edu or on Twitter @MayoClinicCV and @MayoCVservices. LinkedIn: Mayo Clinic Cardiovascular Services Cardiovascular Education App: The Mayo Clinic Cardiovascular CME App is an innovative educational platform that features cardiology-focused continuing medical education wherever and whenever you need it. Use this app to access other free content and browse upcoming courses. Download it for free in Apple or Google stores today! No CME credit offered for this episode. Podcast episode transcript found here.
The following question refers to Section 7.8 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by Stony Brook University Hospital medicine resident and CardioNerds Intern Dr. Chelsea Tweneboah, answered first by Mayo Clinic Cardiology Fellow and CardioNerds Academy Chief Dr. Teodora Donisan, and then by expert faculty Dr. Michelle Kittleson.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #29 A 69-year-old man was referred to the cardiology clinic after being found to have a reduced left ventricular ejection fraction and left ventricular hypertrophy. For the last several months he has been experiencing progressively worsening fatigue and shortness of breath while getting to the 2nd floor in his house. He has a history of bilateral carpal tunnel syndrome and chronic low back pain. He takes no medications. On exam, his heart rate is 82 bpm, blood pressure is 86/60 mmHg, O2 saturation is 97% breathing ambient air, and BMI is 29 kg/m2. He has a regular rate and rhythm with normal S1 and S2, bibasilar pulmonary rales, and 1+ pitting edema in both legs. EKG shows normal sinus rhythm with a first-degree AV delay and low voltages. Transthoracic echocardiogram shows a moderately depressed LVEF of 35-39%, severe concentric hypertrophy with a left ventricular posterior wall thickness of 1.5 cm and strain imaging showing globally reduced longitudinal strain with apical sparring. There is also biatrial enlargement and a small pericardial effusion. A pharmacologic nuclear stress test did not reveal any perfusion defects. A gammopathy panel including SPEP, UPEP, serum and urine immunofixation studies, and serum free light chains are unrevealing. A 99mTc-Pyrophosphate scan was positive with grade 3 uptake. In addition to starting diuretics, what is the next most appropriate step for managing for this patient? A Start metoprolol succinate B Start sacubitril/valsartan C Perform genetic sequencing of the TTR gene D Perform endomyocardial biopsy Answer #29 Explanation The correct answer is C – perform genetic sequencing of the TTR gene. This patient has findings which raise suspicion for cardiac amyloidosis. There are both cardiac (low voltages on EKG and echocardiogram showing marked LVH with biatrial enlargement and small pericardial effusion as well as a characteristic strain pattern) and extra-cardiac (bilateral carpal tunnel syndrome and low back pain) features to suggest amyloidosis. The diagnosis of cardiac amyloidosis requires a high index of suspicion and most commonly occurs due to a deposition of monoclonal immunoglobulin light chains (AL-CM) or transthyretin (ATTR-CM). ATTR may cause cardiac amyloidosis as either a pathogenic variant (ATTRv) or as a wild-type protein (ATTRwt). Patients for whom there is a clinical suspicion for cardiac amyloidosis should have screening for serum and urine monoclonal light chains with serum and urine immunofixation electrophoresis and serum free light chains (Class 1, LOE B-NR). Immunofixation electrophoresis (IFE) is preferred because serum or urine plasma electrophoresis (SPEP or UPEP) are less sensitive. Together, measurement of serum IFE, urine IFE, and serum FLC is >99% sensitive for AL amyloidosis.
This week we review a recent work from the UK on the causes of death in adolescents who die suddenly. The novelty of this week's work is that all the individuals in this very large study had specialized cardiac pathologists perform careful assessments of the hearts of these subjects. What is the most common cardiac cause of SCD in the adolescent and how do the findings of this work compare with prior works on this topic? What sort of screening should be considered when encountering a patient with SCD? Why would LVH (without HCM) possibly be a cause of SCD in the young? Should all SCD victims have evaluation by a cardiac pathologist? What is the role of molecular autopsy? These are amongst the many topics reviewed with the senior author of this week's work, noted Professor of Pathology, Dr. Mary Sheppard of St. George's, University of London, London UK. https://doi.org/10.1016/j.jacc.2023.01.041
The following question refers to Section 4.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by Texas Tech University medical student and CardioNerds Academy Intern Dr. Adriana Mares, answered first by Rochester General Hospital cardiology fellow and Director of CardioNerds Journal Club Dr. Devesh Rai, and then by expert faculty Dr. Eldrin Lewis.Dr. Lewis is an Advanced Heart Failure and Transplant Cardiologist, Professor of Medicine and Chief of the Division of Cardiovascular Medicine at Stanford University. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #26 A 45-year-old man presents to cardiology clinic to establish care. He has had several months of progressive dyspnea on exertion while playing basketball. He also reports intermittent palpitations for the last month. Two weeks ago, he passed out while playing and attributed this to exertion and dehydration. He denies smoking and alcohol intake. Family history is significant for sudden cardiac death in his father at the age of 50 years. Autopsy has shown a thick heart, but he is unaware of the exact diagnosis. He has two children, ages 12 and 15 years old, who are healthy. Vitals signs are blood pressure of 124/84 mmHg, heart rate of 70 bpm, and normal respiratory rate. On auscultation, a systolic murmur is present at the left lower sternal border. A 12-lead ECG showed normal sinus rhythm with signs of LVH and associated repolarization abnormalities. Echocardiography reveals normal LV chamber volume, preserved LVEF, asymmetric septal hypertrophy with wall thickness up to 16mm, systolic anterior motion of the anterior mitral valve leaflet with 2+ eccentric posteriorly directed MR, and resting LVOT gradient of 30mmHg which increases to 60mmHg on Valsalva. You discuss your concern for an inherited cardiomyopathy, namely hypertrophic cardiomyopathy. In addition to medical management of his symptoms and referral to electrophysiology for ICD evaluation, which of the following is appropriate at this time? A Order blood work for genetic testing B Referral for genetic counseling C Cardiac MRI D Coronary angiogram E All of the above Answer #26 Explanation The correct answer is B – referral for genetic counseling. Several factors on clinical evaluation may indicate a possible underlying genetic cardiomyopathy. Clues may be found in: · Cardiac morphology – marked LV hypertrophy, LV noncompaction, RV thinning or fatty replacement on imaging or biopsy · 12-lead ECG – abnormal high or low voltage or conduction, and repolarization, altered RV forces · Presence of arrhythmias – frequent NSVT or very frequent PVCs, sustained VT or VF, early onset AF, early onset conduction disease · Extracardiac features – skeletal myopathy, neuropathy, cutaneous stigmata, and other possible manifestations of specific syndromes In select patients with nonischemic cardiomyopathy, referral for genetic counseling and testing is reasonable to identify conditions that could guide treatment for patients and family members (Class 2a, LOE B-NR). In first-degree relatives of selected patients with genetic or inherited cardiomyopathies, genetic screening and counseling are recommended to ...
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Please join author Subodh Verma and Guest Editor Christopher Granger as they discuss the article "Empagliflozin and Left Ventricular Remodeling in People Without Diabetes: Primary Results of the EMPA-HEART 2 CardioLink-7 Randomized Clinical Trial." Dr. Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the journal and its editors. We're your co-host. I'm Dr. Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. Dr. Peder Myhre: And I'm Dr. Peder Myhre, social media editor and doctor at Akershus University Hospital at University of Oslo in Norway. Dr. Carolyn Lam: Peder, I am so excited to be discussing this issue. So many great articles and a feature discussion coming up on the SGLT2 inhibitor, empagliflozin. And do you think it's got effects on left ventricular remodeling in people without diabetes? Very interesting question. Dr. Peder Myhre: That is so interesting, Carolyn. I can't wait to hear this discussion. Dr. Carolyn Lam: Yep, I agree, but we got to wait till we discuss the other papers in today's issue. I want to go first. So we know that non-vitamin K oral anticoagulants, or NOACs, they've become the standard therapy for preventing stroke and ischemic thromboembolism in most patients with atrial fibrillation. But, what is the effectiveness and safety of NOACs in patients on dialysis? That is hemodialysis. The AXADIA-AFNET 8 study sought to test the hypothesis that apixaban would be non-inferior to vitamin K antagonists in these very patients undergoing hemodialysis. Dr. Peder Myhre: Oh wow. This is really a gap of knowledge that we've been waiting to hear more about. NOACs in patients with hemodialysis. Tell us about this trial, Carolyn. Dr. Carolyn Lam: Sure. So this is from corresponding author, Dr. Reinecke, and colleagues, from University of Munster in Germany. And it's an investigator initiated prospective randomized open-blinded outcome assessment of 97 patients with atrial fibrillation on chronic hemodialysis randomized to either apixaban 2.5 mg BID, or a vitamin K antagonist, aiming for an INR between 2 and 3. Over a median follow-up time of 429 days for apixaban, and 506 days for the vitamin K antagonist, the composite primary safety outcome of first, major bleeding, clinically relevant, non-major bleeding, or all cause death, occurred in 46% of patients on apixaban, and 51% of patients on the vitamin K antagonist. That would be a hazard ratio of 0.91, with a p for non-inferiority being 0.157. How about the primary efficacy outcome? While this was a composite of ischemic stroke, all cause death, myocardial infarction, or deep vein thrombosis, and/or pulmonary embolism, and that occurred in 21% of patients on apixaban and 31% of patients on the vitamin K antagonists. Again, no difference when there was testing. So, in summary, Peder, there were no differences in the safety or efficacy observed between apixaban and vitamin K antagonists in patients with atrial fibrillation on chronic hemodialysis. Of note, however, even receiving oral anticoagulations, these patients remain at very high risk of cardiovascular events. So these data really support the consideration of apixaban for prevention of cardiovascular complications in patients with atrial fibrillation on chronic hemodialysis, but larger studies are definitely needed. Dr. Peder Myhre: Oh wow, Carolyn, that is so clinically relevant. And the next paper is also a clinically relevant paper. And it comes to us from the SPRINT authors. And to remind you, the SPRINT study was a study of intensive systolic blood pressure lowering compared to standard blood pressure lowering. And the results demonstrated that there was a robust reduction in both heart failure endpoints and all cause mortality. And in this sub-study that comes to us from corresponding author Jarett Berry from University of Texas Tyler School of Medicine, these authors look at the mechanisms through which intensive blood pressure lowering reduces the risk of these endpoints. And given the important role of cardiac injury and neurohormonal activation in the pathways leading from hypertension to heart failure, and strong association that has been observed between hypertension and levels of cardiac troponin and NT-proBNP, the authors hypothesized that intensive systolic blood pressure lowering would decrease levels of high sensitivity cardiac troponin T and NT-proBNP. Dr. Carolyn Lam: Cool. That's interesting. So how did they do this, and what did they find? Dr. Peder Myhre: So, as expected, Carolyn, the authors found that increases in troponin and NT-proBNP from baseline to 1 year were associated with a higher risk of heart failure and death. And there were really no significant interaction by treatment assignment. But let's look at the changes in troponin. And these results showed that randomization to intensive blood pressure lowering versus standard blood pressure lowering resulted in a significant 3% increase in cardiac troponin T level over 1 year follow up, and a higher proportion of participants with more than 50% increase, and that's with an odds ratio of 1.47. And Carolyn, in contrast, NT-proBNP decreased by 10% in intensive blood pressure arm. And these patients had substantially lower probability of increasing more than 50% in NT-proBNP, with an odds ratio of 0.57 compared to the standard arm. And now, to the most interesting part of this analysis, Carolyn, the association of randomized treatment assignment on changes in troponin was completely attenuated after accounting for changes in eGFR during the follow up, whereas the association of treatment with NT-proBNP changes were completely attenuated after adjusting for changes in systolic blood pressure. So Carolyn, the authors highlight in their discussion the importance of non-cardiac factors influencing variation in cardiac biomarkers, and raise questions about the potential role of cardiac troponin T as a surrogate marker for heart failure or death in blood pressure lowering studies. Dr. Carolyn Lam: Wow, very interesting. Thanks, Peder. Can I tell you now about a preclinical study? Very interesting, because it shows that cardiac inflammation and hypertrophy are regulated by a heart-brain interaction. Dr. Peder Myhre: Wow, Carolyn, a heart-brain interaction. I'm excited to hear more about this. Please explain. Dr. Carolyn Lam: I'd love to, but first some background. Interleukin-1 beta, now that is a pro-inflammatory cytokine that causes cardiac hypertrophy and heart failure. I need to familiarize you with this, the nucleotide-binding domain leucine-rich containing family, pyrin domain-containing-3, NLRP3 for short, which is an inflammasome, which is a cytosolic multiprotein complex that mediates active interleukin-1 beta production. Okay? So you know these terms, and now I want to tell you about the study. This is an elegant series of experiments performed by co-corresponding authors, Dr. Higashikuni, from University of Tokyo, and Dr. Sata, from Tokushima University Graduate School of Medicine, and their colleagues. They first showed that genetic disruption of the NLRP3 inflammasome resulted in significant loss of interleukin-1 beta production, cardiac hypertrophy, and contractile function during pressure overload. Next, a bone marrow transplantation experiment revealed an essential role of NLRP3 inflammasome in cardiac non-immune cells in myocardial interleukin-1 beta production and the cardiac phenotype. It was extracellular ATP released from sympathetic nerve terminals that induced the hypertrophic changes of cardiac cells in an NLRP3 and interleukin-1 beta dependent manner in vitro. And finally, depletion of ATP release from sympathetic efferent nerves, or ablation of cardiac afferent nerves, or a lipophilic beta-blocker, all reduced cardiac extracellular ATP, and inhibited the NLRP3 inflammasome activation, the interleukin-1 beta production, and the adaptive cardiac hypertrophy during pressure overload. So all of this suggests that controlling the neuronal brain signals might have therapeutic potential for the treatment of hypertensive heart disease. Neat, huh? Dr. Peder Myhre: Oh, that is so interesting. The heart and brain interaction. And, Carolyn, we're going to stay in the field of preclinical science. And now we're going to talk about another field that is really interesting, and that is regeneration of cardiomyocytes. Because, Carolyn, developmental cardiac tissue holds remarkable capacity to regenerate after injury, and consists of regenerative mononuclear and deployed cardiomyocytes. Whether reprogramming metabolism promotes persistence of these regenerative mononuclear and deployed cardiomyocytes that enhance cardiac function in repair after injury is unknown. Therefore, these researcher, led by corresponding author, Mohsin Khan, from Temple University School of Medicine, investigated whether the RNA binding protein, LIN28a, which is a master regulator of cellular metabolism, plays a role in cardiac repair following injury. Dr. Carolyn Lam: Wow. That is always, always interesting, regeneration and repair following injury. So what did the authors find? Dr. Peder Myhre: Well, Carolyn, through a number of elegant experiments, the authors made the following key findings. For the first time, they documented a role for RNA binding protein LIN28A in regulating cardiomyocyte turnover in the postnatal and adult heart. And LIN28a overexpression promotes cardiomyocyte cell cycle activity during postnatal development and extends cardiac regenerative ability of the mammalian heart to postnatal day 7. And in the adult heart, the authors could demonstrate that LIN28a drives new myocyte formation, augmenting cardiac structure and function after myocardial injury. And Carolyn, I'm sure you're going to ask the clinical implications of this study. Dr. Carolyn Lam: Indeed. Dr. Peder Myhre: And that is that these results may suggest a novel translational role for LIN28a based strategy to replenish cardiomyocytes in the adult heart after injury. Dr. Carolyn Lam: Very nice, Peder. Thank you. Also in the issue is a Research Letter by Dr. Bick on interleukin-6 receptor polymorphism attenuates clonal hematopoiesis mediated coronary artery disease risk among many individuals in the UK Biobank. There's also Cardiology News by Tracy Hampton, where she highlights few really interesting things, like aging cardiomyocytes accumulate new genetic mutations that was published in Nature Aging, cytokines promote tissue repair after a heart attack in mice, and that was published in Science, and scientists identifying molecular alterations in a failing heart at a single cell resolution, which was published in Nature. Dr. Peder Myhre: And there are a couple of other papers also in this issue, Carolyn. And there's first, an exchange of letters by Drs. Halushka, Lu, and Mayr, regarding the article "Circulating MicroRNA-122-5p is Associated with a Lack of Improvement in Left Ventricular Function after TAVR and Regulates Viability of Cardiomyocytes Through Extracellular Vesicles." And finally, we have an "On My Mind" piece by doctors Monda and Limongelli entitled "An Integrated Sudden Cardiac Risk Prediction Model for Patients with Hypertrophic Cardiomyopathy." Dr. Carolyn Lam: Oh, nice. Nice full issue. Thank you, Peder. Let's go to our feature discussion now. Shall we? Dr. Peder Myhre: Let's go. Dr. Greg Hundley: Welcome listeners to this feature discussion on January 24th. And we have with us Dr. Subodh Verma, from St. Michael's University in Toronto, Canada. And a guest editor, Dr. Christopher Granger, from Duke University in Durham, North Carolina. Welcome gentlemen. Well, Subodh, we will start with you. Can you describe for us some of the background information that went into the preparation of your study, and what was the hypothesis that you wanted to address? Dr. Subodh Verma: First, my great pleasure to be here, and thank you very much for the opportunity to discuss this paper with your viewers. As you know, SGLT2 inhibitors have been truly transformative therapies. From a heart failure perspective, we know that they prevent incident heart failure in people with diabetes who have vascular disease or risk factors. They also have been shown to treat prevalent heart failure in people with heart failure and either a reduced, mildly reduced, or preserved ejection fraction independent of glycemic status. And really, these have been the basis of very strong recommendations to use these agents in the prevention of heart failure in people with diabetes, and also in the treatment of prevalent heart failure in people with and without diabetes. Now, the fact that these drugs have such broad effects in people with heart failure has led to a theory that maybe these drugs could be introduced earlier on in the natural history of heart failure in people who neither have diabetes nor have significant heart failure, the so-called sort of stage A or stage B patient. But there really have been no clinical trials evaluating this question. There've been a lot of translational randomized trials that have provided some mechanistic insights about LV remodeling in people with diabetes or in people with prevalent heart failure. And we hypothesized that maybe the first step to evaluate whether SGLT2 inhibitors may have favorable effects on cardiac remodeling in people without diabetes or without heart failure would be to conduct a randomized double-blind control trial looking at indices of left ventricular remodeling in a population that I've just described. Dr. Greg Hundley: Very nice, Subodh. So you've started us into your study design. Maybe describe that a little more fully, and then who was included in your study population? Dr. Subodh Verma: So EMPA-HEART 2 CardioLink was a multi-center double-blind placebo control randomized trial in which we studied the effects of empagliflozin, an SGLT2 inhibitor, at a dose of 10 mg per day versus placebo in people who did not have type 2 diabetes or significant heart failure. We included people who were adults between the age of 40 and 80 who met 1 of 2 entry criteria. Either they had to have one major criteria, which was an increase in left ventricular mass index by specific echo criteria or MRI criteria, or they could have increased LVH as identified by ECG or by intraventricular septal or posterior wall thickness. They could also get in if they had resistant hypertension, hypertension despite being on 3 antihypertensive agents, or the second strata was entry through 2 minor criteria, which included a history of myocardial infarction, a GFR between 30 or 60, or evidence of overweight or obesity. Dr. Greg Hundley: And how many subjects did you randomize? Dr. Subodh Verma: So we randomized, of the 318 that we screened, 169 were randomized to receive empagliflozin 10 mg or a placebo. Patients had a baseline cardiac MRI done, and then the exposure was 6 months. They had a follow-up MRI at the end of 6 months. And the primary outcome measure was a 6-month change in left ventricular mass index from baseline to 6 months between the two groups. Dr. Greg Hundley: Very nice. And so , Subodh, can you describe for us now, what did you find? What were your study results? Dr. Subodh Verma: So, first and foremost, what we found in terms of baseline characteristics was that we enrolled a population of people with a mean age of around 60 with a BMI of around 30 kg/m2, predominantly men, about 80% or so were men. These were patients who did not have significant heart failure. The NT-proBNP at baseline was around 50 pg/mL. The eGFR was around 80 mL/minute, and the vast majority of these patients actually had a history of hypertension. Of course, none of them had diabetes by definition. The hemoglobin A1C was around 5.8%. Now what we found was, despite the fact that we went after patients who we thought would be enriched for a baseline increase in LV mass indices, the baseline LV mass index was mildly elevated, was around 63 g/m2. And over the course of 6 months, we did not find any significant difference in terms of LV mass regression between the placebo and empagliflozin groups. In fact, the adjusted treatment effect was minus 0.30 g/m2, which was not statistically significant. No other differences were found in terms of other indices of a remodeling, including left ventricular and diastolic or end systolic volume indices or in terms of left ventricular ejection fraction. There was a 2% increase in ejection fraction, and the p-value for that was 0.07, but really was not statistically significant. Dr. Greg Hundley: And very nice. And realizing that women may have smaller LV masses, any stratified analysis that evaluated effects on men versus women? And then what about, perhaps in the higher quartile versus lower quartile, of age? Dr. Subodh Verma: Right. So, Greg, we actually did look at various subgroups and covariates, including gender, including age. And age or gender did not really influence the overall result that we obtained. There was really a neutral result in empagliflozin, irrespective of these 2 covariates. We also looked at baseline blood pressure, baseline NT-proBNP, LV mass indices, the presence or absence of heart failure, chronic kidney disease. So for the covariates that we have evaluated over a short term of 6 months in this relatively low risk population, we did not find any heterogeneity the result, per se. Dr. Greg Hundley: Very good. Well, Subodh, thank you so much for that beautiful presentation. And listeners, now we're going to turn to our guest editor, Dr. Chris Granger. And Chris is an expert in the field of heart failure. Also, a lot of familiarity with HFpEF, which sounds a little bit, we're looking at precursors. We don't have HFpEF yet, but maybe trying to inhibit this from happening using empagliflozin. How do you put these results in the context with other studies that have emphasized utilizing SGLT2 inhibitors in patients with sort of a preserved ejection fraction and absence of diabetes? Dr. Christopher Granger: Yeah. Well thanks, Greg. And again, congratulations, Subodh, to your study. And I think you framed some of the context here as these drugs, the SGLT2 inhibitors, as being transformative, which I think is exactly right. And it's such a fascinating story. Right? These drugs, which we thought originally, with their cause of glucose spilling in the urine, and a modest decrease in blood glucose, might have a role for modestly improving glucose control in diabetes. And low and behold, they've turned out to be one of the great stories I think in recent, across all of medicine, in terms of their consistent and substantial improving clinical outcomes for patients with heart failure, with diabetes and cardiovascular disease, and now even kidney protection, and much broader implications. And their well tolerated, and they don't have dose titration. So there's some practical appeal to this class of drugs in terms of their benefits, in terms of clinical outcomes. But we're left with having this amazing evidence-based generated without really understanding why are these drugs so effective? And what are they doing? And you've provided, I think, an important piece to the puzzle. We did have the data from patients with diabetes and heart failure, with diabetes and left ventricular hypertrophy, that there is a modest reduce in LV mass with SGLT2 inhibitors. And what you've shown is that for patients that with mild LVH, with risk for LVH, that we simply don't see a substantial reduction in LV mass with the use of these drugs. So I think that provides this evidence that that's not a major cause of benefit, at least in this earlier phase of development of heart failure. And I think it really underscores the fact that there's a lot of work to do still to understand. We know that the renal effects are obvious place that these drugs have such an important benefit. And then the linkage of renal disease and cardiac performance is one of the areas, I think, that's a very exciting aspect of a probable contribution of the mechanism of these drugs. But I think in the end, we're left with still not really understanding why these drugs are so beneficial. But understanding that, I think, will be important, both for opening new avenues of targeting pathways, as well as being able to tell the clinical community, okay, you have these important benefits, but people do want to also know why are we seeing these benefits. Dr. Greg Hundley: Very nice. Well, listeners, we're going to turn back to Dr. Verma here. Subodh, what do you see is the next study to be performed in this sphere of research? Dr. Subodh Verma: Well, first, my thanks to Professor Granger, Chris, for handling this paper and for his very thoughtful comments. And he's absolutely right. We have such wonderful clinical data, and these results, of course, should not in any way take away from the importance of using empagliflozin or other SGLT2 inhibitors in the prevention of heart failure in people with diabetes, or in the treatment of HFpEF or HFrEF. But we're struggling with trying to understand what is the dominant mechanism of action here. And, in the previous precursor to EMPA-HEART 2, we did EMPA-HEART 1 in people with diabetes, and we saw a modest effect that was statistically significant of reduction in LV mass index. And we did not see this, of course, in a lower risk population without diabetes. And that tells me that remodeling may be occurring to a modest effect, it may require a longer time to actually show its benefits, but that this is unlikely a dominant sort of mechanism through which these drugs are working. And I do share Chris's thoughts that one of the key mechanisms of benefit that needs to be further explored is looking at the renal cardiac axes. We know that these drugs are profoundly renal protective, and that the benefits may actually be secondary to improvements in renal hemodynamics, improvements in renal function. And I think that is a population that needs to be, that's a mechanism that needs to be studied further. So I think the next generation of translational mechanistic studies need to really tease out the renal cardiac axes, maybe tease out populations that are at risk but have more significant left ventricular hypertrophy, maybe evaluate patients for a longer duration of treatment, or select people who truly have significant hypertension at baseline. I think those are groups and questions that need further exploration. And, of course, the translational science needs to be also studied in the context of larger completed clinical trials, where biomarkers are currently available and they can be linked, of course, to the outcomes in those trials. So those are some of my thoughts as to where the field could move towards. Dr. Greg Hundley: Very nice. And Chris, do you have anything to add? Dr. Christopher Granger: Subodh, I think that was a great summary. And I might just make a comment on the other end of the spectrum. That is, we have these drugs and the evidence of their benefit, and yet they're grossly underused in the populations that have proven to have benefit. Now it takes some time to educate, to get people familiar with, and get them to integrate these treatments into practice, but there's an enormous opportunity, and I think there is a linkage here. I think when people understand the mechanism, and when they're thoughtful about how these drugs may be working, that that really helps to make the case that the drug should be used, and that people are on board with using them. So I think there's this linkage here, there's the need to both better understand mechanism, and there's the need to have systems of care where these treatments are integrated to provide the benefit that's been so clearly shown in the randomized trials. Dr. Greg Hundley: Very nice. Well, listeners, we want to thank Dr. Subodh Verma, from St. Michael's University in Toronto, and our guest editor, Dr. Chris Granger, from Duke University in Durham, North Carolina, for bringing this paper highlighting that among people with neither diabetes nor significant heart failure but with risk factors for adverse cardiac remodeling, that SGLT2 inhibition with empagliflozin did not, did not, result in a meaningful reduction in LV mass index after 6 months. Well, on behalf of Carolyn, Peder, and myself, we want to wish you a great week, and we will catch you next week on the run. This program is copyright of the American Heart Association 2023. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more, please visit ahajournals.org.
ECG Diagnosis of Left Ventricular Hypertrophy Guest: Ljuba Bacharova, M.D., D.Sc, M.B.A. Hosts: Anthony H. Kashou, M.D. (@anthonykashoumd) Joining us today to discuss the diagnosis of left ventricular hypertrophy (LVH) by means of the ECG is Ljuba Bacharova, senior researcher in the International Laser Centre, CVTI, in Bratislava, Slovakia and instructor at Comenius University's Medical School. Dr. Bacharova's main focus in research has been in the evaluation of the cardiac electric field with a special interest in left ventricular hypertrophy. Tune in today to learn more about the ECG and LVH. Specific topics discussed: What do you see as the major problem in ECG-LVH diagnosis? And why is it still interesting/ actual? What are other key factors influencing the resultant QRS voltage in LVH? Thoughts around relative high specificity in ECG diagnosis of LVH. How to escape from the mental high-QRS-voltage trap in LVH diagnosis. Connect with Mayo Clinic's Cardiovascular Continuing Medical Education online at https://cveducation.mayo.edu or on Twitter @MayoClinicCV and @MayoCVservices. Facebook: MayoCVservices LinkedIn: Mayo Clinic Cardiovascular Services NEW Cardiovascular Education App: The Mayo Clinic Cardiovascular CME App is an innovative educational platform that features cardiology-focused continuing medical education wherever and whenever you need it. Use this app to access other free content and browse upcoming courses. Download it for free in Apple or Google stores today! No CME credit offered for this episode. Podcast episode transcript found here.
It's another session of CardioNerds Rounds! In these rounds, Dr. Loie Farina (Advanced Heart Failure and Transplant Fellow at Northwestern University) joins Dr. Jane Wilcox (Chief of the Section of Heart Failure Treatment and Recovery at Northwestern University) to discuss the nuances of HFpEF diagnosis and management. Dr. Wilcox is also the Associate Director of the T1 Center for Cardiovascular Therapeutics in the Bluhm Cardiovascular Institute and Director of the Myocardial Recovery Clinic at Northwestern University. Dr. Wilcox is a prolific researcher, clinician, and thought leader in Heart Failure and we are honored to have her on CardioNerds Rounds! Notes were drafted by Dr. Karan Desai. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. Speaker disclosures: None Challenging Cases - Atrial Fibrillation with Dr. Hugh Calkins CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes - Antithrombotic Management with Dr. Deepak Bhatt Case #1 Synopsis: A woman in her 80s with a history of HFpEF presented with worsening dyspnea on exertion over the course of a year but significantly worsening over the past two months. Her other history includes prior breast cancer with chemotherapy and radiation therapy, permanent atrial fibrillation with AV node ablation and CRT-P, and CKD Stage III. She presented for an outpatient RHC with exercise to further characterize her HFpEF. Her echo showed normal LV size, no LVH, LVEF of 50%, decreased RV systolic function, severe left atrial enlargement, significantly elevated E/e' and mild MR. Right heart catheterization showed moderately elevated bi-ventricular filling pressures at rest but with passive leg raise and Stage 1 exercise the wedge pressure rose significantly. We were asked to comment on management. Case #1 Takeaways Amongst the things that were discussed were the role of specific therapies in symptomatic patients with HFpEF. In patients with HFpEF and documented congestion, they will require diuretic therapy for symptomatic relief. But in addition to diuretic therapy, we discussed starting HFpEF-specific therapies. Amongst, those specific therapies mineralocorticoid receptor antagonist (MRA) and sodium-glucose co-transporter 2 (SGLT2) inhibitor. In multiple trials that have included patients with HFPEF, SGLT2i have reduced the risk of hospitalization. This includes the EMPEROR-PRESERVED Trial (see the CardioNerds Journal Club discussion on the trial) in which nearly 6000 patients with NYHA Class II-IV symptoms, EF > 40% and elevated NT-proBNP with a prior HF hospitalization within the past 12 months were randomized to Empagliflozin or placebo. The primary outcome – death from CV causes or hospitalization for Heart Failure – was significantly lower in the SGLT2i arm (13.8% vs 17.1%, 95% CI 0.69-0.90, P 45% to receive either spironolactone or placebo. The primary endpoint (death from CV cause, aborted cardiac arrest, or hospitalization for HF) was not statistically different between treatment arms. Of note, however, there were concerns for regional differences which is outlined well in this NEJM Evidence piece. Case #2 Synopsis: A woman in her 70s with history of hypertension, obesity,
LiveHire (ASX: LVH) CEO and executive director Christy Forest joins Small Caps to discuss the ongoing growth of the company's globally awarded recruitment, talent mobility and direct sourcing software platform. The human resources technology company recently posted a record performance in the Australia-Pacific region, along with accelerated growth in the North American market. Ms Forest says North America is a huge market ripe for disruption for its talent recruitment technology, which attracts quality personnel, while reducing hire costs and shortening position filling times. Articles:https://smallcaps.com.au/livehire-appoints-financial-expert-board-of-directors/ https://smallcaps.com.au/livehire-provide-recruitment-platform-fortune-500-oil-gas-company/ For more information on LiveHire:https://smallcaps.com.au/stocks/LVH/See omnystudio.com/listener for privacy information.
Computerized Left Ventricular Hypertrophy Detection Guest: Bob Farrell, Ph.D. Hosts: Anthony H. Kashou, M.D. (@anthonykashoumd) When the heart in the human body's source to pump blood has decreased, it is referred to as the left ventricle. Furthermore, the hypertrophy or the heart's wall eventually loses its firmness, which leads to a higher risk of hypertension or high blood pressure. Often, the heart tends to lose its ability to pump blood. In addition, some signs to stay aware of are feeling fatigued, dizziness, fainting, and frequent chest pain. Patients affected by Left Ventricular Hypertrophy are more at risk of becoming diagnosed if they experience decreased or increased heart rhythm signals or congestive heart failure. Therefore, when the doctor recommends testing, an Electrocardiogram is used to record signals to test the heart rhythm and abnormalities. In addition, an MRI or Echocardiogram is used to test Computerized Left Ventricular Hypertrophy as well. Joining us today to discuss Computerized Left Ventricular Hypertrophy Detection is Bob Farrell, M.D., professor of medicine at Queen's University in Kingston, Ontario, Canada. Furthermore, Dr. Farrell is currently a member of the board of directors of the International Society of Computerized Electrocardiology. Specific topics discussed: With other modalities available to clinicians (e.g., echo, cardiac MR), is ECG still relevant in the discussion of LVH? You have recently made some updates in the GE “12SL” program related to LVH. What drove the changes that you made? Customer feedback, opaqueness of the criteria, ACC/AHA recommendations to manufacturers So what were the changes you made? How did you pick which of the many criteria out there to use and how important was it to explicitly list the positive criteria in the interpretation? You mentioned earlier that ECG-LVH is an entity in its own right and is associated with poorer outcomes. Can you talk about ECG-LVH and risk prediction, and how the changes you've made in the GE 12SL program aid in the risk prediction? Connect with Mayo Clinic's Cardiovascular Continuing Medical Education online at https://cveducation.mayo.edu or on Twitter @MayoClinicCV and @MayoCVservices. Facebook: MayoCVservices LinkedIn: Mayo Clinic Cardiovascular Services NEW Cardiovascular Education App: The Mayo Clinic Cardiovascular CME App is an innovative educational platform that features cardiology-focused continuing medical education wherever and whenever you need it. Use this app to access other free content and browse upcoming courses. Download it for free in Apple or Google stores today! No CME credit offered for this episode. Podcast episode transcript found here.
The JournalFeed podcast for the week of July 18-22, 2022. These are summaries from just 2 of the 5 article we cover every week! For access to more, please visit JournalFeed.org for details about becoming a member. Very Sensitive Trops Spoon Feed A single high sensitivity cardiac troponin T (hs-cTnT) measurement* less than the limit of quantitation (the lowest reportable concentration) appears to be sufficient in ruling out acute MI in a low risk population. Seaman's Sign Spoon Feed: The Seamens' Sign performs better than commonly used criteria for ruling in left ventricular hypertrophy (LVH) by ECG.
DEAR DR. ROACH: What is the difference between eccentric LVH and concentric LVH? Which one is more dangerous and needs more attention? My mother was diagnosed with severe eccentric LVH for body surface area with adequate systolic and diastolic functions. What does that mean? — C.F. ANSWER: The left ventricle is the chamber of the heart that pumps blood to the entire body, except for through the lungs; that is the job of the right ventricle. When the job is too hard, usually because of high blood pressure, the left ventricle hypertrophies, meaning its walls get thicker as a response...Article Link
Merhaba arkadaşlar, bu yazımda sizlere hipertansif akut kalp yetmezliğinde (AKY) yüksek doz IV nitratların rolünün değerlendirildiği bir makaleden bahsedeceğim. Makalenin tamamına buradan ulaşabilirsiniz. Öncelikle, yüz kişiye 'IV nitrogliserini hipertansif AKY'de nasıl kullanırsınız?' diye sordum ama popüler bir cevap alamadım. '10 µg/dk dan başlarım, 5 dk'da bir kontrol ederim, düşmezse iki katına çıkarım' diyen oldu, '5 µg/dk dan başlarım, öncesinde 2 mg puşe de yaparım' diyen oldu, '2 mg puşe yaparım, yüksek dozdan infüzyon da açarım, düşmezse araya tekrar puşe de girerim' diyen oldu, “Primum non nocere” demiş Hipokrat, yüksek doz riskine girmem, standart dozdan başlarım.' diyen de oldu. Her yiğidin yoğurt yiyişi farklı fakat kılavuz bu konuda ne önermiş hatırlayalım; İntravenöz vazodilatörler, yani nitratlar veya nitroprussid, venöz ve arteriyel damarları genişleterek kalbe venöz dönüşün azalmasına, daha az sıkışıklığa, daha düşük afterload, artan atım hacmine ve bunun sonucunda semptomların azalmasına neden olur. Nitratlar esas olarak periferik damarlar üzerinde etkilidir, oysa nitroprussid daha dengeli bir arteriyel ve venöz dilatatördür. Akut pulmoner ödeme; artmış afterload ve akciğerlere sıvı birikiminin neden olduğu hastalara etki mekanizmaları nedeniyle IV vazodilatörler diüretiklerden daha etkili olabilir. Erken, yoğun ve sürekli verilen IV vazodilatörlerin yüksek doz diüretiklere karşı yararlı etkisi gösterilememiştir. SKB >110 mm Hg olduğunda AKY semptomlarını hafifletmek için intravenöz vazodilatörler düşünülebilir. Klinik iyileşme ve KB kontrolünü sağlamak için düşük dozlarda başlanıp, titre edilebilirler. Nitratlar genellikle bir ilk bolus ve ardından sürekli infüzyon ile uygulanır. Ancak tekrarlayan boluslar olarak da verilebilirler. Akut pulmoner ödemi olan şiddetli hipertansif hastalarda nitrogliserin 1-2 mg bolus olarak verilebilir. Ön yükte ve art yükte aşırı azalmaya bağlı hipotansiyon oluşmamasına özen gösterilmelidir. Bu nedenle LVH (sol ventrikül hipertrofisi) veya ciddi aort darlığı olan hastalarda çok dikkatli kullanılmalıdırlar. Bununla birlikte, hemodinamik parametreler dikkatle izlenerek vazodilatörler verildiğinde, LV (sol ventrikül) sistolik disfonksiyonu ve aort stenozu olan hastalarda olumlu etkiler tanımlanmıştır. 2021 ESC kılavuzu akut kalp yetmezliği bölümünü daha önce sizlerle paylaşmıştık. Makaleye gelecek olursak; İki randomize kontrollü çalışma, üç prospektif çalışma, iki retrospektif çalışma, iki vaka serisi ve bir vaka raporunun incelenmesiyle yazılmış olan makalede; yüksek doz nitratlar IV bolus ve IV infüzyon şeklinde uygulanmış, fakat çalışmada kullanılan dozlar arasında önemli ölçüde farklılık görülmüş. Çalışmaların heterojenliği nedeniyle yüksek doz nitrat kullanımıyla ilgili güçlü sonuçlar sınırlı ancak mevcut literatürden elde edilen kanıt düzeyine dayalı öneriler sunulmuş. Heterojenlikten kastımız şu; Nashed ve arkadaşlarının çalışmasında bolus dozlar klinisyenlerin yaklaşımına göre değişkenlik göstermiş, Cotter ve arkadaşlarının çalışması yüksek doz furosemid ve düşük doz nitrogliserin tedavisini, yüksek doz nitrogliserin tedavisi ile karşılaştırmış. Sharon ve arkadaşları yüksek doz nitrat tedavisi alan hastaları, standart doz nitrat ve BİPAP tedavisi uygulanan hastalarla karşılaştırmış. Wilson ve arkadaşları, 395 hastayı retrospektif olarak incelemişler; yüksek doz nitrogliserin alan ve devamlı nitrogliserin infüzyonu alan hastaları karşılaştırmışlar. İntravenöz bolus dozları, her 3 ila 5 dakikada bir 2 mg'a kadar artışlarla uygulanmış, devamlı nitrogliserin infüzyonu alan hastaların dozları ve titrasyon parametreleri ise doktorun takdirine göre belirlenmiş. Hsieh ve arkadaşlarının yüksek doz nitrogliserin ve BİPAP tedavisini başarıyla kullandığı 3 vakasında; hastalara BİPAP başlanmış ve dispne düzelene kadar her 2 dakikada bir 1 mg bolus nitrogliserin verilmiş; toplam dozlar 3-6 mg arasında olup bir hastaya yüksek doz nitrogliseri...
Ann-Marie Hosang Archer is the founder and CEO of Mauritian-based Lignum Vitae Health Africa (LVH) and the founder of LVH International Ltd based in South Africa. Ann-Marie started LVH after 23 years in the pharmaceutical industry with Eli Lilly pharmaceuticals serving in senior leadership positions in Central America, the Caribbean, Brazil, and South Africa. She is also an angel investor with Future Females Invest (FFI).What you will learn from this episode: Mentorship is important for women entrepreneurs to thrive in addition to funding and FFI Angels provides both to its portfolio companies. Sharing knowledge and experience is a value-add to investing. Not to be afraid of fundraising but the process will be hard and you have to do your research and do the work that is required to fundraise Women +Health = Wealth and Healthy women make healthy economies Get in touch with FFI Angels if you are an African female founder (or a non-Africa-based female founder with a business that serves the African market) looking for seed capital, business, and moral support to help you grow and scale your business. Thanks for joining us for another episode of the WTF podcast.If you would like to be a guest or sponsor the podcast, please contact us at whereisthefunding@gmail.com.Where to find us: Anchor, Apple Podcasts, Google Play, Spotify, or wherever you get your podcasts.Help us grow: Please subscribe, stream or download, leave a rating or review and share your favorite episodes with family, friends, and colleagues.Social Media: Follow the WTF podcast on Instagram.Follow Michelle on LinkedIn: Michelle J. McKenzieJoin us for the next episode!
Ann-Marie Hosang Archer is the founder and CEO of Mauritian-based Lignum Vitae Health Africa (LVH) and the founder of LVH International Ltd based in South Africa. Ann-Marie started LVH after 23 years in the pharmaceutical industry with Eli Lilly pharmaceuticals serving in senior leadership positions in Central America, the Caribbean, Brazil, and South Africa. She is also an angel investor with Future Females Invest (FFI).What you will learn from this episode: Mentorship is important for women entrepreneurs to thrive in addition to funding and FFI Angels provides both to its portfolio companies. Sharing knowledge and experience is a value-add to investing. Not to be afraid of fundraising but the process will be hard and you have to do your research and do the work that is required to fundraise Women +Health = Wealth and Healthy women make healthy economies Get in touch with FFI Angels if you are an African female founder (or a non-Africa-based female founder with a business that serves the African market) looking for seed capital, business, and moral support to help you grow and scale your business. Thanks for joining us for another episode of the WTF podcast.If you would like to be a guest or sponsor the podcast, please contact us at whereisthefunding@gmail.com.Where to find us: Anchor, Apple Podcasts, Google Play, Spotify, or wherever you get your podcasts.Help us grow: Please subscribe, stream or download, leave a rating or review and share your favorite episodes with family, friends, and colleagues.Social Media: Follow the WTF podcast on Instagram.Follow Michelle on LinkedIn: Michelle J. McKenzieJoin us for the next episode!
Ann-Marie Hosang Archer is the founder and CEO of Mauritian-based Lignum Vitae Health Africa (LVH) and the founder of LVH International Ltd based in South Africa. Ann-Marie started LVH after 23 years in the pharmaceutical industry with Eli Lilly pharmaceuticals serving in senior leadership positions in Central America, the Caribbean, Brazil, and South Africa. She is also an angel investor with Future Females Invest (FFI).What you will learn from this episode: Mentorship is important for women entrepreneurs to thrive in addition to funding and FFI Angels provides both to its portfolio companies. Sharing knowledge and experience is a value-add to investing. Not to be afraid of fundraising but the process will be hard and you have to do your research and do the work that is required to fundraise Women +Health = Wealth and Healthy women make healthy economies Get in touch with FFI Angels if you are an African female founder (or a non-Africa-based female founder with a business that serves the African market) looking for seed capital, business, and moral support to help you grow and scale your business. Thanks for joining us for another episode of the WTF podcast.If you would like to be a guest or sponsor the podcast, please contact us at whereisthefunding@gmail.com.Where to find us: Anchor, Apple Podcasts, Google Play, Spotify, or wherever you get your podcasts.Help us grow: Please subscribe, stream or download, leave a rating or review and share your favorite episodes with family, friends, and colleagues.Social Media: Follow the WTF podcast on Instagram.Follow Michelle on LinkedIn: Michelle J. McKenzieJoin us for the next episode!
Ann-Marie Hosang Archer is the founder and CEO of Mauritian-based Lignum Vitae Health Africa (LVH) and the founder of LVH International Ltd based in South Africa. Ann-Marie started LVH after 23 years in the pharmaceutical industry with Eli Lilly pharmaceuticals serving in senior leadership positions in Central America, the Caribbean, Brazil, and South Africa. She is also an angel investor with Future Females Invest (FFI).What you will learn from this episode: Mentorship is important for women entrepreneurs to thrive in addition to funding and FFI Angels provides both to its portfolio companies. Sharing knowledge and experience is a value-add to investing. Not to be afraid of fundraising but the process will be hard and you have to do your research and do the work that is required to fundraise Women +Health = Wealth and Healthy women make healthy economies Get in touch with FFI Angels if you are an African female founder (or a non-Africa-based female founder with a business that serves the African market) looking for seed capital, business, and moral support to help you grow and scale your business. Thanks for joining us for another episode of the WTF podcast.If you would like to be a guest or sponsor the podcast, please contact us at whereisthefunding@gmail.com.Where to find us: Anchor, Apple Podcasts, Google Play, Spotify, or wherever you get your podcasts.Help us grow: Please subscribe, stream or download, leave a rating or review and share your favorite episodes with family, friends, and colleagues.Social Media: Follow the WTF podcast on Instagram.Follow Michelle on LinkedIn: Michelle J. McKenzieJoin us for the next episode!
Ann-Marie Hosang Archer is the founder and CEO of Mauritian-based Lignum Vitae Health Africa (LVH) and the founder of LVH International Ltd based in South Africa. Ann-Marie started LVH after 23 years in the pharmaceutical industry with Eli Lilly pharmaceuticals serving in senior leadership positions in Central America, the Caribbean, Brazil, and South Africa. She is also an angel investor with Future Females Invest (FFI).What you will learn from this episode: Mentorship is important for women entrepreneurs to thrive in addition to funding and FFI Angels provides both to its portfolio companies. Sharing knowledge and experience is a value-add to investing. Not to be afraid of fundraising but the process will be hard and you have to do your research and do the work that is required to fundraise Women +Health = Wealth and Healthy women make healthy economies Get in touch with FFI Angels if you are an African female founder (or a non-Africa-based female founder with a business that serves the African market) looking for seed capital, business, and moral support to help you grow and scale your business. Thanks for joining us for another episode of the WTF podcast.If you would like to be a guest or sponsor the podcast, please contact us at whereisthefunding@gmail.com.Where to find us: Anchor, Apple Podcasts, Google Play, Spotify, or wherever you get your podcasts.Help us grow: Please subscribe, stream or download, leave a rating or review and share your favorite episodes with family, friends, and colleagues.Social Media: Follow the WTF podcast on Instagram.Follow Michelle on LinkedIn: Michelle J. McKenzieJoin us for the next episode!
Ann-Marie Hosang Archer is the founder and CEO of Mauritian-based Lignum Vitae Health Africa (LVH) and the founder of LVH International Ltd based in South Africa. Ann-Marie started LVH after 23 years in the pharmaceutical industry with Eli Lilly pharmaceuticals serving in senior leadership positions in Central America, the Caribbean, Brazil, and South Africa. She is also an angel investor with Future Females Invest (FFI).What you will learn from this episode: Mentorship is important for women entrepreneurs to thrive in addition to funding and FFI Angels provides both to its portfolio companies. Sharing knowledge and experience is a value-add to investing. Not to be afraid of fundraising but the process will be hard and you have to do your research and do the work that is required to fundraise Women +Health = Wealth and Healthy women make healthy economies Get in touch with FFI Angels if you are an African female founder (or a non-Africa-based female founder with a business that serves the African market) looking for seed capital, business, and moral support to help you grow and scale your business. Thanks for joining us for another episode of the WTF podcast.If you would like to be a guest or sponsor the podcast, please contact us at whereisthefunding@gmail.com.Where to find us: Anchor, Apple Podcasts, Google Play, Spotify, or wherever you get your podcasts.Help us grow: Please subscribe, stream or download, leave a rating or review and share your favorite episodes with family, friends, and colleagues.Social Media: Follow the WTF podcast on Instagram.Follow Michelle on LinkedIn: Michelle J. McKenzieJoin us for the next episode!
Ann-Marie Hosang Archer is the founder and CEO of Mauritian-based Lignum Vitae Health Africa (LVH) and the founder of LVH International Ltd based in South Africa. Ann-Marie started LVH after 23 years in the pharmaceutical industry with Eli Lilly pharmaceuticals serving in senior leadership positions in Central America, the Caribbean, Brazil, and South Africa. She is also an angel investor with Future Females Invest (FFI).What you will learn from this episode: Mentorship is important for women entrepreneurs to thrive in addition to funding and FFI Angels provides both to its portfolio companies. Sharing knowledge and experience is a value-add to investing. Not to be afraid of fundraising but the process will be hard and you have to do your research and do the work that is required to fundraise Women +Health = Wealth and Healthy women make healthy economies Get in touch with FFI Angels if you are an African female founder (or a non-Africa-based female founder with a business that serves the African market) looking for seed capital, business, and moral support to help you grow and scale your business. Thanks for joining us for another episode of the WTF podcast.If you would like to be a guest or sponsor the podcast, please contact us at whereisthefunding@gmail.com.Where to find us: Anchor, Apple Podcasts, Google Play, Spotify, or wherever you get your podcasts.Help us grow: Please subscribe, stream or download, leave a rating or review and share your favorite episodes with family, friends, and colleagues.Social Media: Follow the WTF podcast on Instagram.Follow Michelle on LinkedIn: Michelle J. McKenzieJoin us for the next episode!
Ann-Marie Hosang Archer is the founder and CEO of Mauritian-based Lignum Vitae Health Africa (LVH) and the founder of LVH International Ltd based in South Africa. Ann-Marie started LVH after 23 years in the pharmaceutical industry with Eli Lilly pharmaceuticals serving in senior leadership positions in Central America, the Caribbean, Brazil, and South Africa. She is also an angel investor with Future Females Invest (FFI).What you will learn from this episode: Mentorship is important for women entrepreneurs to thrive in addition to funding and FFI Angels provides both to its portfolio companies. Sharing knowledge and experience is a value-add to investing. Not to be afraid of fundraising but the process will be hard and you have to do your research and do the work that is required to fundraise Women +Health = Wealth and Healthy women make healthy economies Get in touch with FFI Angels if you are an African female founder (or a non-Africa-based female founder with a business that serves the African market) looking for seed capital, business, and moral support to help you grow and scale your business. Thanks for joining us for another episode of the WTF podcast.If you would like to be a guest or sponsor the podcast, please contact us at whereisthefunding@gmail.com.Where to find us: Anchor, Apple Podcasts, Google Play, Spotify, or wherever you get your podcasts.Help us grow: Please subscribe, stream or download, leave a rating or review and share your favorite episodes with family, friends, and colleagues.Social Media: Follow the WTF podcast on Instagram.Follow Michelle on LinkedIn: Michelle J. McKenzieJoin us for the next episode!
Ann-Marie Hosang Archer is the founder and CEO of Mauritian-based Lignum Vitae Health Africa (LVH) and the founder of LVH International Ltd based in South Africa. Ann-Marie started LVH after 23 years in the pharmaceutical industry with Eli Lilly pharmaceuticals serving in senior leadership positions in Central America, the Caribbean, Brazil, and South Africa. She is also an angel investor with Future Females Invest (FFI).What you will learn from this episode: Mentorship is important for women entrepreneurs to thrive in addition to funding and FFI Angels provides both to its portfolio companies. Sharing knowledge and experience is a value-add to investing. Not to be afraid of fundraising but the process will be hard and you have to do your research and do the work that is required to fundraise Women +Health = Wealth and Healthy women make healthy economies Get in touch with FFI Angels if you are an African female founder (or a non-Africa-based female founder with a business that serves the African market) looking for seed capital, business, and moral support to help you grow and scale your business. Thanks for joining us for another episode of the WTF podcast.If you would like to be a guest or sponsor the podcast, please contact us at whereisthefunding@gmail.com.Where to find us: Anchor, Apple Podcasts, Google Play, Spotify, or wherever you get your podcasts.Help us grow: Please subscribe, stream or download, leave a rating or review and share your favorite episodes with family, friends, and colleagues.Social Media: Follow the WTF podcast on Instagram.Follow Michelle on LinkedIn: Michelle J. McKenzieJoin us for the next episode!
Ann-Marie Hosang Archer is the founder and CEO of Mauritian-based Lignum Vitae Health Africa (LVH) and the founder of LVH International Ltd based in South Africa. Ann-Marie started LVH after 23 years in the pharmaceutical industry with Eli Lilly pharmaceuticals serving in senior leadership positions in Central America, the Caribbean, Brazil, and South Africa. She is also an angel investor with Future Females Invest (FFI).What you will learn from this episode: Mentorship is important for women entrepreneurs to thrive in addition to funding and FFI Angels provides both to its portfolio companies. Sharing knowledge and experience is a value-add to investing. Not to be afraid of fundraising but the process will be hard and you have to do your research and do the work that is required to fundraise Women +Health = Wealth and Healthy women make healthy economies Get in touch with FFI Angels if you are an African female founder (or a non-Africa-based female founder with a business that serves the African market) looking for seed capital, business, and moral support to help you grow and scale your business. Thanks for joining us for another episode of the WTF podcast.If you would like to be a guest or sponsor the podcast, please contact us at whereisthefunding@gmail.com.Where to find us: Anchor, Apple Podcasts, Google Play, Spotify, or wherever you get your podcasts.Help us grow: Please subscribe, stream or download, leave a rating or review and share your favorite episodes with family, friends, and colleagues.Social Media: Follow the WTF podcast on Instagram.Follow Michelle on LinkedIn: Michelle J. McKenzieJoin us for the next episode!
Ann-Marie Hosang Archer is the founder and CEO of Mauritian-based Lignum Vitae Health Africa (LVH) and the founder of LVH International Ltd based in South Africa. Ann-Marie started LVH after 23 years in the pharmaceutical industry with Eli Lilly pharmaceuticals serving in senior leadership positions in Central America, the Caribbean, Brazil, and South Africa. She is also an angel investor with Future Females Invest (FFI).What you will learn from this episode: Mentorship is important for women entrepreneurs to thrive in addition to funding and FFI Angels provides both to its portfolio companies. Sharing knowledge and experience is a value-add to investing. Not to be afraid of fundraising but the process will be hard and you have to do your research and do the work that is required to fundraise Women +Health = Wealth and Healthy women make healthy economies Get in touch with FFI Angels if you are an African female founder (or a non-Africa-based female founder with a business that serves the African market) looking for seed capital, business, and moral support to help you grow and scale your business. Thanks for joining us for another episode of the WTF podcast.If you would like to be a guest or sponsor the podcast, please contact us at whereisthefunding@gmail.com.Where to find us: Anchor, Apple Podcasts, Google Play, Spotify, or wherever you get your podcasts.Help us grow: Please subscribe, stream or download, leave a rating or review and share your favorite episodes with family, friends, and colleagues.Social Media: Follow the WTF podcast on Instagram.Follow Michelle on LinkedIn: Michelle J. McKenzieJoin us for the next episode!
Ann-Marie Hosang Archer is the founder and CEO of Mauritian-based Lignum Vitae Health Africa (LVH) and the founder of LVH International Ltd based in South Africa. Ann-Marie started LVH after 23 years in the pharmaceutical industry with Eli Lilly pharmaceuticals serving in senior leadership positions in Central America, the Caribbean, Brazil, and South Africa. She is also an angel investor with Future Females Invest (FFI).What you will learn from this episode: Mentorship is important for women entrepreneurs to thrive in addition to funding and FFI Angels provides both to its portfolio companies. Sharing knowledge and experience is a value-add to investing. Not to be afraid of fundraising but the process will be hard and you have to do your research and do the work that is required to fundraise Women +Health = Wealth and Healthy women make healthy economies Get in touch with FFI Angels if you are an African female founder (or a non-Africa-based female founder with a business that serves the African market) looking for seed capital, business, and moral support to help you grow and scale your business. Thanks for joining us for another episode of the WTF podcast.If you would like to be a guest or sponsor the podcast, please contact us at whereisthefunding@gmail.com.Where to find us: Anchor, Apple Podcasts, Google Play, Spotify, or wherever you get your podcasts.Help us grow: Please subscribe, stream or download, leave a rating or review and share your favorite episodes with family, friends, and colleagues.Social Media: Follow the WTF podcast on Instagram.Follow Michelle on LinkedIn: Michelle J. McKenzieJoin us for the next episode!
Ann-Marie Hosang Archer is the founder and CEO of Mauritian-based Lignum Vitae Health Africa (LVH) and the founder of LVH International Ltd based in South Africa. Ann-Marie started LVH after 23 years in the pharmaceutical industry with Eli Lilly pharmaceuticals serving in senior leadership positions in Central America, the Caribbean, Brazil, and South Africa. She is also an angel investor with Future Females Invest (FFI).What you will learn from this episode: Mentorship is important for women entrepreneurs to thrive in addition to funding and FFI Angels provides both to its portfolio companies. Sharing knowledge and experience is a value-add to investing. Not to be afraid of fundraising but the process will be hard and you have to do your research and do the work that is required to fundraise Women +Health = Wealth and Healthy women make healthy economies Get in touch with FFI Angels if you are an African female founder (or a non-Africa-based female founder with a business that serves the African market) looking for seed capital, business, and moral support to help you grow and scale your business. Thanks for joining us for another episode of the WTF podcast.If you would like to be a guest or sponsor the podcast, please contact us at whereisthefunding@gmail.com.Where to find us: Anchor, Apple Podcasts, Google Play, Spotify, or wherever you get your podcasts.Help us grow: Please subscribe, stream or download, leave a rating or review and share your favorite episodes with family, friends, and colleagues.Social Media: Follow the WTF podcast on Instagram.Follow Michelle on LinkedIn: Michelle J. McKenzieJoin us for the next episode!
Ann-Marie Hosang Archer is the founder and CEO of Mauritian-based Lignum Vitae Health Africa (LVH) and the founder of LVH International Ltd based in South Africa. Ann-Marie started LVH after 23 years in the pharmaceutical industry with Eli Lilly pharmaceuticals serving in senior leadership positions in Central America, the Caribbean, Brazil, and South Africa. She is also an angel investor with Future Females Invest (FFI).What you will learn from this episode: Mentorship is important for women entrepreneurs to thrive in addition to funding and FFI Angels provides both to its portfolio companies. Sharing knowledge and experience is a value-add to investing. Not to be afraid of fundraising but the process will be hard and you have to do your research and do the work that is required to fundraise Women +Health = Wealth and Healthy women make healthy economies Get in touch with FFI Angels if you are an African female founder (or a non-Africa-based female founder with a business that serves the African market) looking for seed capital, business, and moral support to help you grow and scale your business. Thanks for joining us for another episode of the WTF podcast.If you would like to be a guest or sponsor the podcast, please contact us at whereisthefunding@gmail.com.Where to find us: Anchor, Apple Podcasts, Google Play, Spotify, or wherever you get your podcasts.Help us grow: Please subscribe, stream or download, leave a rating or review and share your favorite episodes with family, friends, and colleagues.Social Media: Follow the WTF podcast on Instagram.Follow Michelle on LinkedIn: Michelle J. McKenzieJoin us for the next episode!
Ann-Marie Hosang Archer is the founder and CEO of Mauritian-based Lignum Vitae Health Africa (LVH) and the founder of LVH International Ltd based in South Africa. Ann-Marie started LVH after 23 years in the pharmaceutical industry with Eli Lilly pharmaceuticals serving in senior leadership positions in Central America, the Caribbean, Brazil, and South Africa. She is also an angel investor with Future Females Invest (FFI).What you will learn from this episode: Mentorship is important for women entrepreneurs to thrive in addition to funding and FFI Angels provides both to its portfolio companies. Sharing knowledge and experience is a value-add to investing. Not to be afraid of fundraising but the process will be hard and you have to do your research and do the work that is required to fundraise Women +Health = Wealth and Healthy women make healthy economies Get in touch with FFI Angels if you are an African female founder (or a non-Africa-based female founder with a business that serves the African market) looking for seed capital, business, and moral support to help you grow and scale your business. Thanks for joining us for another episode of the WTF podcast.If you would like to be a guest or sponsor the podcast, please contact us at whereisthefunding@gmail.com.Where to find us: Anchor, Apple Podcasts, Google Play, Spotify, or wherever you get your podcasts.Help us grow: Please subscribe, stream or download, leave a rating or review and share your favorite episodes with family, friends, and colleagues.Social Media: Follow the WTF podcast on Instagram.Follow Michelle on LinkedIn: Michelle J. McKenzieJoin us for the next episode!
Ann-Marie Hosang Archer is the founder and CEO of Mauritian-based Lignum Vitae Health Africa (LVH) and the founder of LVH International Ltd based in South Africa. Ann-Marie started LVH after 23 years in the pharmaceutical industry with Eli Lilly pharmaceuticals serving in senior leadership positions in Central America, the Caribbean, Brazil, and South Africa. She is also an angel investor with Future Females Invest (FFI).What you will learn from this episode: Mentorship is important for women entrepreneurs to thrive in addition to funding and FFI Angels provides both to its portfolio companies. Sharing knowledge and experience is a value-add to investing. Not to be afraid of fundraising but the process will be hard and you have to do your research and do the work that is required to fundraise Women +Health = Wealth and Healthy women make healthy economies Get in touch with FFI Angels if you are an African female founder (or a non-Africa-based female founder with a business that serves the African market) looking for seed capital, business, and moral support to help you grow and scale your business. Thanks for joining us for another episode of the WTF podcast.If you would like to be a guest or sponsor the podcast, please contact us at whereisthefunding@gmail.com.Where to find us: Anchor, Apple Podcasts, Google Play, Spotify, or wherever you get your podcasts.Help us grow: Please subscribe, stream or download, leave a rating or review and share your favorite episodes with family, friends, and colleagues.Social Media: Follow the WTF podcast on Instagram.Follow Michelle on LinkedIn: Michelle J. McKenzieJoin us for the next episode!
Ann-Marie Hosang Archer is the founder and CEO of Mauritian-based Lignum Vitae Health Africa (LVH) and the founder of LVH International Ltd based in South Africa. Ann-Marie started LVH after 23 years in the pharmaceutical industry with Eli Lilly pharmaceuticals serving in senior leadership positions in Central America, the Caribbean, Brazil, and South Africa. She is also an angel investor with Future Females Invest (FFI).What you will learn from this episode: Mentorship is important for women entrepreneurs to thrive in addition to funding and FFI Angels provides both to its portfolio companies. Sharing knowledge and experience is a value-add to investing. Not to be afraid of fundraising but the process will be hard and you have to do your research and do the work that is required to fundraise Women +Health = Wealth and Healthy women make healthy economies Get in touch with FFI Angels if you are an African female founder (or a non-Africa-based female founder with a business that serves the African market) looking for seed capital, business, and moral support to help you grow and scale your business. Thanks for joining us for another episode of the WTF podcast.If you would like to be a guest or sponsor the podcast, please contact us at whereisthefunding@gmail.com.Where to find us: Anchor, Apple Podcasts, Google Play, Spotify, or wherever you get your podcasts.Help us grow: Please subscribe, stream or download, leave a rating or review and share your favorite episodes with family, friends, and colleagues.Social Media: Follow the WTF podcast on Instagram.Follow Michelle on LinkedIn: Michelle J. McKenzieJoin us for the next episode!
Ann-Marie Hosang Archer is the founder and CEO of Mauritian-based Lignum Vitae Health Africa (LVH) and the founder of LVH International Ltd based in South Africa. Ann-Marie started LVH after 23 years in the pharmaceutical industry with Eli Lilly pharmaceuticals serving in senior leadership positions in Central America, the Caribbean, Brazil, and South Africa. She is also an angel investor with Future Females Invest (FFI).What you will learn from this episode: Mentorship is important for women entrepreneurs to thrive in addition to funding and FFI Angels provides both to its portfolio companies. Sharing knowledge and experience is a value-add to investing. Not to be afraid of fundraising but the process will be hard and you have to do your research and do the work that is required to fundraise Women +Health = Wealth and Healthy women make healthy economies Get in touch with FFI Angels if you are an African female founder (or a non-Africa-based female founder with a business that serves the African market) looking for seed capital, business, and moral support to help you grow and scale your business.Thanks for joining us for another episode of the WTF podcast.If you would like to be a guest or sponsor the podcast, please contact us at whereisthefunding@gmail.com.Where to find us: Anchor, Apple Podcasts, Google Play, Spotify, or wherever you get your podcasts.Help us grow: Please subscribe, stream or download, leave a rating or review and share your favorite episodes with family, friends, and colleagues.Social Media: Follow the WTF podcast on Instagram.Follow Michelle on LinkedIn: Michelle J. McKenzieJoin us for the next episode!
Ann-Marie Hosang Archer is the founder and CEO of Mauritian-based Lignum Vitae Health Africa (LVH) and the founder of LVH International Ltd based in South Africa. Ann-Marie started LVH after 23 years in the pharmaceutical industry with Eli Lilly pharmaceuticals serving in senior leadership positions in Central America, the Caribbean, Brazil, and South Africa. She is also an angel investor with Future Females Invest (FFI). What you will learn from this episode: Mentorship is important for women entrepreneurs to thrive in addition to funding and FFI Angels provides both to its portfolio companies. Sharing knowledge and experience is a value-add to investing. Not to be afraid of fundraising but the process will be hard and you have to do your research and do the work that is required to fundraise Women +Health = Wealth and Healthy women make healthy economies Get in touch with FFI Angels if you are an African female founder (or a non-Africa-based female founder with a business that serves the African market) looking for seed capital, business, and moral support to help you grow and scale your business. Thanks for joining us for another episode of the WTF podcast. If you would like to be a guest or sponsor the podcast, please contact us at whereisthefunding@gmail.com. Where to find us: Anchor, Apple Podcasts, Google Play, Spotify, or wherever you get your podcasts. Help us grow: Please subscribe, stream or download, leave a rating or review and share your favorite episodes with family, friends, and colleagues. Social Media: Follow the WTF podcast on Instagram. Follow Michelle on LinkedIn: Michelle J. McKenzie Join us for the next episode!
Chris Conway from Marcus Today and Mark Gardner from Maqro Capital go in-depth and stock specific. Stocks covered: LVH, GNC, PPG, TLS, WAM, LGL, TPW, CSL, WR1, SRV. Stock of the day is Latitude Group Holdings (LFS). See acast.com/privacy for privacy and opt-out information.
Episode Summary:Elon Musk Sells $5 Billion of Tesla Shares$500 Shiba Inu Giveaway Guests:Ben Rabizadeh StoryTrading 10:00Vivi Biotech Queen https://twitter.com/Biotech_SD 24:00Zandy Forbes, Ph.D. President & CEO of MeiraGTx (NASDAQ: MGTX) 41:00Ronen Samuel, CEO of Kornit (KRNT) 55:00Scott Mathis, CEO and Chariman of Guacho Holdings $VINO 70:00Renato Capelj, Benzinga, Physik Invest 110:00https://physikinvest.com/Hosts:Spencer IsraelTwitter: https://twitter.com/sjisraelAaaron BryTwitter: https://twitter.com/aaronbry5Subscribe to all Benzinga Podcasts hereClick here for BENZINGA TRADING SCHOOL Get 20% off Benzinga PRO here Become a BENZINGA AFFILIATE and earn 30% on new subscriptionsDisclaimer: All of the information, material, and/or content contained in this program is for informational purposes only. Investing in stocks, options, and futures is risky and not suitable for all investors. Please consult your own independent financial adviser before making any investment decisions.Unedited Transcriptwe got a lot of guests today. Here's that's what I said. Here's what we got. We got Ben from story trading in like eight minutes. We've got Vivi biotech, uh, or the Bio-Queen at, uh, 1215. We've got Zandi Forbes from Mira GTX. She's a presidency yet.We're talking gene editing at 1230. We got Ronan Senor from Coronet digital we're talking, uh, fashion and the fashion supply chain at 1245. Did I get all that right? As far as timing goes. Yep. We got Scott Mathis from Gaucho holding sicker V I know, uh, at one and that Renato, uh, Capella, he is a Benzinger writer and also does some really, really cool options trading on the side.Uh, he'll be on the show at one 30. So we got what we got. 1, 2, 3, we got six guests today. We have all that's a lot, frankly. Uh, maybe a few too many, but nonetheless, here we are. So before we get to those guests, uh, we're going to talk about what's what's moving. We're going to talk about, uh, crypto. We're going to do a guest that sharp sediment.Cause we got some good feedback from that yesterday. So, um, AB where should we start? Um, well, let's start with just looking at the overall market. Spencer. I see Christian in the chat asking who do we have on for a guest today? You just ran through them, but you can also check the description in the YouTube, uh, the YouTube description for the guests for the day.Um, and shout out to the chat yesterday. We had some good trade ideas thrown out in the chat yesterday. We did, uh, easy Mike was talking about Uber puts. I played those. They were up nicely. Um, and we were talking about playing Disney for a big move on either side. We got talked out of it by our main man, Nick Shaheen.But yeah, I don't know. Maybe we should have done it. Yeah. I felt bad about that one going and they got talked out of it, but, uh, you know, it was a pretty brutal quarter. So, um, anyway, I don't even know why I look at Disney it's in my never sell portfolio. That's my first mistake is don't look at and stuff and your never sell portfolio.Otherwise you're just giving yourself anxiety. Rowan DAS pips is saying audio levels. Are we good, Bruce? Or Ron? Are you awake? I'm here. Okay. Oh, he's coming through us through the sky. I did not know that was coming from Terminator. I'm hanging out on the background, like a good idea. Hey, uh, while we figure out those levels, if you all want to do a solid, as DK suggested and hit that like button ladies and gentlemen, we'd appreciate that.Thank you very much. Um, Hey, what's do a guest, that chart segment. We're going to start doing this every day yesterday. Wasn't it easy one a B I don't even remember what it was. It was D whack. Oh yeah. That was that. That was yours. Full disclosure, I guess the one today. No, because I changed it. Shoot. So beforehand Spencer showed me the guests that chart and I guessed it and he didn't like the fact that I got it so easily.So he went out and picked a new one. I don't know what it is. I went out and I picked her from, Ooh, this will be a good drawer. And then he gets to like right away. So it's not a firms that don't get that, um, drop your answers on the chat and whoever's right. Uh, email us afterwards and we'll send you some swag.Um, here is two days chart of the day. This is going back to like February, or actually this is going back to the start of the year. This is going back to the interests of the start of the year. Now I will give you some hints because otherwise it'd be impossible. I feel like, um, in some respects, this is a technology stock in some respects.Oh man, we can have a winner already. Holy moly. Christian Gallagher. Wait, it was PayPal. This is PayPal. How so are we looking at weekly candles right now? Is this a daily PayPal has gotten beat up over the past month or so it looks like, yes, it has gotten beat up is, is, is, is a nice way of putting it, but yes, Christian Gallagher.Did anyone yesterday? No, Frendo on yesterday. Christian email us shows app benzinga.com. Hey, why is PayPal down so much? Didn't they just announce a Venmo, Amazon integration. So yeah, you would think that tell me you don't own PayPal or maybe you do and you don't know it. Um, I think in my like real portfolio, the one that I don't manage it's in there scourge.It's too easy with showing prices. Well, that's an idea. I take the price off ridiculously hard, but we could do that. Should I buy? I like calls on PayPal. No, it's gotta be coming back up at some point, right? That's one way of putting it. Um, you want to throw out like, uh, you know, you want to buy the, the, the, the, the two 80 strikes expiring and like six months.Really worth looking at. I'm sure it's not very much money. I do think though we have to, um, you know, keep up, like if we start doing obscure biotech stocks, you know, it'd be nearly impossible. So what we'll probably try to stick to, I dunno, S and P 500. Yeah. That's, that's, that's a good plan. Stick to the S and P 500.So we're going to do this everyday. Christian email us shows up and it's going to come. We will hook you up with some schwag before we go to our first guest AB I seem working backstage. Let's do our first crypto update of the day. Sure. Yeah. So yesterday Bitcoin spiked on the CPI data and then gave up all those gains and more.Let's take a look today to see how the, the crypto markets are responding to that yesterday. Uh, we, we have a lot of people in the chat that have been asking kind of how are they supposed to be trading crypto right now? So I know you and I, Spencer are in that boat where we're just like adding Ethereum and not really touching it or selling it.I haven't even added recently. It's been a while for me. I hadn't bought a theorem. I wanted the board. So yesterday, w like I've mentioned, once that CPI data came out, Bitcoin spiked and actually hit brand new, all time highs, um, gave all those gains up is currently trading about $65,000 a coin down 4.8%.Ethereum is also down, albeit not as much Ethereum currently, right around $4,800. So we talked about that $5,000 level being a big level for Ethereum. I think once we see a theory and finally breakthrough that $5,000 level, we can really see it run. Um, but yeah, everything pretty much in the red, like you can see from this heat map Sheba, he knew though in the green up 5%, um, we're actually going to have a big Shiba Inu guest on the show tomorrow.Uh, his name is Ross. He was an early investor and also a kind of co-developer of Sheba. So he's someone that I think I can say confidently knows more about Shiba Inu than 99.9% of people in the world. Um, so if you're interested in Sheba or what's next for the coin tune in tomorrow, he'll be on about one 30, uh, Spencer, any thoughts on this crypto heat map?I I'm trying to get a link right now because we're actually doing a sheep giveaway. I'm trying to get the link for that. I don't have it handy, but we're giving away some free shipping. I hope somebody gets me that link so I can get it to you. Uh, that's my thought, my thought is no. I mean, Bitcoin is an inflation hit crypto isn't inflation, hedge.Um, I don't quite understand the why it's down like this today, but you don't. All you need to do is look at the reaction to Bitcoin at 8:30 AM. Eastern time yesterday, right? Inflation comes out. It's harder than expected. It's it's more than expected. What does Bitcoin do? It goes up. Mike is saying, Hey, be it.It's a good play. Definitely go for PayPal options. Um, so I don't know if he's, you know, facetiously saying that he wants to see me lose some money, but I'm looking at him. I'm looking at the calls. Um, but yeah, Spencer, like you mentioned get some free Bitcoin we'll we'll throw that zing token up real quick.Go to Voyager. You put in a hundred dollars, you get $50 free Bitcoin, if you use the code zing. Uh, so not a bad deal at all. I mean, who doesn't want $50 of free Bitcoin checkout Voyager for that? Use the code zing. Um, all right. Real quick before we get to Ben. Yeah. Yeah. And, and I'm going to post the link to the ship giveaway.Um, when I, once you find that I find it. Yeah, no problem. Somewhere out there, easy Mick, you might be the guy who knows technicals what they're talking about when it comes to technicals, I'm watching a. Dash, which has been up a lot over the past, I don't know, week or so. Is this, is this, this the kind of subtle head and shoulders forming on the, on the one day chart?I think we're looking at five minute candles right here. I see one shoulder here. This could be the head, if this is the, the second shoulder, um, you know, could it start falling down or should I be looking at some dash puts, I need someone who knows technicals better than I do to let me know if this is, uh, you know, I'm not a big patterns guy, so I'm not really know, but we have some people out there that are outsourcing.And I know, I know when I need to listen to someone that knows more than I do. Yeah. Um, Alvin say, and he's looking at Wayfair puts an ADSL. K what's ADSL desk. Autodesk. Yeah, by the way, I just put the link in the chat for the ship giveaway. There it is. There it is. You can't click it on the screen, but it's in the chat.I'm just throwing up there. So y'all know it is there. All right. Y'all so story train. If you guys have watched a show before you've seen Ben on the show, he gave us a E H R at, I don't know, four bucks, three bucks. What does it now? It's like, I like 20 let's check real quick before he comes on. He'll give us an update on AHR.Um, it's at $23. So let's see. I mean, it's, it's up. I want to say like at least 200% since he pitched us to us on the show, he's got a couple more stocks. We're going to talk about, uh, Should we bring them on easy MC RSI? Isn't it. If the RSA is 90, isn't that a sign it could come to? I don't know. You, you know, more about technicals than I do.Let me know. All right. Without further ado, let's go ahead and get BenOh, Ben, what was the, what was the price of AHR when you first came on the calendar? What's up guys? Yeah. When I first came on, the show was around $5, five 40, somewhere that somewhere in the low fives, I believe it was. Yeah. And when we first presented it to our VIP community, when I presented as a trade idea, it was $2 and 74 cents.What, all the way up to 27. So it was a 10 bagger if you captured that. And I happened to pretty much captured that I was done. I'm handing this from 2 74. I didn't sell my first shares until 16. And then, um, I sold a lot more in the, in the 20 to 25, 26 weeks and maybe even gotten a little bit at 27. So, um, yeah, I've got a few updates for you on, on that.And a couple other sucks. Yeah. You got a new background. This is the first time we're seeing this. It looks pretty good. Yeah. A lot more work to do. We got to get that our mikes and cameras and everything, but yeah, this is the first time anyone's seen this background. Cool. And you said too, it looks like we did.It took us far too long, but we eventually got it together. You get a zoom out so Ben can see our beautiful. Oh, wow. That's great, man. Um, all right, Ben, you want to go ahead and get your screen shared and we can go ahead and run through those slides real quick. I know we only got about 10 minutes, so we've got a few I'll work.I'll be fast. All right, there we go. All right. So yeah, first we got that quick disclaimer, we got to always do that. A story is not investment advisor and missing his spirit is in most gimmick where some losses of you who are new to store trading, what is associate is the practice of understanding market pricing.We also call that the story behind the trade through the four pillars, which we say are sentiment catalyst, fundamentals, and technicals. That allows us to take a holistic look at markets and make choices based on all of these factors, not just one of them. So air story, trade idea, update. I officially opened that in my community on July 8th of 2 74, I did close it on November 8th of 25, 79.I still own some shares. Uh, I ended up selling about nine giving 95% of my shares. Um, Monday morning was really the trigger for me and that's because I saw something, the technicals and also the sentiment, which caused me to say, let me, let me lock in these games. And the technicals last Friday was the.Solid green candle on the chart, you can go look it up the first solid green channel and then tire run-up, which, which means it started the day high and then went down lower throughout the day. And throughout this entire run, it was starting low and going higher throughout the day. I took that to be a reversal sign plus the sentiment, I think when reached peak Eby sentiment for now, for this cycle with, uh, Elon Musk selling shares of Tesla with the Caribbean IPO, with excitement, but Eby infrastructure.I'm trying to time that sentiment top. So I took my profits. I am keeping about 5% of my shares because it could go much higher still if they get the right contracts in the future. Got it. Um, so it took some money off the table, trim some of your position and air took those profits, never a bad move. Uh, Ben, what else?I was on your radar today. I wanted to give you an update on side, cause I was on your show. July 26, we presented this at $5 and 70 cents. Uh, this is stuff that's been up 66% since it was initiated in our community. At the time we said, Hey, T-Mobile's come in. End of month in August. It didn't happen then.But it happened last night. Uh, so a few updates. They have earnings last year. Um, so this T-Mobile deal came three months late, but it's finally here. Now, key, this was announced last night on the conference call only. There's no PR yet. So people who are in the know who are listening to the conference call, they have a big edge getting into the stock right now.Um, there probably will be a PR at some point in the future, and there's also tremendous traction with their other customers, 18 T and Verizon. Um, there was an upgrade today to $9 and I'm not even sure that Benzinga caught it, that upgrade by the analyst and $9 by lake street. But we think in our community, it can go much higher.Uh, there's uh, estimates out there in our community saying we can do go up to a dollar 33 DPS by 2024, which would be a $40 price target. So that's the update on SSI. You know, our investigative research worked and we're read about T-Mobile just a few months late. So this company is going to start printing lots of tests going to be a very profitable company.Do, do you have a target? Um, yeah, no, I don't have to stop losses. God forbid men. No, I do stories yet. I never do stop losses. So I've been holding the stock for like two or three years. I increase in decrease my position around catalysts. So, um, I was buying and after hours last night I bought a lot more today.It's now my largest position actually. And uh, I'm not going to put a price target. I see how it goes. I, I assess the fundamental sets of metallics and technicals on an ongoing basis to determine. There you have it. Yep. So I do have a new pig that I'll get to in a second. But before that, just a little quick alert, maybe something for you guys to look into and talk about, because this is a big kind of big cap for us.At $1.5 billion company GoPro. We presented it to our community Sunday night, um, because the fundamentals are super strong. They had earnings last Friday and we have anticipated a technical breakout of the 200 DMA, which just happened this morning. And this is really, it could be a really fun situation, wanted to bring your attention because it has, this has short and gamble, squeeze potential, very high, short position.He has sense of it has been very, very low, but the financials have completely turned around with this company and they're printing tons of cash. Now you see the technicals broke. The options are very liquid, very cheap. And if it gets into the right hands and the Reddit community, et cetera, this could be a crazy profit potential, you know, with shorten game of squeezes.So keep your eye on that. But go. So GoPro's up about 9% today on the strong earnings. Um, so I, I mean, I, I don't know, personally, Ben, if I'm going to go in and try to chase GoPro and it's already up 10%, but I, or 9% today, but I definitely like having it on my radar. Uh, J rice in the chat was also talking about GoPro saying that he thinks it could be a long-term turnaround play.Uh, I don't know. Munis has been one of those stocks that has just been like beaten down over time historically. Um, but you know, at some point I don't think you can ignore the fundamentals or Fridays when I got in added more Monday, uh, I got a little bit messed up on the options than playing the options.So I actually lost some money. Cause I got scared with the whole inflation thing yesterday, but I'm in it now and yeah, the sense of it's sport, that's the only thing people hate this company, but they're printing cash like crazy. The technicals are turning and shorting, given squeeze potential, such that this, yeah, my all hold back a GoPro has always been that.I feel like they have a very limited, uh, customer base, you know, it's like who, who who's going out and buying GoPros. It's people that take part in extreme sports, you know, mountain bikers, snowboarders, skiers, et cetera, outside of that. Um, I don't, I don't know how many, you know, everyday people are GoPro customers.It's absolutely correct. And I'm not, you know, I wouldn't take issue with that, but the amount of earnings they have like 60 million EBITDA this last quarter. And if you compare it with their market cap, I mean, this thing can easily be 17 bucks. Even with that knock against it. Got it. Um, I been, what else is on the radar?I have a presence. It's my first story. Trade ideas. Since air. I presented this to my VIP community last week. Okay. Listen to the presentation. Don't just jump into buying guys. Okay. Because of what happened with their, every stocks, not air, I can guarantee you, this is not going to go a thousand percent in the next three months, like heritage.Okay. So that sock is Gaia, ticker symbol, G a I a. All right. So we're going to look at it and yeah, it's a smaller company on the ground, 200 million market cap or so, but you know, what's the story behind the trade. That's what we're trying to figure out. And again, we look at the sentiment, the fundamentals, catalyst and technical.So let's start with the fundamentals guys, digital video subscription service, like in some ways like, like Netflix, they sell, um, they make original content for yoga, alternative health, holistic healing, nutrition. It's a monthly subscription service. They've been growing steadily over the last many quarters.They're profitable. Uh, fundamentally I think their inflection really happened to a quarter or two ago when they became profitable. And you can see some of the, uh, the trends here in terms of their, um, their revenue and their EPS, although in the right direction. So in our community, we collaborate with people who are really steeped in fundamentals, just charts, courtesy of Mark Holmes.He has a risk reward chart here in terms of what is the value of this stock and. You know, it's worth, it could be worth at least $17 a share. And the stock is very cheap here. So, so that's the fundamentals. You can check it out on your own. Go look at the earnings report and you'll be able to verify everything I'm saying about, uh, the growth and the subscriber growth and money they're making written it now.And it could potentially be, uh, you know, Netflix may buy them out one day. You know, there's, there's a lot of opportunities here. So, um, yeah, catalyst let's go to the next pillar. Uh, in these sorts trading four pillars, they had their earnings just recently, November 1st, it was 20, 20, 20 2% revenue growth, uh, year to date compared to last year Q3 EBITDA of $4 million.Uh, even a margin of 20% was their fifth straight quarter positive earnings in cashflow. Um, and then they had an additional catalyst the next day. So we'll talk about that catalyst in just a second. What happened the day after earnings, but first let's go to sentiment. So the sentiment is kind of poor with the stock because fundamental investors are frustrated at the price action.I know a lot of fundamental investors saying this should be worth 17, 20, 25 bucks. Why is it $10? Why is it moving yet? So I listened to other participants. I say, I talked to people in social media. I talked to people in my community. Why aren't you interested in the stock? And this is what I'm hearing.The total adjustable market may be too small. It may be too niche, their content. We talked about alternative medicine, yoga, meditation, and things like that. So it feels like I'm just not interested. It doesn't seem like a huge part. Other people say, Hey, the content, they have some content that's kind of fringe on their French content.Like some of that alternative medicine, there might be some videos on, you know, some vaccine hesitancy type stuff or who knows, like some things are it's alternative content, right? So some ESG, uh, buyers, uh, may stay away from that environmental social governance. So that's another knock on the sentiment.The other knock is this is just slow and steady growth it's and where's the hockey stick potential on that. So just remember, this is the poor sentiment. This is what happened. Going back to the catalyst the next day after earnings, after we know the fundamentals are great, the next day another catalyst hit the other, the catalyst was there was a PR that Demi Lovato became a brand ambassador for.And there was a press release that a lot of people didn't see a where Demi Lovato says I'm excited to be one of Dias. First celebrity ambassadors, and honor to join a platform. I've been a fan of for some time she has 118 million followers on Instagram. And the market cap is again like 189 million. So this company has been growing slow and steady.And all of a sudden, they hit you with this news of Demi Lovato is a huge mainstream personality, that and company, I want to go back to this. Airpoints the one thing I saw that the thing about Demi Lovato, uh, in, and I, I guess I didn't realize this was the same company, but like they got a lot of weird shit on their platform.And that was the sentiment I was talking to. They're saying, oh, there's stuff is weird. I just don't want to own this company. But you know, I think that, you know, they're growing steadily, they're getting to a place where they can really focus on growth now, and to me, and let me go back to that bad point.You just made that pinpoint. You brought it up for me, right? Yeah. They have weird stuff. It's too niche. The French content. They keep some buyers away. But this is where I think that Demi Lovato news is really significant because they're in a financial position now to really grow the company. And to me, this signals.And in fact, in that PR said, I'm excited to be one of guys. First celebrity ambassador, And I have a feeling this company is going to start growing their content and start getting into more mainstream content. And based on what you're saying, I think they may be looking for more celebrity ambassadors.And it's just a great situation because the downside is so limited. You have a fundamental floor here and now you have optionality upside. If the company starts doing things to get that hockey stick growth potential. And that's why I really add it to my position here. And I'm very excited for the next several months on this stuff.Um, let me just go to the last or technical resulted with her awesome technician Rex. And this is a monthly chart is saying, uh, this can go to the twelves if it breaks out of the yellow.here, which thought is that shorter than I think the current breakout circled right there. It's got a breakout of, I guess, 10 70 area.He thinks it can go to 12 for the month. And here's another view which looks much more bullish. This is a long view of the monthly chart is a sometime in the future. When the 12 to 13 breakout at the blue line, it should proceed to break out the all-time trend at the white line. And he thinks this is a several month play for that to happen, but you can kind of see where this can go.Uh, if that happens. Uh, any questions on that or any of the other stops, man? I didn't see this one coming. I didn't realize this. I read about this company and I was like, man, I didn't even realize they were a public company until you came on here. So, um, I'm all I'm putting two and two together here. Uh, Ben, thank you as always for coming on the show, we appreciate it and uh, and have a good rest of your day.Please follow us on YouTube. Thank you guys. Thanks a lot, Dan. We got to get moving. We got our next guest. She's already here. We're going to talk biotech guys. I know that we, we always get asked. We always get questions like when's Vivian. When's Vivian. When well she's on right now. Not right now. She'll be on in like five seconds when we bring her on.But Vivi Bio-Queen will be joining us every Thursday. At this time, I told you all to save your questions for your bites. The questions for right now, let's bring her on Vivi. How are we doing today? Good. How are you guys? Can you hear me? Well, we hear you. We see you and we have questions. Oh, awesome. And before we do any questions, I think, um, we can do some updates.I did have a request on Twitter to cover it stock. Um, like at my old good lawyer friend, mellow at Twitter, I, this is out for entertainment purposes. So, uh, is only my opinions are for entertainment, purpose, not a financial advice. So I wanted to, uh, first of all, um, talk to you guys, um, just given up a date, we just had the, uh, ER, on KMP.H can you guys put that up over there? Yeah, this is a daily chart. Okay. And P Hit's quiet. So, yeah, so we just had the ER and I want to, so when I, when everybody kept asking me, like, what do you, what are you going to do for 'em? What are you going to do for K MPH? My position was this small because he is a, some of the concerns I had. I spoke to the manager and he interviewed me. And, uh, he said, you know, we're not going to put any reps in New York yet.And it's just going to be certain regions in the United States. And for me, it showed a little bit of a weakness because for me, if you launching a drug, you should have put reps all over the map. But I think they're just trying to be cautious. So they report around like, I think 2 million in revenue, but here's what I'm bullish.Now. They just launched the rest of the Salesforce. And this company here, you know, their burn rate is really, really small because Korean is doing all the selling. So the burn rates is like a million a quarter and they have a, still have 135 million. And he is what I'm bullish of. Um, there's a company that sells a scripts and there's a guy that, uh, his friend works for this company and feeds him all the script.So for you guys to have an idea, right, the, the feedback has been amazing. So July, they had a nine scripts for the monthly and then August, they had 173 scripts, um, September 416, October 886, still low because there were not out throughout the nation. But I think the feedback has been tremendous from psychiatrist, from the drug and the differentiator.And I feel like as they deploy, uh, the other sales reps, we going to just ramp up the sales. So I feel like at this moment, I wanted to add a little bit more to my position because I, I see the future being very bright here, KMBH. And I think that, um, we gotnot yet. Not yet. I, I should have now I have an, I am waiting for some of my swings to flourish, so I haven't been able to, to add, but I wanted to for sure. Okay. And then I want it to put you guys out. Somebody asking me to, uh, to, uh, cover a, uh, a N N S. Hmm. Okay. Now I want I'm familiar with, but it is biotech.So it's a biotech it's under the radar. So I wanted to explain to you guys some of the reasons how I invest in biotech, and I told you guys, if there's no commercial products, there's, there's got the most important thing you can look at is cash, right? Because if you don't have a cash, no product, are they going to burn too much?And they also gonna have a, to do offerings. And if the stock is low, they do reverse the split. So the first thing I do is to look what was the cash burn and how much cash they have left in a would the future and what the catalysts are going to be. So this company here, the first thing that got me to, to look at it was they have a $271 million in cash.So they're really the city really strong. So I thought that was a really, really, uh, um, uh, valid, uh, information, very important. Then I look at a financial institution on. EVestment, which is a goblin, was the director of FDA is a partner on their firm. So they own 2.5 million shares. So I thought that was another very important information because goblet is well connected to FDA.Not that you know, it nobody's going to be bought out, but when you have investors that work with FDA, they know what it takes to, to be compliant, to get a drug approved, right. Because it's just so much behind to get a drug approved. So manufacturing, you know, how the studies are designed. So I like the fact that there's Nia investment behind.And then I also know VOD is, oh, 2.1 million. So Novartis has some interested and, and the pipeline, it looks really, really amazing is all CNS, um, uh, and mass. Um, they're going to have, uh, Gilliam Barre syndrome, which is a very rare disease. So I really like this company. I really do. I, I'm not, uh, obviously I can't be in every single stock.Uh, but I, I, I, I think this is a really good a long-term, uh, stock to hold for sure. So that would be one. And then if you can, um, bring back, uh, pro GPRO G we have a lot of fans PRG. It's like almost like a min stock, but also a really good stock to hold long and, um, really. Yes. Yes. So, so what, what do you see that the market doesn't see, um, what I see that the market doesn't see.Um, I will tell you why this company is going to be huge. They have a two types of, of delivery system. They have a, um, on, I'll tell you guys, they have a two to two technologies and I wanted to bring to you guys, let me see. I can share a screen. Okay. But I have it here right in front of me. So they have two things.They have the OBDs okay. Which is oral Biotherapeutics delivery system. So what it does is, is able to take big formulations and put in a form of a pill. So for example, Humira is one of the biggest blockbuster drugs in the world. If they found a $10 billion. So you imagine if Abby, I think Abby is a Humira honor.If, imagine if Humira is loses patterns and five years, right. And all of a sudden, because doctors love the efficacy of this drug, and that's why it's so well prescribed. Right? But it's an injection. Imagine for this company sell their technology. And all of a sudden you can have a drug, like a Humira being, um, given orally, all of a sudden you create a whole new patent for that drug.Do you follow me? Because a different formulation. So all of a sudden you gaining another 15, 20 years. I have a patent on that drug. Now imagine how many pharmaceutical companies would have be jumping all over because they like, geez, I have this, this drug that's high formulation. And now I have a, I would love this drug to be an oral form because patients do prefer to be an oral form.So I see, um, they announced that they have three partnerships with the big pharma, but they have announced who, so everyone is kind of on a suspense, like who are going to be the big pharma. So they have, uh, right now with the Pfizer there, just to have an idea, they, the not only the delivery, the delivery system does this to the big formulation, but also one of the drugs of four in any boat to the second one, the oral bio biotherapeutic delivery system.The OBDs, what it does is it's designed it to, to, um, to take it a pill and the pill, the way this delivers it, doesn't go all over your bloodstream. So it's it's for the GI tract. So is GI specific drugs and there's one. For for, for, uh, uh, Pfizer they're there. The preclinical, what they found was not only that, that would their delivery system, that drug was 25 times more potent than the Pfizer drug, but had a no toxicity because it doesn't go to the bloodstream.Like the other drugs would go. So you have a less toxicity, less, less side effects. So imagine what they can do if they already doing this with Pfizer drug, they're studying the Humira. Imagine like for me, this drug should have just literally like get royalties for every farmer, choose the technology instead of it being bought out.Right? So I believe this, the future of this company is super, super bright. Uh, you know, it's heavily shorted. So I think that a lot of people are here for the, the, the, the gum is squeezed because if you look at the amount of, of, uh, of, uh, options, that the options chain is crazy, uh, for this, for this company.But I, I will, like, I have a big position because I wanted to, you know, to trade around my core, but it's some, it's a company that I wanted to keep it. And, um, and a long term, uh, option, because I feel this company is going to be huge. So they just appointed also geo hall, believe it or not do, how do you, how, um, she's in a board of directors and this woman, it's like a powerhouse in biotech, a friend of my work.As so maximum, so messenger gas sold. So she comes in with a lot of experience in pharma and a lot experience in acquisition. So, uh, the team is fabulous. They are four miles away from my house. I should have just bring them a bottle of champagne when we hit $10. But I believe in this company, this company has a bright future and that, um, right now there's a lot of people on it, you know, waiting for that short squeeze.But, uh, it's been keeping really it's being holding like it dipped to, to like 2, 3 0 3 today and it went right back up. So it's been keeping, you know, I think the short sellers were expecting after der cause you know, there's, you know, a yard for a state, uh, initial stages of biotech doesn't produce revenues.Right? So it, it dipped to fund 360 2 all the way to three, but it's been holding for weeks at that average. So people are not selling people believe in this company for sure. Uh, can I ask you, what do you, what do you get, do you have any favorites in the, in the gene therapy space? I do. I, um, I, uh, I, I'm a loan holder for ADP and they have the, uh, it's one of the car T therapies, but it's not the car T is the RTC, uh, ADP.And, uh, the reason I like this company is, uh, not only they have a partnership with Genentech, uh, the Genentech partnership is up to three. And, uh, they already have enough funny from Genentech cause they got, they gave them a prompt payment payment. They have funded into 2024. So I feel like this is a very safe play in regards to not having offerings and that they are sitting with 285 million in the bank and they do have, uh, some, um, some, uh, catalyst coming.And, uh, I, I believe this company will be a multibagger on day, you know? Uh, so it's one of those that you set and forget it, but I like the position of cash because it gives me the comfort that they're not going to be throwing in offerings after a big catalyst. You know, they, they have they're in a really strong position.And when you look at, uh, um, institutional ownership matrix, all 15 million shares of this company, baker brothers owned 18 million, the institutional ownership. It's so strong in this company. And obviously Jen at that has a huge, huge portion of the company and has their eyes on the company. So, uh, this, this is a big one for me.I got to ask you about, about BCR X here. That's the rule. Every week we got to talk about BCR ex of course, it's this year access to my unicorn. You guys, for sure. So, um, it's, it's funny. I held this space as on Twitter yesterday, and I was talking to a pharm D you know, I do respect, they have a lot more knowledge than me, you know, uh, in terms of a clinical.And he validates my position on the CRX and GRTs, which is great stone. And he says to me, you know, be CRX is, is a rare diseases monster in the making. So they, um, they just released the earnings. They put 38 million for the quarter, and people, BU people were really upset that it wasn't 7 million like this huge numbers, but for the mentally long-term, it's still there, right.Because the science hasn't changed. So I see this as an amazing opportunity, uh, if you're not in the CRX, but, uh, just, you guys have an idea. Uh, the biggest drug for, um, for Alex yawn is, uh, Alto Morris. And they are not even that good because it's not only an infusions for PNH, but patients still need transfusion, uh, taking this infusion every eight weeks.Uh, BCRA X has the competitor, which is going to be an oral oral, uh, competitor factor D and not only patients that have been on this study up to now, not only they jumped from phase one to phase three, because they did so. Patients to this date. I think there's 40 weeks, 30 weeks of, could it be this fusion to this date?So imagine having a drug that is, it's already a rare disease for PNH and patients only at the choice on the available is in Jackie, no infusions. And you still have to go through the transfusions. Imagine having an oral pill that you don't have to have a transfusion at all. So just make them do the math and Alex, the on 70% of its revenue, 70 was on PNH for this drug and they got bought out for $39 billion that would have put the CRX at a $230 a share.And B CRX has a better pipeline with a more potential and it's going to be all oral. So you guys do the math, if you don't think this is a monster in the making. Alright, Vivi the bio queen, she joins his every single Thursday at biotech. Underscore SD is for Twitter handle it's up on the screen. And uh, and then please.Yeah, please, if you, I will post my DD there because this is a very short, so you guys searched the bioclean on Twitter and you can find me all right. Thanks a lot. Viva, talk to you again next week, next week. All right. Uh, Hey, let's stick with biotech for a second here because our next guest is the CEO of a gene editor.Company, hence why I asked to VV about that one to get her thoughts. So, uh, if we can, let's go ahead and, uh, and, and, uh, bring her on guys. Andy Ford. She's the president CEO of Mira GTX. His company is a lot going on right now. They're at a very critical point. So let's get Zandy onum, Ford,by the way. Yes. Thank you. Thank you. Where we're actually, it's on our to-do list to get new music, but, um, thank you for, for, for the compliment. Uh, so as I said, it's a pretty critical time for, for mirror DGX. Uh, you guys just presented at, uh, uh, the virtual, uh, oh gosh, uh, the European society of gene and cell therapy Congress, right?Uh, yes, we did add three abstracts. Yes. Right. And then there's a, we're due for another, a little bit surprised when I found out you're on the calendar. Cause I thought you guys, you have another, uh, presentation coming up in a few weeks. I, I, I think I believe right. We do. So we have, um, quite a number of presentations in the second half of this year, uh, which included, uh, some presentations at the meeting.You just mentioned on our programs and our switch that allows you to switch gene therapies on and off with a pale. Um, related to what video was just talking about, actually, that's what I do want to talk about. I'm sorry about, and then, uh, at the beginning of December, we, uh, having a clinical update on our xerostomia program for patients who've been cured of had a neck cancer, but don't make saliva.So we'll be completing that study this year and we'll be updating on the clinical progress so far at the beginning of December. And then a couple of weeks later in mid December, we're having a science day to discuss in some more detail, uh, Ribas switch technology and our promoter platforms, which allow us to really optimize gene therapy.And for the first time switched gene therapies on and off with an oral drug and not just switched them on and off, but quite precisely dose the amount of gene therapy at a particular time with a dose of an oral pill. So let's talk about the switching via via pill. Yes, exactly how that. So obviously gene therapies are a virus which contain a gene and there's a coding sequence of the gene, which will make your protein, whether it's Epogen for example, or whatever, uh, gene therapy, it might be RPG or for the eye.And that gene is activated by a promoter, a regulatory sequence at the beginning of the gene. So that's the normal gene therapy promoter and a gene, the promoter switches the gene on, and it remains on for the rest of that patient's life, all that sells life. So you have persistently expressed gene therapy, but what we've been able to do for the first time is we do everything.I've just told you with the promoter that regulates the gene therapy and switches it on. But on top of that, we put into the gene sequence, a small sequence of DNA, which instructs the entire RNA produced from that gene to degrade. However, if we give a small molecule, but via pill, and we've got many small molecules, because we've developed this as a platform, it stops that degradation.It cuts the entire degrading sequence out of the gene. Produced RNA and you'd get the gene switched on as if it was never there. So for the first time we can deliver gene therapies, which are not on, so they're not producing weird proteins or bits of proteins. And we give a pill and bomb that I'll call it.The degrading signal is cut out of the RNA and you get a perfectly normal protein product.I guess I have so many questions. I don't even know where to, I like that all sounds incredibly complicated. Um, I guess, uh, how can you make sure that it works? So it's, we've when we set up the company, this was one of the technologies that we, um, we wanted to build and these switches made of RNA shape.There are thousands of them and bacteria. And for, for decades, people have tried to take bacterial switches and make them work in human cells. And rather than doing that, which hasn't worked very well. We built, we use the theory of Reiber switches and we built based by base our own switch. So we built it in mammalian cells.We then tested many switches and we have a platform of switches we can control. We were able to make these really simple switches, which switched on and off to high dynamic range. So 5,000 fold above the off level when they're switched on. And as a consequence of that, we were then able to change the drug that we activated with.So now we have multiple genes that we've put our switches in sitting in our freezers. So, uh, various antibody, PCSK nine antibody. You'll be aware of, uh, PD, one antibody, the, the very large drugs we can regulate. And then other drugs like GLP one, obviously a diabetes and obesity drug, which we can regulate.So we've got those genes and we can now put them into vivo in mice and NH PS, and we give those animals small molecules and we've already shown. Based specifically on the dose of the small molecule, we see our drug switched on to exactly the right level in each animal, depending on the dose of the small molecule you give.So we have built this over the last five years and we have moved from cells to mice, to non-human primates. And we're currently in a position to start doing I N I N D enabling studies for both the small molecule, all drugs and the genes that they regulate. Uh, and then as far as use cases, I know you're working on, um, you know, you're working on applying this, um, to, uh, I disorders, right.Uh, but is that the only use case right now? Tell us about the other one. No. So, um, we developed this technology of controlling gene therapy with a pill in order to much more broadly open up the space that gene therapy could be used in. So. We do have a lot of expertise in the eye and a partnership with Johnson and Johnson for our rare eye disease programs, but in diseases like wet AMD or dry AMD or uveitis, those large diseases.These are targets for regulation with our cassette and small molecules. In the case of our wet AMD program, we inhibit VEGF like other companies do. But what we're able to do potentially is when we put that gene that blockades by Jeff into the eye, we can formulate one of our small molecules. That's otherwise oral into eyedrops.So what we're working on now is turning our small molecules into eyedrops. So we can put a wet AMD drug or uveitis drug into the eye as a gene and switch it on each day with an eyedrop. So the eye is an excellent place to be able to regulate gene therapy with a small molecule, another place, which is really important is in the brain because it's very difficult to get antibodies or biologics across the blood-brain barrier.But what we're able to do potentially is we have regulated antibodies and we can put the. By an injection into the brain, just a one-time injection within the blood brain barrier. And then all you need is a pill which crosses the blood brain barrier. So it allows us to deliver drugs that really hard to deliver by other routes.And there are many, many more applications. It, it hugely expands what you can use gene therapy for, because for the first time you can control how much you gave. And at what time, uh, it seems like broadly speaking Zandy, um, gene therapy, like what, like as an investment, it was like super sexy a couple of years ago.Right. And then it sort of, it was super hot and then came down a little bit and was like, oh, wait a minute. This is still really days. Where, where are we now? Are we like back to, is gene therapy being like the hot, the hottest topic in biotech? Or, or are we still sort of, is it like the off cycle? I dunno how else to phrase it?W well, I think there are, there are many different gene therapy companies and there is cell therapy companies. There are very, very large number of, of, uh, therapies in the genetic medicine space. And, um, and there are some companies that just have a product or a platform or a particular organ that they focus on and that.Is a somewhat higher risk to those companies that depend on data around a particular study, right? What is quite different about mirror is that we established the company to really innovate in gene therapy and shows indications in the clinic that had good proof of concept and highly likely to work and to support a future pipeline.We built everything you need to be a gene therapy company in-house so we have multiple promoter platforms, multiple capsid discovery efforts. We have our own internal manufacturing, which is probably the broadest engine therapy today in that we manufacture our own GMP plasmid. We have two, uh, viral vector manufacturing facilities, which are flexible and scalable to commercial scale.And we do our own QC and analytics as well as potency assays. So we have a very, very broad, I suppose, toolkit that's required for anything. That you need to do in gene therapy and went out, positioned with this regulation ability with a deep pipeline of regulated genes that we can then take through to the clinic with our vector ecology and our own GMP manufacturing,not of the regulatory by putting all that in house. I was just gonna ask, as, as we get more developed in this space, like Spencer said, it seems like a couple of years ago, you know, that the gene editing space was huge for investors. Uh, what advice would you give investors that are looking at different, uh, you know, genomics companies to, to be able to discern which ones are going to have an advantage in the, in the field once the industry does become more hot among investors?Again, I do think that right now, manufacturing is not just a bottleneck with respect to capacity, but, um, Dealing with regulatory agencies globally and an expertise in manufacturing process. And, uh, and the assets required to show the release and stability of your products is very, very important. And to be able to either have that, to have as much of that as possible in house dearest clinical programs that you'll see, particularly if you have those sorts of capabilities at the time of D you really don't want to see companies that are starting manufacturing their product in one way.And then at phase two, switched to another way and then have to scale it later. Ideally, you would look for companies that have capabilities that allow them not to necessarily rely on CRS for plasmid manufacturing or in DQC. And we learned that over the last five years, it's one of the reasons we've bought, uh, so many of these capabilities in house, but I do think that's very important.Um, in addition to obviously, you know, do the targets work or is this, is this an appropriate, um, disease for gene therapy, the nuts and bolts of being able to produce and show the agencies that you've produced the right thing, a really important. Zanni Forbes is the presidency of Mira GTX. As I mentioned, there's a lot going on.You guys also got some positive in Canberrans over the weekend and, uh, uh, a lot of presentations after being in stealth mode for quite some time. So, uh, looking forward to seeing how things develop here and, uh, and, and, and good luck going forward. Thanks a lot for coming on today. Thank you so much. All right.Hey, w we got to keep the train running on time here. We've got so many guests today, back to back to back to back let's pivot. If we can, maybe we just spent the last half hour or so talking biotech, uh, let's pivot to like supply chain, specifically, uh, supply chain of textiles, right fashion. And what exactly is going on there?What to find out? We're going to bring on our next guest here in just a second and running Samuel. He is the CEO of a cornea technology, and, uh, let's bring coordinates and a Ronan. W that's been running on this show. Now, if we can guys, I guess I'm Spencer, I guess I'm doing that. All right. I got you right.There you go. Good morning for us this afternoon for you it's later on in the evening. So I appreciate you, uh, coming on, uh, the, the, uh, the show here today. So, uh, let's talk about textile supply chains, right? Uh, what exactly is going on there right now are things as bad there as they are in other areas of the.Well, um, yeah, it's bad. And it has to change the supply chain is broken, but even more than that textile industry and fashion industry in particular is the second most polluted industry in the world. Um, from different reasons. One of the reason is that 30% of whatever put use on textile is actually never been sought.Uh, and this create a huge amount of waste, both of materials and water, and we have to save the world. Um, uh, so we have to change the industry. Now, the reason for that is some of it is because the supply chain of today doesn't meet or doesn't fit the need of the consumer of today. The supply chain of the textile industry is like centuries ago, you produce in large quantities in forest, in China, in Magilla dish, you trying to forecast what the consumer, what the people would like to buy a year in advance, sometimes 18 months in advance, which is impossible.It's crazy to think that you can predict what the consumer today would like to wear in a year and a half from now. So we have to change it. The world move to digital in many, many industries. And in this industry is still fully. Yeah, I'm glad you brought up the, uh, you know, the environmental impact of the textile industry, because that's something that's gained a lot of attention over the past year or so.I mean, you have a quote unquote fast fashion companies, such as sheen and people have kind of started attacking the, the idea that, oh, buying, you know, a cheap t-shirt for $15 or some pants for $15 that you see an ad for an Instagram, uh, causes a lot of environmental distress. So what do you think needs to be done in the industry to address that?So they, this would need to change in order to try to predict what the consumer would like to buy and put, use Lauder moms of products, which will never been sold is to produce, to demand, to produce after the consumer.But that's not efficient. I mean, it you're saying it is, but that's not a necessarily inefficient use of capital though, right? No, no. It's, it's actually a very, very efficient, um, hold on, explain to me, explain to me, yeah, let's begin with, first of all, what we see that production is really moving on shore.Why it's moving on shore, not only because the, the, the supply chain is broken because you have to be closer to the consumer. You have to react fast for the consumer trends. Now, the world of fashion and textile move is moving online today. 30% of all purchases being done online. So e-commerce the focus by 2025, that it will be more than 60%.Now, the online the e-commerce of today is still trying to sell you what they have in the inventory or what they have in the shops, in the stores. Uh, and if you going to order products, sometimes it does not exist at all. Um, and uh, sometimes, um, for the brands is really, really difficult to. Okay. Can you hear me okay?Yeah, we, we, you we're fine. We just got disconnected, but we're back. Okay. So, so I missed everything you just said. Okay. Okay. So let me try to explain again. So the world is moving digital. What does it mean? The consumer today's buying? So e-commerce online. 30% of all sales is being done online and the focus by 2025, that it will be 60%, but the online is today's actually a mirror of the store.Doesn't allow you to choose your product. They're trying to sell you what they have in inventory, which doesn't fit what this consumer would like, what we believe needs to be done, that the online should be filterable. You shouldn't have any real physical products. You can have endless amount of product virtually and connect the virtual wall to the physical world.And this is exactly what committee's doing is enabling on demand, production. You order what you want only. Then you produce it. You produce it close to the consumer. Onshore and delivering, you know, the same day on the next day to the consumer, the product, I feel like this is I'm in now. It sounds great. I think that, but that's like, that's more difficult, right?Well, I give it a few examples. Well, one example, great example. Thinking about the books book markets, um, back at 25 years ago was fully analog. You went to a bookshop, you tried to buy a book. You only have them, the shelf, the books that we're selling in millions of copies, Amazon disrupt this market. They created a digital world.You could go to Amazon buy any type of book, even from 200 years ago. But what they create is actually much more, the impact was much more than that because now everybody can become a writer. You can write a book about your family, about cooking, about anything you like, you publish it. Virtually doesn't cost you anything.Only when someone is ordering, then you print it and send it to the consumer. So the same thing is happening now in the fashion world, you don't need to have it physically. You actually unleashing creativity because you can have endless creativity and each one of the consumer can choose whatever they want in any Colleen, any design.And once you choose it only, then you produce. So this is efficient and there is no way. And you produce it using coordinate technology, which is a fully sustainable green technology. That was my next question was just if you to clarify that, so I come up here like Amazon, for example, uh, could have used your technology, right.Or, or any retailer, right? Could just buy your technology and, and use that along their supply chain to make it more and more green, more efficient. Right? Actually, Amazon is our biggest customers. Okay. Amazon is our biggest customer, but we have many, many more customer. We are worth more than 1000, 300 customers that using our technology all over the world.Some of them very big companies like Amazon, like Adidas, like fanatics, but using our technology. And you can go online and order products and customize the product and order your t-shirt here. You can see with coordinate on top of that or on any color, any size, any shape. And this is the new world. Look what the world is moving into.What is moving into metaverse. So metaverse is everything is virtual. You will have. Your image in the metaverse. Yeah. You will be able to dress it as you wish with any, any type of, of, of goods. Uh, and only when you feel that you lack it, then you order it and then it would connect it to the physical world, which will be big produce next to you.If you are in New York, it will produce in New York. If you are in Beijing, will be produced in Virgin and shipped to you the same day. So the impact on the environment in terms of sustainability is huge and their efficiencies and believable, and the creativity is unleashing the creativity for the designers and for the brands.W why is no one else doing this? Or are they well, uh, there are some, uh, companies, our customers that using our technologies like Amazon are doing it. If you go to Amazon and you're doing what you're doing, right. That's what I meant because, well, we are kind of unique festival in terms of the physical world.We out technology, what we have developed is systems Inc services that is all sustainable, which are digital systems that can produce one off. If you want it to produce a t-shirt or any, any government or any fabric in the, in, in the past using analog technology, you had to print where to produce hundreds of meters in order that it will be economical and.The sustainability impact is huge. Um, there's a lot of pollution and consumption of water for every meter without technology, because it's digital, you are not limited. You can print one t-shirt, you can print one meter, one fit, there's no limitation and every feed can be different design. So this is the advantage of digital is unleashing the limitations that you had before, and we are not using water.So there's no, there's no water consumption. It's pigment ink. So it's fully green. So no impact on the environment. So like who couldn't use corny Amazon obviously, but they're the largest retailer in the world could, could, could I use it on my online Shopify store that make, that sells? I dunno, 10 shirts a year.Exactly the point it's off form. The biggest retailers, biggest e-commerce biggest brands like Adidas, Nike. They of course can use it to anyone, any consumer that would like to open a shop in Shopify. Now, what is the problem with Shopify? If you are now at this time? And you see somewhere in India and you would like to, to sell your product.You open the shop in Shopify in five minutes, you put your design, what is the problem? Once you get the order, what are you going to do with it? How are you going to produce it? Are you going to ship it out? We can compete against other marketplaces. What call Nita Naples is to connect all those and marketplaces all those designers in to a network of fulfiller that can fulfill for them.So you need to take care of only on the design, open a shop, and then connected to Coney ticks. And kinetics is a platform that connect them to a network or fulfiller that using our technology and can produce it anywhere around the world. And it sounds good. The market clearly likes it. Cause if you, if you look at your stock, it's had a pretty tremendous run actually, even, even last year, uh, seemed to, uh, COVID, didn't seem to hold it down too long.So, uh, the market agrees with you. Uh, so I, I guess keep doing what you're doing. Uh, running Samuel was the CEO of, uh, coordinate, uh, digital. Uh, we will have to get you back on the show. Uh, hopefully, uh, now maybe next year when, when the supply chain starts to work itself out a little bit, but I, I I'm, I'm very curious about this space because, uh, you're, you're one of the best performing stocks, uh, I think out there probably right now.So, uh, Ronan, thank you so much for coming on the show today. Thank you very much. Pleasure being here. All right. Uh, it is, uh, 1259. We've got our next guest coming on in couple minutes. Whenever minute when it, whenever they join, to be honest, cause they're not even here yet, but that's okay. Uh, Scott Mathis is the CEO and chairman of Gacha holdings, ticker V I N L a.And then we have, I'm very excited for our one to 30 guests, but we're not a Capels from Benzinga and, uh, really Benzinga is, is a side it's his side gig. His main gig is, uh, is doing really complex. Trading stuff, strategies. So, uh, I'm, I'm very, I'm very much looking forward to that, uh, in a half hour. Uh, if we can think of who executive though, and I have not grabbed, voted for likes yet this hour as we enter our two of our show keyword yet, uh, if you could be so kind and hit that thumbs up button on your screen, I'm not sure where we're at on the light counter right now.Let's look, we're at the de come on computer 74, 75. We can do better than that. We do over a hundred easy, easy. The goal for the goal for the day is 200, but we can get you a hundred right now. I suspect. Yeah. So before we get to Scott Mathis with a wild show holdings, um, the, uh, the previous guest, I liked that idea of cause basically what he's saying is that companies now are producing clothes for a year down the line, right?But they don't know what's going to be hot on Instagram and Tik TOK and what the trends are going to be efficient. It's not efficient. So what, what he's saying they're doing is waiting and basically it's print on demand, but on a huge scale, like what Shelly was talking about in the chat with the economies of scale, they're able to produce, uh, the goods for cheaper when they're doing it on a large scale.If everyone, if they're, if their technology is able to kind of shift that whole industry, it would have a tremendous impact on, uh, the environmental right now, the negative environmental impact that the textile industry has. Another fun fact. Spencer, did you know this, that a lot of luxury brands, um, such as, you know, Gucci, Louis Vuitton, do you know what they do with their extra extra goods?No, I don't want to say something that's politically incorrect, but I know I have no idea. What could, what would the, I don't know. They, they, they, they give it the, give it to animals. I don&
This week's episode features author Benjamin Levine and Guest Editor Walter Paulus as they discuss the article "One-Year Committed Exercise Training Reverses Abnormal Left Ventricular Myocardial Stiffness in Patients with Stage-B HFpEF." Dr. Greg Hundley: Well, welcome listeners. This is the September 21st podcast for Circulation on the Run. Sadly, I'm without Carolyn today, but I am your host today, Dr. Greg Hundley, associate editor and director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Dr. Greg Hundley: Our feature discussion today is really interesting. It's from Dr. Ben Levine, and he's evaluating the utility of exercise training and actually trying to reverse abnormal left ventricular myocardial stiffness in individuals that have stage B, it's a very early heart failure and preserved ejection fraction. But before we get to that, let's grab a cup of coffee and we're going to work through some of the other articles in this issue. Dr. Greg Hundley: So the first one comes to us from Göran Bergström from University of Gothenburg in Sweden. He and his team used coronary computed tomography angiography or CCTA to determine the prevalence, severity and characteristics of coronary atherosclerosis and its association to coronary artery calcification scores in a general population of greater than 25,000 individuals all aged 50 to 64 years and without known coronary heart disease. It really comes to us from the Swedish CArdioPulmonary BioImage Study or SCAPIS. Well, Carolyn would ask me that is a really large study, and what did they find? Well, let's get to the results. Dr. Greg Hundley: So using CCTA to detect silent coronary atherosclerosis, the investigators showed that any coronary atherosclerosis was actually quite common, 42% of individuals and significant stenosis of greater than 50% was less common, only 5% of individuals. More severe forms were rarely found, only 1.9% in this very large, random sample of middle-aged individuals. Dr. Greg Hundley: Now disease onset was delayed by 10 years in women and a higher prevalence of coronary atherosclerosis was observed with higher age and accumulation of risk factors. Interestingly, CCTA detected atherosclerosis increased with an increasing coronary artery calcium score. All those with a high CAC score of greater than 400 had atherosclerosis and 45% had significant stenosis. 5.5% of those with no coronary artery calcification had atherosclerosis and 0.4% had significant stenosis. So although there was a strong association with high coronary artery calcium scores and significant stenosis, atherosclerosis was not excluded in those with zero coronary artery calcification especially in those with high baseline risk. Dr. Greg Hundley: Well, our second article comes to us from the world of preclinical science and it's from Dr. Nathan Palpant from the University of Queensland. So the article pertains to ischemia reperfusion injury, and it's one of the major risk factors implicated in morbidity and mortality associated with cardiovascular disease. Now during cardiac ischemia, the buildup of acidic metabolites results in decreased intracellular and extracellular pH that can reach as low as 6 to 6.5, and the resulting tissue acidosis exacerbates ischemia injury and significantly impacts cardiac function. Dr. Greg Hundley: So the authors today use genetic and pharmacologic methods to investigate the role of acid-sensing ion channel 1a or ASIC1a, we'll call it from now, in cardiac ischemia reperfusion injury at the cellular and whole organ level. Human induced pluripotent stem cell-derived cardiomyocytes as well as ex vivo and in vivo models of ischemia reperfusion injury were used to test the efficacy of ASIC1a inhibitors as pre-imposed conditioning therapeutic agents. Dr. Greg Hundley: So what did the authors find in this study? Well, they demonstrated for the first time that acid-sensing ion channel 1a or that ASIC1a mediates cardiac ischemia reperfusion injury. The authors identify that ASIC1a inhibition is a novel therapeutic strategy for preventing acute injury response to myocardial ischemia reperfusion injury. Dr. Greg Hundley: So what are the clinical implications of this research? Well, first there are currently no drugs in clinical use that prevent acute injury response to myocardial ischemia, despite many promising candidates identified over decades of research, all of which ultimately failed in subsequent clinical trials. Second, the identification of new therapeutic targets for preventing the injury response to myocardial ischemia reperfusion injury would therefore have profound implications in cardiovascular medicine. Therefore, the results of this study reveal that ASIC1a inhibiting drugs, they're safe and they have potential applications in heart transplant and myocardial infarction with potential use in other clinical scenarios where myocardial ischemia reperfusion injury is a risk such as those that undergo cardiac surgery. Dr. Greg Hundley: Well, our next article comes from Robin Choudhury from the University of Oxford. Have you ever wondered why cardiovascular risk and diabetes remains elevated despite glucose-lowering therapies? Well, these authors hypothesized that trained immunity in response to elevated glucose accounts for diabetic hyperglycemic "memory", we'll call it, in relation to atherosclerosis. So accordingly, the author sought to determine if hyperglycemia-induced disease relevant changes in monocyte and macrophage function and whether these changes persisted after restoration of normal glucose, thereby implying fundamental reprogramming. So the team combined studies of cellular function, metabolomics, transcriptomics and epigenomics to define how hyperglycemia altered metabolism to modulate long-term activation through epigenetic modifications. Dr. Greg Hundley: Well, what did they find? First, hyperglycemia induced a trained immunity in bone marrow progenitor cells by inducing persistent epigenetic modifications. Second, hyperglycemia-induced trained immunity persisted after differentiation into those macrophages. Finally, hematopoetic stem cells transplanted from mice with diabetes to euglycemic mice promoted exaggerated atherosclerosis. So therefore, the findings of this study may explain the resistance of macrovascular complications of diabetes to conventional glucose-lowering treatments. Dr. Greg Hundley: Well, in the mailbag this week, there are some other articles. Professor Huang has a Research Letter entitled, “Adrenergic-Thyroid Hormone Interactions Drive Postnatal Thermogenesis and Loss of Mammalian Heart Regenerative Capacity.” Dr. De Caterina has an In Depth article on coronary artery anomalies. Finally, Professor Merid has a Perspective piece entitled, “Digital Redlining and Cardiovascular Innovation.” Dr. Greg Hundley: Well, listeners, what a great group of articles, and now we're going to turn to that feature discussion with Dr. Ben Levine. Dr. Greg Hundley: Welcome listeners to our feature discussion today and we're very fortunate. We have with us, Dr. Ben Levine from UT Southwestern in Dallas, Texas and also Dr. Walter Paulus from Amsterdam. Welcome gentlemen. Dr. Greg Hundley: Ben, we'd like to start with you. Could you describe for us a little bit of the background related to your study and what was the hypothesis that you wanted to test? Professor Benjamin Levine: Sure. Oh, nice to talk with you, Greg. As you know, our lab has been very interested in the effects of both aging and physical activity on cardiac mechanics. To cut a very long story short, what we know is that sedentary aging leads to stiffening of the heart. We also know that HFpEF, heart failure with preserved ejection fraction, is a disorder predominantly of the aged. I don't know about you, Walter, but I've never seen any lead masters athlete HFpEF. Professor Benjamin Levine: What we've shown is that if you regularly exercise over a lifetime that the heart can preserve its youthful compliance and flexibility. But if you wait until somebody is older, meaning over 65, 70, regardless of how hard or intense we train, the heart seems to lose its plasticity. It can't actually get that much better. But if we start in late middle age, it turns out that you can actually reverse some of the adverse effects of sedentary aging. So we said, "Okay, we know what the dose is, how much exercise you need to do. We know what the sweet spot in time. Now how do we find those people who are most likely to go on to develop HFpEF in whom getting them on a regular exercise program might help forestall this very challenging syndrome." Professor Benjamin Levine: So as part of an AHA-funded strategically focused research network and prevention, we identified a group of patients who had left ventricular hypertrophy, but evidence that they were on the wrong path. Their biomarkers were elevated. They have an elevated NT-BNP or a high sensitivity troponin. We did a right heart catheterization and we looked at their cardiac stiffness using a technique that we've done now for the past 25 years or so, and showed that indeed those patients' hearts are clearly stiffer than healthy, but otherwise sedentary middle-aged individuals. Professor Benjamin Levine: So our key question was what happens if we put them on a long sustained high intensity exercise program? Can we reverse the effects of sedentary aging superimposed with hypertension, left ventricle hypertrophy and elevated biomarkers? Dr. Greg Hundley: Really interesting, Ben. So describe your study design for us. How are you going to set up? It sounds like a very elaborate experimental setup here. Then also, maybe just define for us your study population. Did you have men and women or- Professor Benjamin Levine: Yeah, we started by going to the Dallas Heart Study. We're blessed here in Dallas by having this room access to our remarkable population where we know a lot about them. So we picked people in late middle age of all races, both sexes, and we reached out to the members of the Dallas Heart Study if they had left ventricular hypertrophy by echo or MRI and were of the right age range. We enriched that database by going to an EKG database and looking at the Ecolab database, trying to find people who did not have heart disease already. That was important. They couldn't have had a heart attack. They couldn't have had heart failure. They couldn't have had infiltrative disease. They had to be generally healthy except had left ventricular hypertrophy. Professor Benjamin Levine: We screened a lot of patients to get there, I have to acknowledge that, almost 4,000 of them or so to get the small number who were interested in doing a one-year exercise training program. But as we eventually got a good solid number that because we use such high resolution techniques, we were able to define the key outcome variable, which is cardiac stiffness. Professor Benjamin Levine: Briefly in our lab, we put a right heart catheter in to measure wedge pressure. We use 3D-echo to measure volume and then we use something called lower body negative pressure to unload the heart. It's almost like standing up progressively or tilting upright and then we give them a rapid saline infusion, 200 mls a minute. So a lot of saline, 15 and 30 mls/kg. We can get the left atrial pressure from about three or four up until about 18 to 20 and define the entire physiologic range of left ventricular filling. We look not just at the wedge pressure of course, but the transmural pressure. Professor Benjamin Levine: John Tyberg and his colleagues in Canada have shown clearly that the pericardial pressure is pretty close to right atrial pressure. So transmural pressure, which is the distending pressure of the heart, is left atrial minus right atrial pressure. We use that as the input into a pressure volume relationship. Dr. Greg Hundley: Very nice, and then what did you find? Professor Benjamin Levine: Well, what we found is after demonstrating that these patients with LVH and elevated biomarkers have increased stiffness, what we found quite remarkably actually was that we were able to reverse that by a year of training. Professor Benjamin Levine: Now when I say training, I mean, we do use the optimal approach to training that we've demonstrated in our lab. We didn't just pick one thing, get on a bike, do that for 30 minutes three times a week, right? These were sedentary people so we built them up slowly over about seven months. We added frequency, we added duration, we added intensity. Professor Benjamin Levine: I am enamored by the four by four in old Norwegian ski team workout, which is four minutes at 95% of max followed by three minutes of recovery repeated four times. We added interval training and long slow distance battle lasting about an hour on the weekends and a little bit of strength training, too. Professor Benjamin Levine: So what we consider the ideal prescription for life, four to five days a week, one long session, one high intensity session, two or three moderate intensity sessions and a little bit of strength. We did it for a year. It took a lot of effort. We had dedicated trainers. We gave them all heart rate monitors. Each person had a trainer to follow them. Professor Benjamin Levine: We did have a control group. We randomly assign them to a group that did stretching and yoga and mindfulness and a little bit of strength training, which makes people feel better. But we know from experience, it doesn't make them fitter and doesn't change their cardiac compliance. Dr. Greg Hundley: What happened with the treatment group? Professor Benjamin Levine: Oh, they got much more compliant. They got as compliant as if they had been training most of their lives. It was quite remarkable, actually, frankly, better than we expected it to be. We check the data multiple times by multiple people to make sure that this was a real finding. We really reversed much of the effects of the adverse effects of sedentary aging plus LVH. We hope that if that would be sustained over more than a year, years of long training study, there are very few training studies that go that long. But it's not a lifetime and at least we've set the stage for the concept that if this were to be sustained over a lifetime that we think it could forestall HFpEF. Dr. Greg Hundley: Very nice. Well, Walter, I know serving as a guest editor for us at Circulation and we're most appreciative for you doing that task. What struck you about this particular article and really enticed you to want to help us move it toward publication? Professor Walter Paulus: Well, I felt that the article was very visionary. Of course, as it comes from Ben, I didn't expect anything else. But what struck me were two points. Professor Walter Paulus: First of all, he looks at patients which we would label type B HFpEF. Most of our efforts have always been focusing on sick people, stage C HFpEF, stage D HFpEF. Now Ben was so clever to go to an early stage, and I believe that many of the so-called neutral outcomes in therapy for HFpEF are related to the fact that we actually address patients population who is quite far out on its natural history. So I think this was the first point to me. He, Ben, was addressing a population at the early stages of HFpEF. Professor Walter Paulus: The second point that struck me was that the variable he was looking at is in my opinion the key variable in HFpEF. It's the main reason I appreciated that this is the disease of myocardial compliance of left ventricle stiffness, and then very nicely addressed the stiffness of the heart as its primary outcome. This is something what we miss in all the pharmacological trials. I have always been curious when are we going to see the pharmacological trial whereby somebody is going to evaluate a compound in terms of its effects on left ventricular stiffness on myocardial compliance. Professor Walter Paulus: So these were for me two very salient features and very visionary in terms of treatment of a HFpEF population. Also, a couple of things that need to be clarified for me and I did. The patient's entry criteria were very demanding, has been also already said. I have the feeling that if you have LVH and then you will try NT-proBNP to be elevated and all your required troponins to be elevated, it's probably be very hard to get such a patient population and that may be then the only remark that could come up toward an extent in such a patient population still reflective of everyday health. Dr. Greg Hundley: Very good. Well, Ben, coming back to you, what's your next study? Professor Benjamin Levine: Well, we have a large program project grant, Greg, funded by the NIH, looking at the mechanisms of dyspnea and HFpEF. We're now just entered our third year. We're looking at a strategy to try to lower cardiac filling pressures acutely to see if that improves exercise tolerance and reduce dyspnea. We're looking at peripheral mechanisms of oxygen uptake and utilization and vascular control. We're looking at autonomic function, sympathetic nerve recordings, regulation of the sympathetic nervous system. We have a group focused on pulmonary mechanics, particularly on the effects of obesity. Professor Benjamin Levine: Our team with Tom Sarma is our recruitment core expert and one of the Circulation editors and is really the lifeblood of our study and leads our effort. We have Paul Fidel from UT Arlington who's leading our peripheral function studies, Qi Fu from UT Southwestern leading our autonomic group, and Tony Babb also from Southwestern in the pulmonary division leading our pulmonary mechanics. Professor Benjamin Levine: So we're entering this phase where we're trying to say, "Are there other components?" We know myocardial stiffness is a key factor, but what else in patients with the already manifest HFpEF is causing them to be so short of breath and can we change that? Professor Benjamin Levine: So that's what we're doing next, Greg. I think that if you ask what is the next step from this study, I think it has to be population-based and pushing the concept that exercise is medicine. When you find patients who have hypertension in general, and most of these had hypertension or diabetes, I mean, Walter has led this field and in emphasizing these comorbidities and what they do to the heart and the vasculature and the rest of the body, we have to catch people early. We can't wait until they have full-blown manifest HFpEF. We have to get them to include exercise as part of their personal hygiene. Professor Benjamin Levine: I know that that's a major effort from the American Heart Association. But I think that for the long-term health of our population and preventing this disease that is so difficult to treat when it's firmly established, we have to as cardiologists and as a healthcare system, we have to start by including incentives for reducing healthcare costs to get people to use exercise as part of their personal hygiene and daily life. Dr. Greg Hundley: Very nice. Walter, from your perspective, what do you see are the next studies that need to be performed in this sphere of research? Professor Walter Paulus: Well, I will be very curious to see how many patients would actually go on to develop HFpEF in their life. It should be as if Ben's hypothesis holds, then the control group probably would have an access development of HFpEF compared to his exercise training group. I think that would really extend to study from above, from a mechanical observation to a clinically, epidemiologically more relevant endpoint. So I think that to me would be the first question, how many patients will evolve to clinical HFpEF. Professor Walter Paulus: Second point I would be very intrigued in is, are there SIP groups in the patients who have a positive response to exercise? For instance, what happens with the different ejection fractions? Because we are very intrigued at present in HFpEF that at high ejection fractions nothing seems to work. Sacubitril was notable at high ejection fractions. Empagliflozin was also neutral to ejection fractions. What would happen with exercise? Do the patients who present with the 70% ejection fraction at the angio study, do they still have a positive response? This would be a game change because this would then be the only intervention that is able to cure the HFpEF with high ejection fraction. These are some future projects that come into my mind. Professor Benjamin Levine: Let me just add that we have studied and put patients with HFpEF on a yearlong exercise program with not as much effect as we would like. I think that's one of the things that pushed us to getting earlier into the course of HFpEF, as Walter said earlier. Professor Benjamin Levine: Ambarish Pandey and Jarett Berry, also from UT Southwestern, of course are very interested in this effect of fitness at different points in the lifespan, our fitness test, for example, measured in mid-life and what means for heart failure later. I think it's hard to do the kind of studies that we do and follow patients for 20 years to see if they're going to develop heart failure, and that's where I think being creative and looking at the studies that incorporate an assessment of fitness and that follow people over time will be very informative. I hope with me, Walter's hope and hypothesis that these patients are less likely to develop HFpEF. We've got to get in there early. Dr. Greg Hundley: Very good. Well, listeners, we want to thank Professor Benjamin Levine from UT Southwestern in Dallas and also Dr. Walter Paulus from Amsterdam for bringing us this really interesting study, indicating that in patients with LVH and elevated cardiac biomarkers, sort of the stage B HFpEF that one year of exercise training reduces left ventricular myocardial stiffness. Dr. Greg Hundley: Well, on behalf of Carolyn and myself, I want to wish you a great week and we will catch you next week on the run. This program is copyright of the American Heart Association, 2021. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more, visit ahajournals.org.
Uluslararası Hipertansiyon Derneği tarafından Haziran ayında yayımlanan global hipertansiyon uygulama kılavuzları ışığında hipertansiyonun tanımı, hipertansif acillerin yönetimi ve kullanılan ilaçların yer aldığı bir derleme yapmak istedim.1 2 Keyifli okumalar. Kan basıncı yüksekliği, yılda 10,4 milyon ölüme yol açarak dünya genelinde önde gelen morbidite ve mortalite nedenlerinden biri olmaya devam etmektedir. Dünya çapında rakamlar incelendiğinde, 2010 yılında tahminen 1,39 milyar insanın hipertansiyon tanısı almış olduğu ve hasta dağılımının gelişmiş ülkelerden düşük gelirli ve gelişmekte olan bölgelere kaydığı görülmektedir. JNC 8 uyarınca kan basıncı sınıflaması tablodaki gibidir: EvreSistolik Kan Basıncı (mmHg)Diyastolik kan Basıncı (mmHg)Normal< 120< 80Pre hipertansiyon120-13980-89Evre 1140-15990-99Evre 2> 160> 100HİPERTANSİYON SINIFLAMASI (JNC 8) Kan basıncının ideal ölçümü için 3-5 dakikalık dinlenme sonrası, sessiz bir odada, 30 dakika boyunca sigara ve kahve içmemiş, egzersiz yapmamış olmak gerekir. 1 dakikalık aralıklarla 3 ölçüm yapılmalı ve son 2 ölçümün ortalaması kabul edilen değer olarak alınmalıdır. Uygun manşon seçimi yapılmalı, kolun orta bölümü kalp düzeyinde olmalı ve manşon kolun orta 1/3’üne yerleştirilmelidir. Primer hipertansiyon tanılı hastalar genellikle asemptomatiktir, bulgu veren hipertansiyon sekonder bir nedene ya da hipertansiyona bağlı komplikasyona bağlı olabilir. Anamnezde aile öyküsü ve hastanın medikal geçmişi iyi sorgulanmalıdır. Hipertansiyona eşlik eden ve acil yaklaşım gerektiren göğüs ağrısı, sırt ağrısı, nefes darlığı, çarpıntı, kladikasyo, periferik ödem, baş ağrısı, bulanık görme, bilinç değişikliği, idrar çıkışında azalma, hematüri, baş dönmesi açısından hasta dikkatli değerlendirilmelidir. Anamnez Hipertansiyonun süresi, önceki kan basıncı seviyeleri, varsa mevcut antihipertansif ilaçlar, kan basıncını etkileyebilecek diğer ilaçlar, antihipertansif tedaviye uyum. Risk faktörleri: kardiyovasküler hastalık öyküsü, inme, geçici iskemik atak, diyabet, dislipidemi, kronik böbrek hastalığı, sigara kullanımı, sodyumdan zengin diyet, alkol alımı. Fizik Bakı Kalp hızı/ritmi, juguler venöz dolgunluk, apeks vurusu, ekstra kalp sesleri, periferik ödem, üfürüm varlığı (karotis, renal, femoral), palpabl tiroid, artmış vücut kitle indeksi. Laboratuvar Kan testleri: sodyum, potasyum, serum kreatinin ve glomerüler filtrasyon hızı. Mümkünse, lipid profili ve açlık glikozu. İdrar testi: proteinüri, albümin/kreatinin oranı 12 derivasyonlu EKG Hipertansiyon İlişkili Organ Hasarı Hipertansiyon ilişkili organ hasarı, yüksek kan basıncı nedeniyle organlarda meydana gelen yapısal veya fonksiyonel değişiklikler olarak tanımlanır. End organlar arasında beyin, kalp, böbrekler, merkezi ve periferik arterler ve göz bulunur. Genel kardiyovasküler riskin değerlendirilmesi yanında hipertansiyon ilişkili organ hasarının belirlenmesi iki konu nedeniyle önemlidir: Hafif-orta dereceli tansiyon yükseklikleri olan hastalarda organ etkilenmesi olması nedeniyle yeniden sınıflandırma yapılmasını sağlar. 2) Spesifik etkiye dayalı ilaç tedavilerinin seçimi konusunda önemli terapötik rehberlik sağlar. Beyin: Geçici iskemik atak veya inme yüksek kan basıncının sık bulgularındandır. Erken subklinik değişiklikler (beyaz cevher lezyonları, sessiz mikroinfarktlar ve mikrokanamalar) en hassas şekilde kranial MRI ile saptanabilir ancak rutin uygulamada yeri yoktur. Bilinç değişikliği, nörolojik bozukluğu ve amnezisi olan hastalarda düşünülmelidir. Kalp: Hipertansiyon nedeniyle periferik vaskuler direncin uzun süreli artışına bağlı gelişen sol ventrikül hipertrofisi (LVH), 12 derivasyonlu EKG’de saptanabilse de (Sokolow-Lyon kriteri: SV1 + RV5 ≥ 35 mm, Cornell kriteri: SV3 + RaVL erkekler için > 28mm veya kadınlar için > 20mm ve Cornell voltajı süresi: > 2440mm-ms) sol ön fasiküler bloğu olanlarda ya da genç hastalarda bu kriterlerin duyarlılığı azalacağı iç...
Broderick Chavez is a world-renowned biologist and sports performance coach. Broderick is known as “the drug guy” in the sports performance world, but he also is a book of knowledge when it comes to structuring strength and conditioning programs for elite-level athletes. We discuss more on the controversial topic that is, coronavirus. Later in the podcast, we move on to powerlifting and various complications that may arise throughout their careers. 01:04 - Just how contagious is COVID-19? 02:04 - Can you build an antibody for COVID-19? 03:42 - Has anything other information emerged as far as the deadliness or death rates of COVID-19? 05:46 - How many people are actually dying from COVID-19? 09:49 - The three potential outcomes for ending the coronavirus pandemic. 14:42 - The greedy end up with nothing. How coronavirus benefits no one in the long run. 20:00 - The problem with compounding pharmacies and their similarities to UGL companies. 27:06 - Heavy metal contamination, Fact or fiction? 30:08 - If you don't have symptoms, is it unlikely you have any chronic heavy metal accumulation? 32:18 - How valuable is testing for heavy metal contamination for someone like myself? 35:04 - Discussing my recent lab work with Broderick and the long term complications from dengue fever. 38:32 - How high of a urea value would you have to have to want a deeper look? Is there any kind of threshold? 45:40 - How long do heavy metals stay in the human body? 47:53 - What kind of clinical manifestations could this potential accumulation of heavy metals be causing? 54:01 - Thyroid. The T3 value and the symptoms are where the rubber hits the road? Broderick voices his opinion. 57:13 - Autoimmune diets and how fast they can bring down thyroid antibodies. 01:01:08 - Do females have better survival rates than males from coronavirus due to estrogen levels? 01:08:20 - Is there a difference in drug-induced LVH and a natural athlete? 01:09:51 - Why does Broderick prefer to work with powerlifters over bodybuilders? 01:11:12 - Why on average are strongmen and powerlifters chubbier than bodybuilders even on offseason? 01:28:47 - Estrogen and water retention. Does elevated estrogen directly relate to fat accumulation? 01:40:30 - Short term use of sleep meds and is it okay to use them? 01:41:29 - Increased appetite from THC use and it's common negative trade-offs. 01:42:10 - The psychoactive side effects of THC use. 01:58:50 - The mind-blowing doses of anabolic steroids that some professional athletes use. Instagram - https://instagram.com/danielpekic Twitter - https://twitter.com/daniel_pekic Facebook - https://facebook.com/daniel.pekic.96 My Website - https://danielpekic.com/podcast
Bart and Dave shoot the breeze and do a contest drawing for lucky subscribers who win a free 1% of their WSOP 2014 Main Event action! Congratulations to: Tinodollaz, matts25, LVH, bigirwin23, and gb4780! They also discuss Robocop selling action, a little WSOP ME strategy, and where to use the bathroom at the Rio.
Quad becomes the Linq Hotel & Casino, Westgate buys LVH, Aria fined for gaming violations, Grand Downward Spirial Update, Zippo Vegas, BLVD Creamery Revelation & 24 hours in Vegas.
Druff returns from a 10-day vacation after a stressful WSOP. Chinamaniac guest-co-hosts. We discuss the firing of UB cheating figure Bonnie Leinhos from her new job at the LVH poker room. We talk about PKR.com and their refusal to let go scamming pro Vladmir "Beyne" Geshkenbein, as well as PKR's own shady behavior involving reneging on deals with affiliates. Daniel Negreanu is talking trash about Tom Dwan in an interview. Is NioNio on UltimatePoker actually connected in a way to Russ Hamilton, or just a gimmick account? We talk about PPA getting an "unfavorable" rating in a recent poll on 2+2. There's a new poker show in development called "Poker Night in America", but does it offer anything new? Poker player Masa Kagawa was arrested as part of an Android Malware ring in Japan. The star of an upcoming CNBC sportsbetting show is actually a scammer. We break the bad news that Full Tilt payments won't occur until at least July 2014, and probably later than that. We reveal a surprising guilty plea in the Russian Mob gambling bust from a few months ago. Some baseball discussion occurs at the end of the show, as an elated Druff notices that the Dodgers have won their 27th game in their last 33. The site experienced crashes during the show, but the radio remained broadcasting and properly archiving.
Druff relives his depressing end to the WSOP Main Event, just a hair away from the money. El Chico Loco makes his return, and makes a prank call to UB cheating suspect Bonnie Leinhos (now the LVH Poker Room manager) that is both awkward and hilarious. Druff tells of a terrible bait-and-switch promo currently occurring at the Revel Casino in Atlantic City, and Colonel Fabersham calls up to demand answers. Mark Newhouse has made the WSOP Main final table, and Druff talks about his history with him. Vladimir Geshkenbein finished 62nd in the Main Event, but apparently scammed his original backers. An old man attempted to dump chips to a perplexed Doc Sands at the Main Event, but it backfired badly. Druff plays a video of Dutch Boyd talking about his fallout with Scott Fischman, and gives his own opinion. Bryan "PrimordialAA" Pellegrino defends himself on a BLUFF video, regarding the Lock Poker situation. A happy ending is revealed for Rio theft victim Eric Sonstegard. Druff announces the site's new sponsor, StatClash.
Fremont Shooting, Nugget charges for free experience, LVH supercontest, Krave Massive Opens, the poll, the announcement and Bryan returns to the show
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