Podcasts about diastolic

A recent 12-week randomised controlled trial involving healthy adults aged 55-70 yielded significant positive findings regarding pomegranate extract's effect on blood pressure. While the study might not have shown significant differences compared to placebo across all initially measured markers, it revealed important reductions within the group taking pomegranate extract daily. Specifically, participants supplementing with pomegranate extract saw a statistically significant average decrease in Systolic Blood Pressure (SBP) by 5.22 mmHg and Diastolic Blood Pressure (DBP) by 3.6 mmHg. The researchers highlight the potential clinical relevance of the SBP reduction, noting that a 5 mmHg drop is associated with an estimated 10% decrease in the risk of major cardiovascular events. These findings align with previous research and meta-analyses confirming pomegranate's blood pressure-lowering effects, suggesting pomegranate extract could be a supportive strategy for hypertension prevention in older adults."This information is for educational purposes only and should not be interpreted as medical advice.""The study discussed was a randomised controlled trial in healthy adults aged 55-70.""The significant positive findings highlighted are the reductions in Systolic and Diastolic blood pressure observed within the group taking pomegranate extract. The authors note the SBP reduction is potentially clinically relevant.""These blood pressure findings are consistent with other studies and meta-analyses on pomegranate, strengthening the evidence for this specific effect.""Always consult with a qualified healthcare professional before making any changes to your diet, supplement regimen, or treatment plan, especially regarding blood pressure management or if you have existing health conditions or take medications.""This channel is not monetized and does not provide medical advice."#PomegranateExtract, #BloodPressure, #SystolicBloodPressure, #ClinicalRelevance, #HypertensionPreventionFarhat G, Malla J, Vadher J, Al-Dujaili EAS. Effects of Pomegranate Extract on Inflammatory Markers and Cardiometabolic Risk Factors in Adults Aged 55–70 Years: A Randomised Controlled Parallel Trial. Nutrients. 2025; 17(7):1235.

Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances, discusses a recently published original research paper on Sex Differences in Achieved Diastolic Blood Pressure and Cardiovascular Outcomes in Elderly Patients With Hypertension.

Understanding systolic vs. diastolic heart failure is crucial for anesthesia providers, as both conditions present unique challenges in the operating room. In this episode, Terry and Gary break down the key differences between these two types of heart failure, their underlying mechanisms, and the best strategies for anesthesia management. They discuss the risk factors, symptoms, and pathophysiology of each condition, as well as how preoperative evaluation can help identify high-risk patients. The episode also covers the importance of intraoperative monitoring, fluid management strategies, and why tailoring anesthesia care to each patient can significantly improve outcomes. Tune in as they unpack the latest evidence, share real-world experiences, and provide practical takeaways for managing heart failure patients in the OR. Here's some of what we discuss in this episode:

Hey Heart Buddies! Boots Knighton speaks with Lucinda McDermott about navigating heart health after discovering a severely leaking tricuspid valve. Lucinda shares her journey, from initial chest pain and fainting to being diagnosed with a heart murmur by her OB GYN. After mitral valve replacement in 2017, Lucinda faced additional challenges, including fragmented healthcare and dismissive cardiologists. Both Lucinda and Boots stress the importance of patient advocacy, support networks like WomenHeart, and having a “heart doula” during medical appointments. The episode highlights key issues like secure insurance, patient empowerment, and the significance of clear communication with healthcare providers.Want to contact Lucinda? Email her: lucimc2319@gmail.comJoin the Newsletter for almost weekly content for this podcast and other heart related news.Join the Patreon Community! The Joyful Beat zoom group is where you'll find connection and hope that you aren't alone in your journey.If you just want to support the show as a one-time gift (thank you), go here.**I am not a doctor and this is not medical advice. Be sure to check in with your care team about all the next right steps for you and your heart.**How to connect with BootsEmail: Boots@theheartchamberpodcast.comInstagram: @openheartsurgerywithboots or @boots.knightonLinkedIn: linkedin.com/in/boots-knightonBoots KnightonIf you enjoyed this episode, take a minute and share it with someone you know who will find value in it as well. You can share directly from this platform or send them to:Open Heart Surgery with Boots Mentioned in this episode:Heart Valve Voice - USBe sure to check out HHV - US!HVV-US

In this podcast, Dr. Valentin Fuster discusses a groundbreaking study on using artificial intelligence (AI) in electrocardiograms (ECGs) to assess left ventricular diastolic function and predict outcomes in patients with significant mitral regurgitation. The study demonstrates that AI-driven ECGs can offer comparable prognostic value to traditional echocardiography, identifying high-risk patients and potentially revolutionizing cardiovascular diagnostics, though challenges around sensitivity, specificity, and patient selection remain.

An AI-ECG Algorithm for Left Ventricular Diastolic Dysfunction   Guest: Jae Oh, M.D.  Host: Anthony H. Kashou, M.D.    Diastolic function assessment is crucial in diagnosing, managing, and predicting outcomes in various cardiac conditions. It provides insight into heart health, particularly in diagnosing heart failure. Shortness of breath, a common patient complaint, often indicates elevated diastolic filling pressure if linked to a cardiac condition. Echocardiography is the primary method for assessing diastolic function, but it is operator-dependent and not always available. In contrast, ECGs are standardized and widely accessible. Although subtle changes in ECGs are not easily detectable by the human eye, artificial intelligence can identify specific conditions reflected in the ECG. By training an AI model with labeled ECGs based on diastolic function determined through echocardiography, researchers achieved high accuracy in detecting diastolic dysfunction. AI-enhanced ECGs can significantly impact the identification of both asymptomatic and symptomatic cardiac conditions, potentially streamlining diagnostic strategies and reducing costs. Future developments may enable patients to monitor their heart health using simple wearable devices, enhancing the management of heart failure and other conditions.   Topics Discussed: Your special clinical academic interest is echocardiography. Why are you interested in ECG AI in diastolic function? What is diastolic function and why is it important to assess diastolic function in clinical practice? Why did you decide to create AI-ECG for diastolic function assessment? What did you find and how do you envision AI ECG for diastolic function be used in clinical practice? 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.

In this episode, I take a brief look at blood pressure and why it's important to monitor our body's own canals of life. I studied the circulatory system back in 2008, prior to completing my coursework and exams for my qualifications in sports massage therapy and personal training, of which I recall was a far more complex subject matter than I had anticipated. Blood pressure is essentially the amount of pressure circulating against the walls of blood vessels, the majority coming from the heart pumping blood through our circulatory system. We have the following two terms when measuring this. Systolic (max pressure per heart beat) and Diastolic (min pressure between two heart beats). These measurements are taken in millimeters of mercury above the surrounding atmospheric pressure, this is known as (mmHg). Health care professionals often take our blood pressure readings, alongside various other vital signs, with a normal resting BP of 120 (mmHg) Systolic and 80 (mmHg) Diastolic being ideal for adults. Excessively low BP is known as hypotension and consistently too high is known as hypertension, normal is known as normotension. Chronic hypertension (high blood pressure) can cause a multitude of complications from stroke and heart disease to kidney failure, therefore it's advisable to visit your GP surgery for BP testing, or take your own readings at home with a quality automated kit. Lifestyles are an important factor to consider when addressing our BP, from workplace surroundings and driving to household habits and nutrition. We all know that physical inactivity plays a major role in unhealthy BP and as such cardiovascular exercise (walking, running, swimming, cycling, rowing) or even moderate to high intensity resistance based training are essential in the lifelong maintenance of our circulatory system. Stress induced lifestyles are commonplace in hypertension, often brought on by external factors, such as highly populated towns and cities, elevated crime rates, increased road traffic, target driven sales professions, cluttered households, raising children, marriage, divorce, financial problems and mentally/ emotionally subscribing to political ideologies, through mass hysteria social media outlets. As a professional personal trainer I often take clients blood pressure readings, alongside body composition and grip strength, with an eye on reducing hypertension through exercise, sleep and nutritional improvements. Alcohol and salt consumption are discussed during appointments, which clients can immediately make inroads to reducing one or both, by way of complete abstinence form alcohol and removing added salt in cooking / avoiding salt laden processed foods until hypertension readings are lowered. This is possibly more beneficial than a weekly exercise appointment, as salt and alcohol are generally available morning to night, seven days a week, whereas structured exercise appointments are usually one hour per week, or two if a client has excessive weight / body fat loss targets. Look after your heart and blood vessels folks and remember to ask for professional advice if you have concerns regarding low or high blood pressure. Listen to the episode here or on Spotify, Apple Podcasts and Amazon Music or watch the video on YouTube. Please subscribe to the channel for more free content and feel free to comment and share with your friends, family and colleagues. Thanks for listening.

How does a cardiologist treat heart failure? Diastolic and systolic heart failure. Which medications to start, what to choose next and what do the guidelines say about heart failure meds. ARNI - EntrestoACE InhibitorsARBSAldosterone Antagonists - Spironolactone and EplerenoneBeta Blockers - Metoprolol Succinate, CarvedilolSGLT2 - Farxiga, JardianceGLP1 - Ozempic, Wegovy, Mounjaro https://dralo.net/links

February is American Heart Month. When's the last time you measured your blood pressure? Do you know what "good" blood pressure even is? Or what about "good" cholesterol?Brush up on the fundamentals – and get some clear guidelines for keeping tabs on your heart health - from Dr. Marc Eisenberg, a cardiologist from NewYork-Presbyterian and Columbia.Click here for the episode transcript. 

Commentary by Dr. Candice Silversides and Dr. Florian Rader

What is HFpEF? Heart failure with preserved ejection fraction? It used to be called non systolic heart failure and diastolic heart failure. What is it? https://dralo.net/links

What is the difference between right and left sided heart failure? Diastolic and systolic? Right and left sided heart failure? https://dralo.net/links

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.02.546740v1?rss=1 Authors: Yoshinaga, D., Feng, R., Prondzynski, M., Shani, K., Tharani, Y., Milosh, J., Walker, D., Carreon, K., Boss, B. M., Parker, K. K., Pu, W. T., Bezzerides, V. J. Abstract: BACKGROUND: N-terminal-acetyltransferases catalyze N-terminal acetylation (Nt-acetylation), an evolutionarily conserved co-translational modification. Nt-acetylation regulates diverse signaling pathways, yet little is known about its effects in the heart. To gain insights, we studied NAA10-related syndrome, in which mutations in NAA10, which catalyzes Nt-acetylation, causes severe QT prolongation, hypotonia, and neurodevelopmental delay. METHODS: We identified a missense variant in NAA10 (c.10C greater than A; p.R4S) that segregated with severe QT prolongation, arrhythmia, cardiomyopathy, and sudden death in a large kindred. We developed patient-derived and genome-edited human induced pluripotent stem cell (iPSC) models and deeply phenotyped iPSC-derived cardiomyocytes (iPSC-CMs) to dissect the mechanisms underlying NAA10-mediated cardiomyocyte dysfunction. RESULTS: The NAA10-R4S mutation reduced enzymatic activity, decreased expression levels of NAA10/NAA15 proteins, and destabilized the NatA complex. In iPSC-CM models of NAA10 dysfunction, dysregulation of the late sodium and slow rectifying potassium currents caused severe repolarization abnormalities, consistent with clinical QT prolongation and increased risk for arrhythmogenesis. Engineered heart tissues generated from mutant NAA10 cell lines had significantly decreased contractile force and sarcomeric disorganization, consistent with the cardiomyopathic phenotype in the identified family members. Diastolic calcium levels were increased with corresponding alterations in calcium handling pathways. We identified small molecule and genetic therapies that reversed the effects of NAA10 dysregulation of iPSC-CMs. CONCLUSIONS: Our study defines novel roles of Nt-acetylation in cardiac ion channel regulation and delineates mechanisms underlying QT prolongation, arrhythmia, and cardiomyopathy caused by NAA10 dysfunction. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Commentary by Dr. Hector Villaraga

Dr. Martin answers questions sent in by our listeners. Some of today's topics include: Constipation food recommendation  Quickly lowering of blood pressure Niacin Pine Bark Extract effect on kids CoQ10 & ubiquinol Sjogren's High oleic sunflower seed oil Diastolic blood pressure Osteoarthritis in hips & knees Berberine  

Early recognition and resuscitation of patients in septic shock are critical skills for an emergency medicine physician. Many clinical decision-making tools have been developed and validated in their use to identify and define those who are in sepsis or septic shock, as well as predict a patient's overall risk of morbidity and mortality, including tools like the SIRS criteria and SOFA score. The diastolic blood pressure is determined by vascular tone, and thus it can be assumed that a decrease in the diastolic blood pressure should correlate with the pathologic vasodilation in septic shock. As a result, the authors of this study hypothesized that the relationship between heart rate and the diastolic blood pressure (i.e. the diastolic shock index) could provide providers a tool to quickly identify patients that are at risk for unfavorable outcomes.

1.07 Diastolic Heart Murmurs Cardiovacular system reveiw for the USMLE Step 1 exam. Diastolic heart murmurs occur when blood flow is turbulent during the diastolic phase of the heart Two diastolic murmurs discussed: aortic regurgitation and mitral stenosis Aortic regurgitation is caused by blood leaking backwards from the aorta into the left ventricle, resulting in a high pitched decrescendo murmur heard during diastole Aortic regurgitation is associated with conditions such as aortic root dilation, bacterial endocarditis, rheumatic fever, and bicuspid valve "A vacuum adds suction. Aortic regurgitation diastolic decrescendo" Mitral stenosis involves narrowing of the mitral valve, causing an opening snap followed by a rumbling sound during diastole The main cause of mitral stenosis is rheumatic fever "Ms snapped because her husband got strep throat from his lover. MS (mitral stenosis), snap'd (snap diastolic), strep throat (rheumatic fever)"

Today on War on Weight, I have Michelle McCoy from the Treasured Wellness podcast. Michelle is a certified Holistic Health coach and specific passions are: Adrenal Fatigue, Auto-Immune Disorders and Spiritual Health.   I'm super excited to have this conversation with her and talk about the foundations of a healthy life and the goal of optimal health for women over 40. When I listened to her podcast, I was like YES, YES, YES!   She spoke my language and reiterated so many of the basic health principles that are the foundations of the program that helped me lose 56 pounds*, OPTAVIA.  There are many ways to get to optimal health and I love having conversations and learning different ways to get there.    Michelle shares some key ways women over 40 can get to optimal health by putting just a few  healthy habits into place.    I love the wisdom she brings to the show today and how it connects the habits of health I put into practice in my life to finally win the war on my weight.   In the book Habits of Health, Dr. A states “a key study was published in the Arch of Internal Medicine. They evaluated over 25,000 people and concluded that by adhering to four simple lifestyle factors, you can reduce your risk of developing major chronic disease by 80%! Those lifestyle factors are: • No smoking • Have a BMI less than 30 • Perform three and a half hours a week or more of physical activity • Adhere to dietary principles such as a high intake of fruit, vegetables, whole grain bread, and lower your meat consumption Optimal and Ultrahealth™ Guidelines. Here are the key parameters we're aiming for: Systolic blood pressure 110–95 or less Diastolic blood pressure 75–60 or less Body mass index 24.9–19.5 (around 20 is ideal; no less than 18.5) Body fat 10% for men; 17–23% for women HDL (good cholesterol) 50–70 mg/dl Fasting blood sugar 75 mg/dl If I've said it once, I've said it a hundred times, this book is GOLD!  It's why I give a free copy to my clients with their first order because I don't want my clients to miss the magic of the program.  These books take you from diet mentality to lifestyle change. I have a passion to serve women and help them get to optimal health, so I'm here with resources to help you get to your optimal health whether it's a program I coach or another amazing coach that I have met along my journey. Michelle offers a beautiful holistic perspective on health and wellness for women, and I know you are going to love her as much as I do.   If you are interested in finding out more about her podcast, her services and to grab that FREE Foggy & Fatigued Blueprint, head on over to treasuredwellness.com.   Here's the direct link to EPISODE 80 :  Treasured Wellness Episode 80     EXCITING NEWS:  I've Co-authored an amazing new book called UNLEASH HER.  It releases on October 25th, you can order your personally signed copy from me by visiting coachkeatha.com and clicking UNLEASH HER.     You can also contact me, subscribe to my email list to get a weekly newsletter with great new tips and recipes and check out my new program coming: The Revelation Wellness; all on coachkeatha.com      *In a clinical study, the group on the Optimal Weight 5 & 1 Plan® lost 10x more weight than the self-directed group. Average weight loss on the Optimal Weight 5 & 1 Plan is 12 pounds (5.4 kg).  

Host Geoff Pardo talks with Adam Berman, CEO of Alleviant Medical, about the groundbreaking device treating heart failure without hardware or permanent implants. The Alleviant device mitigates shortness of breath in patients with diastolic heart failure by leaving behind a shunt cut from interatrial septum tissue. The shunt moves blood from the left atrium to the right, diminishing pressure on the lungs. Berman speaks about his start in biomedical engineering, gaining invaluable experience in the operating room, developing sales tactics and industry knowledge as a medical device field representative, and switching gears to create novel devices for cardiac care.  Links from this episode:  Alleviant Medical 

When was the last time you had your blood pressure checked? Do you know what your resting heart rate is? If you're exercising to lose weight or change the way you look, there are some important health markers you can use to track your progress instead. On this episode, Dr Sarah explains why you should keep an eye on your blood pressure and your heart rate. The information in this podcast is for general use, always consult your doctor or physiotherapist before undertaking a new exercise program. Contact us:womenlikeyoupodcast@gmail.com   WLY resources and recommendations: Australian guidelines to reduce health risks from drinking alcohol https://www.nhmrc.gov.au/health-advice/alcohol  CVD checkhttp://www.cvdcheck.org.au/calculator Influence of Physical Activity on Hypertension and Cardiac Structure and Function https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4624627/#R6 Physical Activity and the Prevention of Hypertensionhttps://pubmed.ncbi.nlm.nih.gov/24052212/ Target Heart Rate and Estimated Maximum Heart Ratehttps://www.cdc.gov/physicalactivity/basics/measuring/heartrate.htm WLY newsletter subscription  The Women Like You podcast is recorded on the lands of the Gadigal people of the Eora nation. We pay our respects to elders past, present and emerging. We acknowledge Aboriginal and Torres Strait Islander peoples as the First Australians and Traditional Custodians of the land where we live, work, and exercise. See omnystudio.com/listener for privacy information.

The double-blind, randomized phase III EMPEROR-Preserved trial showed a benefit of the sodium-glucose cotransporter-2 (SGLT2) inhibitor empagliflozin in patients with heart failure with preserved ejection fraction (HFpEF). Now let us dig a bit more into those headlines.

Commentary by Dr. Valentin Fuster

On this episode Dave is joined by Dr. Jerry W. Jones, MD FACEP FAAEM, to discuss why ST elevation is not always an infarction. Dr. Jones will highlight why we need to think about morphology and shape when interpreting ECGs and why reciprocal changes are just as important as the primary changes and more!    Dr. Jones is the CEO and Founder of Medicus of Houston. Medicus of Houston is a continuing medical education company that specializes in advanced ECG interpretation and instruction.  He is a Board-certified emergency physician, author, speaker, instructor and and internationally-recognized expert in electrocardiography. Dr. Jones is a diplomate of the American Board of Emergency Medicine who has practiced internal medicine and emergency medicine for over 40 years. Also In This Episode How to diagnose real infarctions How ischemia damages the cell Cells creating electrical current How electrical current creates is responsible for ST depression and elevation Systolic and Diastolic currents of injury How not to confuse subendocardial ischemia with reciprocal change    Subscribe to the video version of this podcast to have access to the visuals that accompany the audio as well as additional tools and resources to help improve your understanding.  Subscribe now at CurrentECG.com  And Stay Current!  

Commentary by Dr. Tozu Suzuki

For more information, contact us at 859-721-1414 or myhealth@prevmedheartrisk.com. Also, check out the following resources:  ·PrevMed's website·PrevMed's YouTube channel·PrevMed's Facebook page

Commentary by Dr. Valentin Fuster

Commentary by Dr. Brijesh Patel

Diabetics who received 1 g of vitamin C daily showed improvements in blood pressure, oxidative stress Khon Kaen University (Thailand), May 21, 2021 Findings from a randomized, double-blind, cross-over trial reported on February 25, 2021 in the Chinese Journal of Physiology revealed an association between intake of vitamin C and a reduction in blood pressure before and after exercise among men and women with type 2 diabetes. “During exercise, mechanical stress on the arterial wall is increased, leading to an increased release of vasodilators by the endothelium (e.g., nitric oxide, bradykinin, etc.),” explained authors C. Boonthongkaew and colleagues at Khon Kaen University in Thailand. “This response can attenuate blood pressure (BP) after acute exercise at low, moderate, and high intensity in normotensive individuals. However, the magnitude of this effect seems to decline in type 2 diabetes patients because of endothelial dysfunction.” The trial included 24 type 2 diabetics with poorly controlled disease who received 1,000 milligrams vitamin C or a placebo daily for six weeks, followed by a six-week washout period, followed by six weeks of the alternate intervention. For inclusion in the study, participants were required to have a blood pressure of ≤140/90 mmHg or less, maintained if necessary with antihypertensive treatment.  Twenty-minute low-intensity exercise sessions were conducted on the day before and the last day of each treatment period. Blood pressure was measured before, immediately after and 60 minutes after the exercise sessions. Blood samples collected before and after exercise were analyzed for plasma vitamin C levels, markers of lipid peroxidation and nitric oxide concentration.  Compared to pre-intake, participants who received vitamin C experienced an average 12.8 mmHg reduction in systolic BP and an 8.9 mmHg reduction in diastolic BP when at rest before exercise. Immediately after exercise, systolic and diastolic BP were lower by 11.4 mmHg and 6.8 mmHg, and an hour after exercise, systolic and diastolic BP were lower by 12.5 mmHg and 8.9 mmHg in the vitamin C group compared to baseline values. No significant differences between pre- and post-treatment measurements occurred in the placebo group. When compared to the placebo, participants who received vitamin C also had lower systolic and diastolic BP before and after the post-supplementation exercise sessions.  Post-intake, plasma vitamin C and nitric oxide levels were higher, and markers of lipid peroxidation were lower among vitamin C patients before and immediately after exercise compared to baseline, while the placebo group experienced no significant changes. And when compared to the placebo, vitamin C and nitric oxide were higher and lipid peroxidation markers were lower before and after the exercise session among participants who had received the vitamin. In their discussion of the findings, the authors remarked that vitamin C’s ability to decrease oxidative stress helps prevent nitric oxide from being degraded by free radicals, which results in higher nitric oxide levels that benefit endothelial function and BP. They announced that the study is the first to report the effect of vitamin C compared to a placebo on BP before and within an hour after exercise. “This study suggests that 6‑week vitamin C [intake] decreased pre-exercise and postexercise blood pressures, possibly due to improved oxidative stress and nitric oxide release,” they concluded.       Making mindfulness meditation more helpful starts with understanding how it can be harmful Brown University, May 18, 2021 Mindfulness-based meditation programs have emerged as a promising treatment for conditions ranging from stress to sleeplessness to depression. In some cases, they're even offered to people—schoolkids or employees, for example—who aren't actively seeking help or who haven't been screened for suitability. Yet most research and discourse about these programs focuses only on their benefits, with little investigation of the risks or the potential for adverse effects. A recent review of nearly 7,000 studies of meditation practices found that less than 1% of them measured adverse effects. Willoughby Britton, an associate professor of psychiatry and human behavior at Brown University, said that this is largely because assessing adverse effects (a process known as "harms monitoring") in non-pharmacological treatments like mindfulness-based meditation programs is difficult to do well. To address that gap, Britton conducted a new study on adverse effects in mindfulness-based programs that identified common obstacles to harms monitoring and, importantly, showed how to address them. The study also found that the rates of adverse effects from mindfulness were similar to those found in other psychological treatments. The study was published on May 18 in Clinical Psychological Science. "Our ultimate goal is to maximize the efficacy of mindfulness-based meditation while minimizing harms," said Britton, who directs the Clinical and Affective Neuroscience Laboratory at Brown. "In order to address risks and modify treatment accordingly, you need thorough and detailed knowledge about potential harms. Our study, the most comprehensive of its kind, provides a blueprint for how to accurately assess the risks of mindfulness-based meditation programs." Why no one wants to talk about meditation's adverse effects The adverse effects of mindfulness-based meditation programs are often an unpleasant topic for providers and participants alike, Britton said. For the study, she and her colleagues reviewed the most current harms monitoring best practices from regulatory agencies like the World Health Organization, the National Institutes of Health and the U.S. Food and Drug Administration. In the paper, they outlined the key considerations around assessing adverse effects, including hesitancy of participants to report negative reactions to treatment because of feelings of shame or a desire to please the researcher or instructor. Researchers and mindfulness teachers (Britton is both) are understandably more focused on the help they can provide than any harm they could cause. As a result, a lack of negative feedback from participants is often interpreted as evidence of absence of harm. "It's very easy for our enthusiasm and desire to help to become a kind of blindness," Britton explained. Another complicating factor, she said, is the lack of knowledge of proper harms assessment. "Often the mindfulness teacher will ask the class, 'Did anyone have any challenges with your meditation practice this week?'" Britton said. "But participants, in general, tend to avoid answering open-ended questions asked by the teacher in a public setting. Research has shown that having someone other than the teacher ask specific questions in a private setting will increase the likelihood of honest reporting." Finally, she highlighted the fact that term "adverse" is a highly subjective judgment that can vary across people and even across the same person in different contexts. "The re-living of a previous trauma may be healing for some and destabilizing for others, in the same way that the drowsiness caused by cold medicine—or meditation—may be undesirable or 'adverse' in the morning but highly desirable before bed," she said. What's more, Britton added, the literature shows that mental health treatment providers (like therapists or doctors) may dismiss patient complaints or reframe them as a sign that the therapy is working. Designing a model assessment Britton's research team followed 24 current harms monitoring guidelines to assess the nature and frequency of meditation-related adverse effects in mindfulness-based programs. The study participants were representative of typical meditators in the U.S.: predominantly middle-age women seeking methods to self-manage mild to severe levels of anxiety, depression and stress. After completing one of three versions of an eight-week mindfulness meditation program, participants were interviewed by a researcher unaffiliated with the treatment about their experiences, with 44 questions based on previous research of meditation-related challenges. To more accurately and thoroughly capture patient perspectives, this study allowed each participant to evaluate the emotional tone or "valence" of each of 44 meditation-related experiences as well as the impact it had on their life and functioning. By asking participants specific questions about duration and impact, researchers were able to differentiate temporary distress, negative-impact side effects and "lasting bad effects." In this way, the researchers sought to clarify which effects were experienced as "adverse" on a case-by-case basis. To accommodate the varying definitions of harm, results were reported in tiers of severity ranging from "transient distress during meditation" (i.e., temporary) to "enduring impairment in functioning"—or "lasting bad effects." The "what" is as important as the "how" The significance of the study, Britton said, has as much to do with what it found as how it found it. "The fact that meditation can cause altered states, for example, isn't news: It's something that people have been talking about for centuries," Britton said. "What we haven't been very good about is measuring the impact and significance of these states on individual participants." Of the 96 participants, 58% reported at least one meditation-related adverse effect, which ranged from perpetual hypersensitivity to nightmares to traumatic re-experiencing. Meditation-related adverse effects with negative impacts on functioning occurred in 37% of the sample. Six percent of the sample had "lasting bad effects," or impairments in functioning lasting more than one month. Notably, the researchers say, this rate is similar to those of other psychological treatments. In the study, meditation-related effects with negative impacts tended to be associated with signs of what's called dysregulated arousal—for example, the participants reported feeling anxious, hyper-stimulated or emotionally flat or disconnected after meditating. This is important for instructors and participants to note, Britton said, because unlike the experiences of anxiety or insomnia, a feeling of being dissociated or emotionally checked-out is not always experienced as unpleasant and can provide some relief, especially for a person suffering from intense anxiety. Yet in the study, this feeling of dissociation tended to predict more significant and lasting impairment in functioning. "This is where the differentiation between valence and impact becomes important, because the valence, or emotional tone, of an experience might be not particularly distressing at the time," Britton said. "Meditators are often taught to reappraise their experience as not being problematic, and to accept it for what it is. Our results are basically saying that when it comes to dissociation, this approach isn't going to work." Britton and colleagues also found that the open-ended question "Have you had any unexpected, unpleasant, adverse or challenging experiences as a result of mindfulness meditation practice during or following the program?" underestimated the true rate by 70%, confirming the inadequacy of open-ended questions compared to specific ones. The study concludes that the active ingredient of these therapeutic programs, which is mindfulness meditation practice, can be associated with both transient distress and enduring negative impacts on life and functioning. Britton said that it is important to note that adverse effects and benefits are not mutually exclusive: many of the same participants who reported adverse effects also reported improvements in depression. Britton noted that the intent of the study, as well as of her broader research, is not to discourage mindfulness-based meditation programs—rather, it is to generate findings on both the positive and negative effects so that providers and meditators can make informed decisions. She compared mindfulness to aspirin, as an example. This medicine-cabinet staple can cause nausea, heartburn and stomach cramps—and taking a daily aspirin can cause gastrointestinal bleeding in some people. But these potential adverse effects do not take away from aspirin's many benefits. Instead, detailed knowledge about the benefits and risks allows practitioners to make educated, effective and safe recommendations to specific patients. "That's where we need to get with mindfulness, too," Britton said. "Our study is an attempt to bring harms monitoring up to the standards of other treatments so that providers can identify events that require monitoring and intervention in order to maximize the safety and efficacy of mindfulness-based meditation."   Vitamin B6, vitamin D and green tea compound could improve uterine fibroids Sandro Pertini Hospital (Italy), May 19, 2021 In an article whose title asks the question, “Uterine fibroids treatment: do we have new valid alternative?” findings from researchers from Sandro Pertini Hospital in Rome suggest the answer may be “yes.” The article, published in the April 2021 issue of the European Review for Medical and Pharmacological Sciences reported a benefit for intake of vitamin B6, vitamin D and epigallocatechin gallate (EGCG, a flavonoid that occurs in green tea) in women with uterine fibroids (myomas), benign tumors of the uterus that affect a significant percentage of reproductive-aged women. Uterine fibroids adversely impact fertility, and unfortunately, there are few treatment options for women who desire to become pregnant. The study included 95 women who had between one and five fibroids. Forty-one participants received 5 milligrams (mg) vitamin B6, 25 micrograms (1,000 international units) vitamin D and 150 mg EGCG twice daily for four months, while a control group of 54 women were monitored without receiving the vitamin B6, vitamin D and EGCG. The number and volume of fibroids was measured using ultrasound before and after the treatment period. Fibroid vascularization was measured by color flow Doppler ultrasound, which color codes blood flow to indicate the direction of flow and/or the presence of high blood turbulence. Other factors assessed at these time points included the presence of heavy bleeding, pelvic pain and health/quality of life. Overall improvement was assessed by a questionnaire, the Patient Global Impression of Improvement (PGI-I), administered to participants who completed the four-month study. After four months, total fibroid volume significantly decreased by 37.9% among participants who received vitamins B6 and D, plus ECGC, while increasing by 5.5% among women who did not receive the nutrients. Similar results were observed in a subgroup of participants who were smokers – fibroid volume was significantly reduced with the supplement combination.  Doppler visualization of blood flow to the myomas suggested reduced vascularization in the intervention group and increased vascularization in the control group. Pelvic pain and health, including the participants’ all-over impressions of improvement, significantly improved in comparison with pretreatment levels in the group that received the nutrients while no change occurred in the control group. Specifically, 85.4% of women taking the supplement reported improvements in their PGI-I score, with 73.2% reporting their symptoms were “very much better”.  No side effects were reported.  Authors Donatella Miriello and colleagues concluded that the study’s findings “showed the effectiveness and safety of a 4-month oral [intake of] a combination of vitamin D, EGCG and vitamin B6 in reducing uterine fibroids’ volume and improving the quality of life of childbearing women. Thus, this…may represent a valid alternative to the classic ‘wait and see’ approach and, at the same time, an adjuvant treatment that could be administered along with pharmacological therapies, even before surgery to reduce the occurrence of possible complications.”       Nitrate-Rich Vegetables Increase Plasma Nitrate and Nitrite Concentrations and Lower Blood Pressure in Healthy Adults Maastricht University (Netherlands), May 21, 2021   Background: Dietary nitrate is receiving increased attention due to its reported ergogenic and cardioprotective properties. The extent to which ingestion of various nitrate-rich vegetables increases postprandial plasma nitrate and nitrite concentrations and lowers blood pressure is currently unknown.   Objective: We aimed to assess the impact of ingesting different nitrate-rich vegetables on subsequent plasma nitrate and nitrite concentrations and resting blood pressure in healthy normotensive individuals.   Methods: With the use of a semirandomized crossover design, 11 men and 7 women [mean ± SEM age: 28 ± 1 y; mean ± SEM body mass index (BMI, in kg/m2): 23 ± 1; exercise: 1–10 h/wk] ingested 4 different beverages, each containing 800 mg (∼12.9 mmol) nitrate: sodium nitrate (NaNO3), concentrated beetroot juice, a rocket salad beverage, and a spinach beverage. Plasma nitrate and nitrite concentrations and blood pressure were determined before and up to 300 min after beverage ingestion. Data were analyzed using repeated-measures ANOVA. Results: Plasma nitrate and nitrite concentrations increased after ingestion of all 4 beverages (P < 0.001). Peak plasma nitrate concentrations were similar for all treatments (all values presented as means ± SEMs: NaNO3: 583 ± 29 μmol/L; beetroot juice: 597 ± 23 μmol/L; rocket salad beverage: 584 ± 24 μmol/L; spinach beverage: 584 ± 23 μmol/L). Peak plasma nitrite concentrations were different between treatments (NaNO3: 580 ± 58 nmol/L; beetroot juice: 557 ± 57 nmol/L; rocket salad beverage: 643 ± 63 nmol/L; spinach beverage: 980 ± 160 nmol/L; P = 0.016). When compared with baseline, systolic blood pressure declined 150 min after ingestion of beetroot juice (from 118 ± 2 to 113 ± 2 mm Hg; P < 0.001) and rocket salad beverage (from 122 ± 3 to 116 ± 2 mm Hg; P = 0.007) and 300 min after ingestion of spinach beverage (from 118 ± 2 to 111 ± 3 mm Hg; P < 0.001), but did not change with NaNO3. Diastolic blood pressure declined 150 min after ingestion of all beverages (P < 0.05) and remained lower at 300 min after ingestion of rocket salad (P = 0.045) and spinach (P = 0.001) beverages.   Conclusions: Ingestion of nitrate-rich beetroot juice, rocket salad beverage, and spinach beverage effectively increases plasma nitrate and nitrite concentrations and lowers blood pressure to a greater extent than sodium nitrate. These findings show that nitrate-rich vegetables can be used as dietary nitrate supplements.       High-intensity interval training improves spatial memory in rats   University of Tsukuba (Japan), May 17, 2021 Researchers at the University of Tsukuba have found that, despite only covering about one-third of the distance in HIIT compared with that covered in endurance training, similar improvements in exercise capacity and brain function were observed for both forms of exercise. "We investigated how rats' muscles and brains—specifically, the region of the brain involved in spatial learning called the hippocampus—adapted to these types of exercise, and how the rats consequently learned and remembered navigating mazes," explains Professor Hideaki Soya, the principal investigator. In the experiment, rats were assigned to one of three groups—resting, endurance running, or alternating intervals (short sprints and rest)—during training sessions on treadmills five days/week for four weeks. Both endurance running and HIIT resulted in weight loss, greater muscle mass, and the ability to exercise longer compared with controls; however, increased cellular aerobic capacity was found in the soleus (a muscle with predominantly slow-twitch fibers that makes it functionally well suited to endurance) and in the plantaris (a muscle with predominantly fast-twitch fibers for meeting high-energy functional demands) in the endurance-running and HIIT groups, respectively. Rats in both groups demonstrated better memory of spatial learning trials in searching for an escape platform in a water maze. In the hippocampus, increased cell development—neurogenesis—was also observed for both forms of exercise; however, levels of a signaling protein that promotes neurogenesis (BDNF) were increased by HIIT but not by endurance running, whereas the levels of its receptor (TrkB) were increased by both. Given that BDNF expression is known to be affected by exercise, why didn't endurance running increase BDNF expression? The answer may lie in the mediating role of stress on BDNF expression; exercise is a type of stress. While stress indicators in both exercise groups were found to be similar, this line of enquiry may lead to future studies: "In this study, we showed that an HIIT exercise regimen with a low exercise volume nevertheless improves spatial memory, and we demonstrated that these improvements are supported by changes in neuronal plasticity in the hippocampus. In a previous study, we found that continuous light-intensity training had a similar beneficial effect, whereas continuous high-intensity training did not," Professor Soya summarizes. "Thus, it seems that the benefits yielded by exercise may actually depend on optimization, that is, a trade-off between exercise time and intensity." A future where exercise regimens can be tailored to improve both physical and cognitive features may be on the horizon.   Hygiene rules are also effective against new coronavirus variants Ruhr-University Bochum (Germany), May 21, 2021 The researchers found that the variants have a similar surface stability as the wild type virus under laboratory conditions, but can be effectively eliminated by disinfection and thorough hand washing, heat or alcohol treatment. They report their results in the Journal of Infectious Diseases from 16 May 2021. For this study, the team from the Department for Molecular and Medical Virology and the Chair of Materials Discovery and Interfaces at Ruhr-Universität Bochum (RUB) cooperated with the European Virus Bioinformatics Center Jena, the University Hospital Duisburg-Essen and Paracelsus Medical University Nuremberg. The fact that viruses change genetically over time is well known. Variants of concern are those that give the virus an advantage, for example by allowing it to replicate faster, become more infectious or enable it to evade the immune response. The British and South African variants have accumulated several mutations which result in an increased transmission and, in some cases, lead to more severe courses of disease. "Therefore, the question arose whether they also differ from the original variant in terms of their sensitivity to hygiene measures," explains Toni Meister from Ruhr-Universität Bochum. Heat, soap, alcohol For this reason, the team analysed how long the variants remain infectious on surfaces made of steel, silver, copper and on face masks and how they can be rendered harmless by means of soap, heat or alcohol. It turned out that both variants, as well as the wild type virus, could be inactivated when treated with at least 30 percent alcohol for at least 30 seconds. "Common disinfectants are therefore effective against all these variants," says Stephanie Pfänder from RUB. Thorough hand washing with soap could also lower the risk of infection. Heat also works against the virus: after 30 minutes at 56 degrees Celsius, all variants were rendered harmless. To find out whether the stability of the different mutant variants on surfaces differs from each other, they analyzed the amount of infectious virus particles on surfaces made of steel, copper, silver and on surgical and FFP2 masks over 48 hours. "The surface stability did not differ between the virus variants," points out Eike Steinmann from the Department for Molecular and Medical Virology at RUB. "As described several times before, copper in particular has a very strong antiviral effect". In conclusion, the team did not detect any differences between the different mutants in terms of their sensitivity to different hygiene measures.     Pink drinks can help you run faster and further, study finds University of Westminster, May 12, 2021         A new study led by the Centre for Nutraceuticals in the University of Westminster shows that pink drinks can help to make you run faster and further compared to clear drinks. The researchers found that a pink drink can increase exercise performance by 4.4 per cent and can also increase a 'feel good' effect which can make exercise seem easier.  The study, published in the journal Frontiers in Nutrition, is the first investigation to assess the effect of drink colour on exercise performance and provides the potential to open a new avenue of future research in the field of sports drinks and exercise. During the study participants were asked to run on a treadmill for 30 minutes at a self-selected speed ensuring their rate of exertion remained consistent. Throughout the exercise they rinsed their mouths with either a pink artificially sweetened drink that was low in calories or a clear drink which was also artificially sweetened and low in calories. Both drinks were exactly the same and only differed in appearance - the researchers added food dye to the pink drink to change the colour.  The researchers chose pink as it is associated with perceived sweetness and therefore increases expectations of sugar and carbohydrate intake. Previous studies have also shown that rinsing the mouth with carbohydrates can improve exercise performance by reducing the perceived intensity of the exercise, so the researchers wanted to assess whether rinsing with a pink drink that had no carbohydrate stimulus could elicit similar benefits through a potential placebo effect.  The results show that the participants ran an average 212 metres further with the pink drink while their mean speed during the exercise test also increased by 4.4 per cent. Feelings of pleasure were also enhanced meaning participants found running more enjoyable. Future exploratory research is necessary to find out whether the proposed placebo effect causes a similar activation to the reward areas of the brain that are commonly reported when rinsing the mouth with carbohydrates.  Talking about the study, Dr Sanjoy Deb, corresponding author on the paper from the University of Westminster, said: "The influence of colour on athletic performance has received interest previously, from its effect on a sportsperson's kit to its impact on testosterone and muscular power. Similarly, the role of colour in gastronomy has received widespread interest, with research published on how visual cues or colour can affect subsequent flavour perception when eating and drinking.  "The findings from our study combine the art of gastronomy with performance nutrition, as adding a pink colourant to an artificially sweetened solution not only enhanced the perception of sweetness, but also enhanced feelings of pleasure, self-selected running speed and distance covered during a run."

This month on Episode 21 of the Discover CircRes podcast, host Cindy St. Hilaire highlights four featured articles from the February 2 and February 19 issues of Circulation Research. This episode also features an in-depth conversation with  Konstantinos Drosatos and Ioannis Kyriazis from Temple University to discuss their study, KLF5 is Induced by FOXO1 and Causes Oxidative Stress and Diabetic Cardiomyopathy.   Article highlights:   Wittenbecher, et al. Lipidomics and Heart Failure Risk   Kryshtal, et al. Flecainide Directly Inhibits RYR2 Ca Release   Chen, et al. Klotho and Heart Aging   Grootaert, et al.  SIRT6 Deacetylase Protects Against VSMC Senescence   Dr Cindy St. Hilaire:        Hi, and welcome to Discover CircRes, the podcast of the American Heart Association's journal, Circulation Research. I'm your host, Dr Cindy St. Hilaire from the Vascular Medicine Institute at the University of Pittsburgh, and today I'll be highlighting four articles from the February 5th and 19th issues of CircRes. After the highlights, Dr Konstantinos Drosatos and Ioannis Kyriazis from Temple University will join me to discuss their study, KLF5 is Induced by FOXO1 and Causes Oxidative Stress and Diabetic Cardiomyopathy. Dr Cindy St. Hilaire:        The first article I want to share is Lipid Profiles and Heart Failure Risk: Results from Two Prospective Studies. The first author is Clemens Wittenbecher, and the corresponding author is Frank Hu from Harvard's Chan School of Public Health in Boston, Mass. Heart failure affects tens of millions of people worldwide, and as the prevalence grows, prevention strategies are becoming ever more important. While factors including age, obesity, and hypertension influence one's risk of developing heart failure, robust biomarkers that are able to pinpoint which individuals will develop heart failure are lacking. Changes in cardiac lipid metabolism predispose animal models of heart failure. Dr Cindy St. Hilaire:        This group hypothesized that blood lipid profiles might be useful to serve as a heart failure biomarker. The team examined 216 blood lipids from a cohort of individuals with various cardiovascular risk factors, but who, at the time of enrollment and blood collection, did not have heart failure. Over the observation period, which averaged out to over 12 years, 331 of the subjects developed heart failure. Dr Cindy St. Hilaire:        When compared to the baseline lipid profiles of individuals who didn't develop heart failure, the group identified two particular lipids, ceramide and phosphatidylcholine, and several networks of lipids and metabolites that were strongly predictive of developing heart failure. Importantly, the findings were corroborated in the second cohort, in which 87 individuals developed heart failure. Together, the results reveal early biomarkers for identifying at-risk individuals and point to particular lipid alterations that may yield insights into heart failure pathology and prevention. Dr Cindy St. Hilaire:        The second article I want to share is titled, RyR2 Channel Inhibition Is a Principal Mechanism of Flecainide Action in Catecholaminergic Polymorphic Ventricular Tachycardia. The first authors are Dmytro Kryshtal and Daniel Blackwell, and the corresponding author is Bjorn Knollmann, from Vanderbilt University School of Medicine in Nashville, Tennessee. Flecainide is a drug that is commonly used to treat various heart arrhythmias. Flecainide works by blocking sodium channel activity. However, the drug also has been found to reduce symptoms of catecholaminergic polymorphic ventricular tachycardia, or CPVT, a condition in which mutations affecting the function of a calcium channel ryanodine receptor, called RyR2, are to blame. In vitro studies have suggested that flecainide can in fact block RyR2 activity, but some researchers have argued that flecainide's inhibition of this receptor is too weak to be clinically relevant, and suggest its sodium channel inhibition instead provides an indirect benefit. Dr Cindy St. Hilaire:        To test that claim, this group synthesized analogs of flecainide that lack RyR2 inhibitory activity, yet retained sodium channel blocking ability. They compared the analogs with the original drug, both in vitro and in vivo. Experiments in cardiomyocytes confirmed flecainide, but not the analogs, could reduce RyR2-mediated calcium release and experiments in catecholaminergic polymorphic ventricular tachycardia model mice showed flecainide, but not the analogs, could suppress induced ventral tachyarrhythmias. These findings suggest that RyR2 inhibition is the principal mechanism of action of flecainide in treating catecholaminergic polymorphic ventricular tachycardia, and therefore, RyR2 may be a valid therapeutic target for the development of additional antiarrhythmia drugs. Dr Cindy St. Hilaire:        The third article I would like to share is titled, Klotho Deficiency Causes Heart Aging via Impairing the Nrf2-GR Pathway. The first author is Kai Chen, and the corresponding author is Zhongjie Sun, and they're from the University of Tennessee Health Science Center in Memphis, Tennessee. Age is a risk factor for many disease states, including heart failure. Even in healthy individuals, the heart size increases and its function declines with age. Aging in humans has also been associated with a decrease in circulating levels of the protein Klotho, which is thought to have anti-aging properties. Previous studies have shown, in a murine model of cardiac hypertrophy, that mice that lack Klotho fare worse than those with normal levels of the protein. Dr Cindy St. Hilaire:        This group, therefore hypothesized that Klotho decline may contribute to age-related heart changes. Similar to humans, heart function declines with age in otherwise healthy mice. Injection of Klotho into old mice reduced the size of the animal's hearts and improved cardiac function. Klotho injections also improve heart size and function in young Klotho-lacking mice with pharmacologically induced cardiac hypertrophy. The team found that Klotho induces these effects by inhibiting the accumulation of damaging reactive oxygen species, and by reducing apoptosis in aged-Klotho deficient heart cells. From these data, they suggest that perhaps boosting Klotho levels may be a strategy to prevent age-related heart failure. Dr Cindy St. Hilaire:        The last article I want to share before our interview is titled, SIRT6 Protects Smooth Muscle Cells from Senescence and Reduces Atherosclerosis. The first author is Mandy Grootaert, and the corresponding author is Martin Bennett from the University of Cambridge in Cambridge, United Kingdom. Vascular smooth muscle cells reside in the medial layer of vessels. They contribute to atherosclerotic plaque progression, as well as to the fibrous cap that helps to stave off plaque rupture. Over time, however, the increased proliferation and differentiation of plaque smooth muscle cells causes them to accumulate DNA damage, senesce, and ultimately die, leading to the destabilization of the plaque. Dr Cindy St. Hilaire:        Functional disruption of the enzyme SIRT6 has been implicated in DNA damage senescence and apoptosis, and certain polymorphisms of the SIRT6 encoding gene are linked to atherosclerosis. From these premises, the team wanted to examine the role of SIRT6 in plaque smooth muscle cells. Compared with healthy aortas, aortas from atherosclerotic mice and humans have lower levels of SIRT6 protein. Inhibiting the activity of SIRT6 and smooth muscle cells caused damage to the telomeres and induced early senescence. By contrast, overexpression of SIRT6 preserved telomeres and prevented senescence. ApoE knockout mice were then engineered to over express SIRT6, specifically in their smooth muscle cells, and these mice showed reduced severity of atherosclerosis compared to control mice. Together, these findings implicate SIRT6 suppression as a cause of plaque senescence, and suggest reversing it may in fact slow disease progression. Dr Cindy St. Hilaire:        Okay, so today we have Dr Konstantinos Drosatos and his postdoctoral fellow, Dr Ioannis Kyriazis from Temple University in Philadelphia, Pennsylvania, and they're here to discuss their study, KLF5 Is Induced by FOXO1 and Causes Oxidative Stress and Diabetic Cardiomyopathy. And this is in our February 5th issue of Circulation Research. So, thank you both so much for being with me today. Dr K. Drosatos:                Thank you for the invitation and for helping to draw attention to our study. Dr Cindy St. Hilaire:        Absolutely. And thank you for doing this at what? What is it, eight o'clock where you are? Dr Ioannis Kyriazis:         It is eight o'clock at night. Dr Cindy St. Hilaire:        Okay. Well, thank you for taking the- Dr Ioannis Kyriazis:         But it's okay, it's okay. It's quite early to be in Greece. Dr Cindy St. Hilaire:        Okay, good. Dr K. Drosatos:                Maybe we need to clarify that Ioannis is a former postdoc. I don’t have a lab at Temple and in Greece. Dr Cindy St. Hilaire:        Former postdoc. Thank you for clarifying that. So I want to start with a question about cardiomyopathy. What is it and how prevalent is it? And what's the different pathogenesis of cardiomyopathy? And how does it differ from diabetic cardiomyopathy? Dr K. Drosatos:                So usually cardiomyopathy arises after heart infracts, after myocardial ischemia, and it actually reflects the reduced ability of the heart to pump blood to the rest of the body, in simple words. Diabetic cardiomyopathy has some unique features. One of those is that it's not related to coronary artery disease, so it does not start with ischemia, but it's still the heart cannot do what it is supposed to. Dr Cindy St. Hilaire:        So it's kind of its own unique driver then, the diabetic cardiomyopathy? Dr K. Drosatos:                Yeah. And there is a lot of, I wouldn't say debate, but there's a lot of discussion in the field about how to best define diabetic cardiomyopathy. It's a different kind of cardiac dysfunction. It has some certain features like oxidative stress, which is the stuff that we work with. It has fibrosis, primarily perivascular fibrosis. Diastolic dysfunction is more prevalent than systolic dysfunction. So there's a number of features that actually define diabetic cardiomyopathy. Dr Cindy St. Hilaire:        I know it's highly prevalent in patients with diabetes, but the inhibitors that people are using to try and treat the diabetic portion, I'm thinking about the sodium glucose transporter SGLT2 inhibitors, those are obviously very good at helping regulate the blood glucose, but they don't appear to alleviate the heart failure. And so what do you think about the pathogenesis or the pathophysiology between the glucose regulation and the cardiomyopathy? Is it kind of like a cliff and it gets too far and is it unrepairable? Dr K. Drosatos:                It's certainly a very trendy question. I mean, you are a scientist so you know that in science will have several trends. So SGLT2 inhibition is one of those right now. And from time to time, there are several, I would say miraculous drugs that do a number of good things, which we're not very certain about the mechanism that underlies the effect. So the SGLT2 inhibitors, which is something that we had also started in a previous paper in Circulation Research four years ago, in relation to KLF5, what it actually does, it targets a transporter in the kidney and this transporter normally returns glucose back to the bloodstream. But when it is inhibited, the extra glucose that we observe in diabetes goes out through the urine. So this is what the drug does, but it has been shown that the drug has its own effects in cardiac function, which do not necessarily pertain to the effect that the drug has in the kidney. And actually I was reading yesterday very interesting paper about using SGLT2 inhibitors in heart failure patients that do not have diabetes. Dr Cindy St. Hilaire:        Oh, interesting. So it might actually have a secondary function that we're just not aware of right now. Dr K. Drosatos:                We do believe that at least in part the beneficial effects has to do with the removal of the extra glucose from the system. My training has been in labs that work on lipid metabolism, so I believe that fatty acid oxidation is the best thing that can happen to the heart. So removing the glucose out of the system is definitely beneficial and actually, Ioannis, before he returned back to Greece, he had performed some experiments showing that removing glucose is definitely beneficial. Dr Cindy St. Hilaire:        That's great. Can you describe the study? What was the former research that the question you were asking in this study was on? Dr K. Drosatos:                That was a study that I started in the lab of Ira Goldberg at Columbia University when I was a postdoc, and we had come up with an interesting observation that in the heart, the protein interception factor, named KLF5, follows an oscillating pattern of expression. So at the early stage of the abyss, it goes down and then it goes up. So we believe that the levels of glucose in the plasma may be one of the defining factors for affecting the expression of KLF5. So this is how it started, why KLF5 goes down and then up. And at that time we observed that KLF5 is an important transcriptional regulator of cardiac PPAR-alpha, a protein that's another transcriptional factor, which seems to be a very important factor that orchestrates gene expression for fatty acid oxidation. So there is more than 20 genes that are important for fatty acid oxidation, and the expression of which has been shown to be affected by PPAR-alpha. Dr K. Drosatos:                So we started working with KLF5 and PPAR-alpha, and that was the paper we published in Circulation Research in 2016, and then Ioannis joined my lab and he works on the effect of KLF5 per se in diabetic cardiomyopathy. And one of the interesting findings from the new study is that the KLF5 has a separate effect on diabetic cardiomyopathy that does not involve PPAR-alpha. Dr Ioannis Kyriazis:         And the whole idea, when I joined Dr Drosatos’ lab, the initial idea was that something is happening initially in the heart and that's why we see KLF5 goes down and we believe initially that has to do with subject utilization. And that's why KLF5 is coming down and then comes up. But after several studies, we figured out that it's actually a big tie in the transcriptional factors that act synergistically and like FOXO1, KLF5, and PPAR-alpha, and KLF5 and PPAR-alphas have distinct roles on regulating diabetic cardiomyopathy. So starting from one point of view, we transferred to a different aspect and we tried to see how KLF5 is involved in that system. And this is two stories in one, actually. And that's why we have this follow up study about glucose, that Dr Drosatos said, before I leave. We try also to make it bigger. Dr Cindy St. Hilaire:        Yeah, it's always complex, but I feel like this story got very complex as it's really interesting. You used a large amount of different mouse models. Can you talk about some of the different mouse models you used and why you had to use them? You had different drivers of CRE, but also over expression, knockout models. Can you maybe give a quick summary of all the different models you use to really test your hypothesis really thoroughly? Dr K. Drosatos:                Are you asking Ioannis why I am forcing him to do a lot of experiments? Dr Ioannis Kyriazis:         No, no. Dr Cindy St. Hilaire:        But they're really well done, so. Dr Ioannis Kyriazis:         I think the answer has to do with how the research community is able to tackle biological questions. You need to use knockout animals and conditional transgenic animals in order to answer biological questions that you are asking. So because we have in front of us a triangle of transcriptional factors that regulate the diabetic myopathy, we were obliged to use all these mouse models to answer all these questions. And we have to understand what is the driving force behind all these systems? Is it FOXO1? Is it KLF5? Is it PPAR-alpha? Do these all add together? So that's why we had two knockout-specific mouse lines for FOXO1 and KLF5. We have the global PPAR-alpha knockout mice, we have transgenic KLF5 specifically in the cardiomyocyte mouse line, and we also have gene therapy. Dr Ioannis Kyriazis:         We construct an AAV that drives KLF5 expressions, specifically in the cardiomyocytes, under the Cardiac Troponin T Promoter. So all these actually helped us combination of therapies to tackle all these biological questions that we wanted to have and to answer. Dr K. Drosatos:                So this is how it's done. So Ioannis started from this point. We were hopeful that there was a flux FOXO1 mouse. So he started working with that, and then we started making more questions. Okay, after we figured out that, yes, FOXO1 regulates KLF5, so the question then was, okay, is it an effective KLF5 through PPAR-alpha? This is where the next mouse model came. When we said, no, it's not PPAR-alpha, we said, okay, what it is then? Dr Cindy St. Hilaire:        What is it? Dr K. Drosatos:                And started thinking about different mechanisms that activate diabetic cardiomyopathy. We started with oxidative stress. I was not very ecstatic about this possibility because antioxidant therapies in diabetic patients did not really improve survival. And actually, we were right not to be so excited about this possibility because we only saw a partial improvement. So then we said, okay, what else? And this is where we started doing high throughput analysis, where we ran out of possible answers to questions. So this is when we did look at dogs and we came up with the observation that ceramides are effective. Dr Ioannis Kyriazis:         And one more thing to add is that, as Dr Drosatos said, that this study, I think, it's one of a lot of studies out there. But I think this is how we, I believe, as an early scientist, the science to know the biological systems, especially in mice. We use the transgenic models and the knockout models and we see in our study that black and white is not good. So in Kosta's, in Dr Drosatos's study in 2016, Circulation Research, he showed that KLF5 knockouts, specifically in the cardiomyocytes, actually is not good for a long time. Initially, we believed that the transgenic KLF5 mouse model will do better in diabetes. Dr Ioannis Kyriazis:         And when we saw that there actually has an accelerated cardiac dysfunction, we were like, okay, this is an interesting phenotype. We need to see how this goes, because we believe in our initial hypothesis that if we induced KLF5 in the early diabetes, then we will have something like we alleviate diabetes. But this was not the case. And I believe that the fine tuning of some proteins will be the future. It's not black, it's not white. If we knock out completely KLF5, it's not good. If we over express KLF5, it's not good. We need some physiological levels. Dr Cindy St. Hilaire:        Yeah. You need to be able to tighter it a bit and tighten it up here or loosen it up there and, yeah. Well, this is a great study to really highlight the intricate dynamics of it all. One of the interesting results, it was just one of the shorter sections, but when KLF5 was increased, you also saw a decrease in mitochondrial DNA integrity in the cardiomyocytes, which I thought was a really interesting finding. It was just a little portion of the paper, but I just thought that was really interesting, and I was wondering if you could expand on it. What does that mean? And do we know what KLF is doing to the mitochondria? Dr K. Drosatos:                We believe that this is an effect of the oxidative stress and the increase of ceramides. It's a secondary effect. But this is something we would like to pursue further because when we did... And Ioannis nicely mentioned about that. In the 2016 paper, in Circ Research, we actually saw that prolonged exhibition of KLF5 results in diabetic cardiomyopathy. So we don't want to inhibit it completely. And in that case, mitochondria number also goes down. Dr Cindy St. Hilaire:        And then, once it's down, it doesn't go back up? Dr K. Drosatos:                We believe that in the most recent papers case, it is the oxidative stress that actually targets mitochondria. Dr Cindy St. Hilaire:        I think, if I got it correctly, the time course of these events happening in the mice is about a 12 week time span you're doing your treatments for? Dr K. Drosatos:                That's correct. Dr Cindy St. Hilaire:        So obviously that's much more accelerated than humans. What do you think about these dynamics on a human scale in terms of KLF being up and then being down? Do we know how this mechanism would translate to humans or is that still kind of a black box? Dr K. Drosatos:                I think that it's a black box. If I know correctly, we still don't know how fast type one diabetes is occurred in humans. And also the majority of people that have diabetes, diabetic cardiomyopathy is not everything. So maybe their cardiac function is bad, and KLF5 is induced, but these patients do not know that they have actually diabetic cardiomyopathy. And the majority, most probably, of the samples of the research community might have is like a endpoint type 1 diabetic patients. And with the help of Professor Kyriazis, it gave us human samples that we have in our study, we saw that KLF5 is increased in isolated cardiomyocytes. So in terms of how KLF5 is induced in human samples, I think it is high, but we don't know if this 12-week timeframe that we put in the mice to have lack of an overt cardiac dysfunction is actually mimicking completely what is happening to humans. Dr Cindy St. Hilaire:        So what do you think about leveraging your findings for the development of potential therapies? What would you want to target first, or how do you think this could potentially move to the clinic setting? Dr K. Drosatos:                So regarding the previous question, first, I think it's important that in our case we observe in both type 1 and type 2 diabetes mice, that KLF5 is going now. And the result of correcting cardiac function, when we see a bit of KLF5, either genetically and specifically cardiomyocytes or pharmacologically, identifies KLF5 as a potential barrier. This is how I see. Dr K. Drosatos:                You know that in the drug discovery world, transcriptional factors are not very popular therapeutic therapies. So right now the lab is investing on identifying what do they regulate? So we are pursuing a proteomic analysis, we are pursuing sequencing analysis to see what may be happening one step earlier. This is how we envision in potential therapeutic approaches in the future. So this is how we see. Dr K. Drosatos:                For me, it's not really a black box. There is a lot of information in the last 20 years on diabetic cardiomyopathy, and you mentioned earlier the SGLT2 inhibition and we don't know how this works, but we have some ideas. I believe we are getting there. And our hope is that the piece of our work we were able to identify any important, novel points of the mechanisms, because it was actually miraculous. I mean, the experiment that excited more than any other experiment in Ioannis's paper was when he started the treatment with the KLF5 inhibitor after diabetic and after cardiac dysfunction had occurred. And the cardiac function became back normal. Dr Cindy St. Hilaire:        Do you think this KLF5 mechanism is operative in kind of traditional cardiomyopathy, kind of non-diabetic cardiomyopathy? Dr K. Drosatos:                We just published a paper in Circulation. This was the work of Matthew Hoffman and Ioannis was also a co-author in that paper. Matthew and Ioannis were working together in the lab. So Matthew showed that KLF5 is increasing ischemic cardiomyopathy as well. And this was shown both in human samples and mouse experiments. And when KLF5 was inhibited, dilated cardiomyopathy was actually the first. KLF5 was such an underappreciated transcriptional factor and when I was doing my postdoc and started working with that, I always say that I took the risk to generate the cardiomyopathy-specific mouse models because by that time there was only one study showing that it was only fibroblast KLF5 that actually protects from a pressure overload cardiomyopathy. Where they knocked out KLF5 and cardiomyocytes they did not see any protection in pressure overload-driven hypertrophy. So they said, because KLF5 has low RNA copy number, probably it's not important. And I still remember when I first presented this data to KLF meeting, and they will all say, "Yeah, but the expression is very low," but we had the results, so. Dr Cindy St. Hilaire:        Yeah. Well, good for you for sticking to your guns. And it's really, really a wonderful study and I want to congratulate you both on this. And it was a huge undertaking with all those mice. Dr K. Drosatos:                Thank you. Dr Ioannis Kyriazis:         Thank you very much. Dr Cindy St. Hilaire:        That's it for the highlights from the February 5th and February 19th issues of Circulation Research. Thank you for listening. Please check out the CircRes Facebook page and follow us on Twitter and Instagram with the handle @CircRes and @DiscoverCircRes and #DiscoverCircRes. Thank you to our guests, Kostas Drosatos and Ioannis Kyriazis. This podcast is produced by Rebecca McTavish and Ashara Ratnayaka, edited by Melissa Stoner, and supported by the Editorial Team of Circulation Research. Some of the copy text for the highlighted articles is provided by Ruth Williams. I'm your host, Dr Cindy St. Hilaire. And this is Discover CircRes, your on-the-go source for the most exciting discoveries in basic cardiovascular research.  

Commentary by Dr. Valentin Fuster

Commentary by Dr. Valentin Fuster

Welcome back to the tasty morsels of critical care podcast. In the main we get excited about systolic dysfunction. We obsess over the ejection fraction with numbers like EF of 12% being reproduced recurrently in handover sheets. But this is ... Read More »

This episode covers diastolic heart failure!

Listen as Deputy Editor Merry Lindsey (University of Nebraska Medical Center) interviews authors Leslie Ogilvie and Jeremy Simpson (University of Guelph) and expert Michael Czubryt (University of Manitoba) about the recent Review by Ogilvie et al. on the importance of evaluating best practices in the hemodynamic assessment of diastolic function for animal models. With significant clinical focus on the role diastolic dysfunction plays in heart failure with preserved ejection fraction (HFpEF), cardiac fibrosis, and diabetes, there is no better time to examine diastolic functional assessments in experimental models. “Diastolic function has emerged as being equally important to systolic function in the overall ability of the heart to function as a pump,” explains Simpson. We discuss rodent models of human diastolic dysfunction in the setting of HFpEF, and understanding diastolic function in terms of its two phases—relaxation and filling. What recommendations do Ogilvie and Simpson make for handling the inherent limitations of software-based algorithms? Listen and learn more.   Leslie M. Ogilvie, Brittany A. Edgett, Jason S. Huber, Mathew J. Platt, Hermann J. Eberl, Sohrab Lutchmedial, Keith R. Brunt, Jeremy A. Simpson Hemodynamic assessment of diastolic function for experimental models Am J Physiol Heart Circ Physiol, published April 21, 2020. DOI: doi.org/10.1152/ ajpheart.00705.2019

Commentary by Dr. Valentin Fuster

Join us as we talk to Dr Altman (WMH cardiologist) about diastolic dysfunction - how it presents, how to diagnose, how to manage and how to watch for complications

In this episode I break down my current diagnosis of Diastolic Dysfunction, which is the decrease in function of the ventricles of the heart. You will also hear about the 4 stages of DD. I will also have a Q&A regarding my health, these questions were submitted via email and DM's. Resources Health Hearty (18, May 2020) Diastolic Dysfunction. Retrieved from: https://healthhearty.com/diastolic-dysfunction #lupusawareness #hearthealth #diastolicdysfunction #heartfailure #heartsmart #lupus #chronicilliness #mystorylivingwithlupuspodcast #podcasting #anchorfm #iHeartRadio **(I don't own the rights to the music that is in this broadcast) --- Send in a voice message: https://anchor.fm/susan-hendrix/message

Heart failure

Diastolic Compliance

We know of our blood pressure as being two numbers: Systolic and Diastolic. The first number or the systolic number is going to represent the pressure in your arteries as your blood goes from the heart. The bottom number or the systolic number that bottom number or the diastolic number. That is the pressure in your arteries when your heart rests between beats.  According to the American Heart Association: Normal is considered 120 over 80 Anything above 140 over 90 is considered hypertension.  If you have a value that's between the normal and high ranges it is considered pre hypertension. Almost 78 million people or one out of three Americans that are currently living with high blood pressure.  Now, one of the things that you'll also hear is, you shouldn't have a lot of salt. Understand that salt is made up of two compounds, Sodium and Chloride. Sodium is a vital component that we need, but the other thing that you have to consider is that salt is actually made of about 40% sodium and 60% chloride. We can get much of the sodium that we need from the vegetables in our diet (if we consume the appropriate amount). The problem comes when you actually take in too much salt. It will cause you to retain water. Your body responds to that by saying, “Wait a minute, I'm getting too much water. Let me raise the blood pressure of my body so that I can get rid of that extra water retention and salt.” It then becomes a problem and creates a very vicious cycle. Fun fact: The recommended amount for us to get in terms of sodium is 1500 milligrams, or about three quarters of a teaspoon of salt. We take in an average of 3500 milligrams daily! So, how do you actually step away from the salt shaker? I actually took away the salt shaker from my table. I stopped, adding salt to my food while I was cooking and opted to lightly add it  at the very end of the cooking process We know that a lot of the processed foods and the junk food that we eat has a high level of sodium. So when you start the process of reducing the amount of processed foods that you consume, naturally your salt intake will go down. Want another fun fact? Beets have a similar effect to what nitroglycerin would have when you experience chest pain. It works by creating nitric oxide, which relaxes your muscle fibers (particularly those in your heart) and allows for more blood flow. The nitrates found in foods such as beets get converted into nitric oxide and our bodies use it the same way (so cool)! Eat your antioxidant rich foods, because, again, you want to make sure that you're supporting nitric oxide production in the body.  Foods that have nitrates: Rhubarb  Cilantro Butter leaf lettuce. Mesclun greens Beet greens/Beets Swiss Chard

In this NB Hot Topics Podcast, Dr Neal Tucker takes an in depth look at coronavirus, the data that scientists need to predict whether it becomes a pandemic, and how this affects UK general practice. He also reviews new research on isolated diastolic hypertension and whether treating this improves outcomes, and on the booster theory for adult exposure to children with chickenpox. As well we look at the latest news in cluding Ian Paterson and the new GP Contract.

Editor's Summary by Howard Bauchner, MD, Editor in Chief of JAMA, the Journal of the American Medical Association, for the January 28, 2020 issue

Commentary by Dr. Valentin Fuster

“Diastolic dyssynchrony assessment by gated myocardial perfusion-SPECT in subjects who underwent cardiac resynchronization therapy” In this episode, Erick Alexanderson-Rosas summarizes the above study, highlights the new information, clinical implications and limitations of the study, and provides suggestions for future studies. The authors of this article have provided a PowerPoint file which summarises the contents of the paper and is free for re-use at meetings and presentations: https://link.springer.com/article/10.1007/s12350-019-01845-2#SupplementaryMaterial The article is available at: https://rdcu.be/bQMsL Be sure to subscribe on your mobile device - search 'JNC/ASNC Podcast'.

Inês Falcão Pires, Faculty of Medicine, University of Porto, Portugal speaks on "Echocardiography in rats – assessing diastolic function". This movie is part of "UltraSound imaging in cardiac and vascular medicine: from pre-clinical to clinical studies" Course, 21-22 February 2019, ICGEB Trieste, Italy.

Giorgio Faganello, ASUITS, Trieste, Italy speaks on "How to assess diastolic function on echocardiography". This movie is part of "UltraSound imaging in cardiac and vascular medicine: from pre-clinical to clinical studies" Course, 21-22 February 2019, ICGEB Trieste, Italy.

“The prognostic value of diastolic and systolic mechanical left ventricular dyssynchrony among patients with coronary artery disease and heart failure”. In this episode, Marat Fudim summarizes the above study, highlights the new information, clinical implications and limitations of the study, and provides suggestions for future studies. The authors of this article have provided a PowerPoint file which summarises the contents of the paper and is free for re-use at meetings and presentations: https://link.springer.com/article/10.1007/s12350-019-01843-4#SupplementaryMaterial The article is available at: https://rdcu.be/bOyc8 Be sure to subscribe on your mobile device - search 'JNC/ASNC Podcast'.

Hypertension is the biggest killer worldwide with an estimated 10 million deaths per year directly attributable to uncontrolled blood pressure. Also known as ‘high blood pressure’, hypertension is a chronic common condition that may cause long term damage to the heart, brain, kidneys, eyes and blood vessels, caused through the blood pressure in the arteries being persistently elevated.Join Professor Markus Schlaich from the Dobney Hypertension Centre as he discusses why it is so important to be aware of this silent killer.

This week in cardiology: Systolic, diastolic BP each tied to adverse CV outcomes Diastolic hypertension can't be ignored, though systolic ultimately has a larger impact.  Almost half of sudden cardiac deaths linked to prior silent MI Prior silent MIs were detected in nearly half of sudden cardiac deaths in people with no coronary artery disease. How does uncontrolled hypertension play into dementia? Findings from a French cohort suggest that a vascular pathway, independent of amyloid, bears on cognitive decline. Vaping device marketers take aim at youth through social media More than a third of JUUL-related posts contained promotional content that highlighted ways to obtain products at reduced cost.  You can contact the Cardiocast by emailing us at podcasts@mdedge.com or interacting with us on Twitter @MDedgeCardio.  

Commentary by Dr. Valentin Fuster

The physical detection of peripheral pulses, and the characterization of those pulses – as strong, moderate or weak, has long been used in triage assessment protocols in both humans and animals – with the assumption that strong pulses correlate with higher blood pressure, whereas weak pulses correlate with lower blood pressure. However, in humans, study of the association between peripheral pulse and arterial blood pressure has revealed that systolic arterial pressure measurements were lower than those expected based on traditional correlations, and this has raised concerns about the reliability of pulse pressure in patient assessment. In this article, we review a veterinary study looking at the validity of this assumption. Prior to this study, there were no clinical studies evaluating the relationship of peripheral pulse to systolic arterial blood pressure in dogs – something the study under discussion aimed to rectify. Pulse quality is determined by the difference between systolic blood pressure and diastolic blood pressure, and is influenced by several factors, including: Systolic blood pressure Diastolic blood pressure Stroke volume Arterial wall compliance, and Intra-thoracic pressure This study [1] was a prospective observational study of 93 dogs that presented to an emergency service where a physical examination and a systolic arterial blood pressure evaluation were performed prior to any intervention or therapy. The results of the study were interesting, and revealed the following: Absent metatarsal pulses reliably predicted hypotension (systolic arterial blood pressure

Relaxing is important an important part of life—especially for the heart. In fact, when the heart has difficulty relaxing between beats, people can develop diastolic heart failure, a serious functional condition. Discover which treatment options can help.   TRANSCRIPT Intro: MedStar Washington Hospital Center presents Medical Intel where our healthcare team shares health and wellness insights and gives you the inside story on advances in medicine. Host: Thanks for joining us today. We’re speaking with Dr. Valeriani Bead, a board-certified cardiologist at the MedStar Heart and Vascular Institute, with extensive experience in nuclear cardiology and echocardiography. Welcome, Dr. Bead. Dr. Valeriani Bead: Thank you for having me. I’m really happy to be here. Host: Today we’re discussing diastolic heart failure which occurs when the left ventricle or the lower left chamber of the heart can’t properly fill with blood. Dr. Bead, is diastolic heart failure a common heart condition? Dr. Bead: Yes. But first we need to understand what diastolic heart failure is. In simple terms, it’s defined as an abnormality of the diastolic filling, or what we call the relaxation, of the left side of the heart, despite the fact that the heart pumping function is normal. And usually it occurs when the ability of the left side of the heart...when it can’t really accept blood or it’s impaired. And this can lead to a higher pressure inside the heart. Then, that can lead to fluid build-up in the lungs and also to the rest of the body. Now, to answer your question, diastolic heart failure is quite common, and it’s thought to be as prevalent as 20 to 70 percent in some patient populations and is thought to be responsible for about two-thirds of the incidence of congestive heart failure that we see in general. Host: What are some of the main symptoms of diastolic heart failure? Dr. Bead: Some of the most common symptoms that we experience with diastolic heart failure are shortness of breath, fatigue, lightheadedness or fainting, and sometimes even an irregular or abnormal heartbeat. Host: How is this condition diagnosed? Dr. Bead: Typically, we diagnose diastolic heart failure by good, comprehensive history and physical exam. And then, based on that, we may order some imaging tests called an echocardiogram, which is a sonogram of the heart. This is often combined with the stress tests to show how blood is flowing in the heart during exercise. Finally, we may do additional blood tests or even an invasive procedure called a cardiac catheterization, which is when a thin tube is inserted into the heart in order to see how the heart is functioning and to determine whether or not there are any blockages in the arteries. Host: Could you tell us a little bit about your patient population for diastolic heart failure? Dr. Bead: So, the most common individuals we see, those at highest risk for diastolic heart failure, is the older population, so typically individuals over 65 years old and those who have high blood pressure. Sometimes those who have problems with their heart valves, particularly the aortic valve, and typically when that valve is narrowed or doesn’t open well. We also see the diabetics and people who have clogged arteries, and, for unclear reasons, you see it more common in women. Host: Once you’ve diagnosed an individual with diastolic heart failure, what treatment options are available for them? Dr. Bead: We always start off with lifestyle modifications, which include smoking cessation, increasing physical activity, and dietary changes. Next, we offer treatment to address the stiffening of the heart and that typically includes controlling the blood pressure, controlling the diabetes, and also, if they have high cholesterol, we also treat that. And some of the medications we use may include a class of medication called beta blockers, which are used to slow the heart rate in order to allow it to function better. We also use medications called calcium channel blockers, which help reduce the stiffness of the heart. Other medications include diuretics that help reduce the fluid accumulation. And, if those are not sufficient, sometimes we offer an invasive procedure called a cardiac catheterization or even surgery to fix any blockages or narrowings in the blood vessels. Host: What are some of the risks if a patient doesn’t receive treatment for diastolic heart failure? Dr. Bead: Now that’s a great question because, the main risk we worry about, if a patient doesn’t receive treatment for diastolic heart failure, is death. The other risk we worry about is congestive heart failure, which is when an individual has a sensation that they can’t breathe, and they have evidence of fluid overload. Other things we may see are abnormal heart rhythms called atrial fibrillation. Other things that we may see are passing out, also called syncope. Host: Is there anything that patients can do to reduce their risk of diastolic heart failure? Dr. Bead: Yes. The most important thing patients can do to reduce their risk of diastolic heart failure is to keep their blood pressure under control, to control their diabetes or their blood sugars, and to control their cholesterol. And, of course, I mentioned lifestyle changes. So, meaning making sure they don’t smoke, they stay active, and they eat a heart healthy diet. Host: Could you explain how diabetes is related to diastolic heart failure? Dr. Bead: Diabetes affects every organ in the body. And in fact, in cardiology, we consider diabetes ‘heart disease’ until proven otherwise. Although the ideology is unclear, diabetes is thought to lead to direct stiffening of the heart, either by having too much glucose in the system or by causing premature stiffening of the blood vessels surrounding the heart and, thereby, stiffening the heart itself. Host: When you said that, it made me think of a ‘starch,’ like you would put in your clothing to make it stiffer. Dr. Bead: You know what!? That’s an amazing analogy! Yeah! Cause that’s basically what it does. When you have all this excess glucose in the circulation. It’s basically, because it can literally surround cells and kind of ‘coat’ them so they don’t function so well, and they can become stiff like a starch. Yeah, like starch. Host: Could you share a treatment success story from your practice? Dr. Bead: This is always my favorite part! I love talking about my patients because they’re so amazing. There was one middle-aged lady who came to me as a consult from her primary care physician. Initially, it was a semi-urgent consult because the EKG, the electrocardiogram, was abnormal and showed, an abnormal rhythm that was initially concerning for atrial fibrillation when, in fact, she had a lot of skipped beats. When I saw the patient, she was complaining mostly of shortness of breath and the inability to do her Zumba exercises. Oh, she loved to exercise about three days a week. But then she started noticing that her legs were more swollen. She got tired easier. She had a ‘flooded’ sensation in her heart and she really couldn’t do her usual activity of daily living. And, I did a good exam. Her lungs were clear. Her heart actually sounded pretty good, with the exception of some skipped beats. But she did have some swelling in her legs and her blood pressure was quite elevated. And so, based on that, we talked, we adjusted her medication in order to get her blood pressure under better control. I prescribed a diuretic in order to reduce the fluid on her legs. And then we discussed her lifestyle changes such as reducing the sodium from her diet. When we saw her back within a couple of weeks, I had her get an echocardiogram or a sonogram of her heart which showed that her heart was strong but, using certain diagnostic techniques, we could tell that her heart was a bit stiff and it was also thickened from long-standing high blood pressure. So, we were very vigilant in terms of getting her blood pressure under good control. We were able to keep the fluid off. She was...did her part by making the lifestyle changes that she wanted to. And then, within about 6-8 weeks, she was back to doing her Zumba classes with no restrictions. And then, when I see her back every 6 months, she’s actually to the point that she’s helping teach the Zumba classes, which is always awesome. Host: Why is MedStar Heart and Vascular Institute the best place for patients to seek care for diastolic heart failure? Dr. Bead: The MedStar Heart and Vascular Institute, really is the best place for general cardiology patients, but, in particular, for patients who have specific diagnoses, such as diastolic heart failure, because it offers comprehensive, state-of-the-art care in a compassionate environment that is patient-centered and evidence based. Host: Well, thanks for joining us today, Dr. Bead. Dr. Bead: Thank you for having me. Conclusion: Thanks for listening to Medical Intel with MedStar Washington Hospital Center. Find more podcasts from our healthcare team by visiting medstarwashington.org/podcast or subscribing in iTunes or iHeartRadio.

Dr Carolyn Lam:                Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the journal and its editors.                                                 I'm Dr Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. The ORBITA Trial of percutaneous coronary intervention and stable single vessel coronary artery disease has to be one of the most hotly discussed in the cardiology world. The featured paper of this week adds important knowledge that will help us understand the physiology stratified results of ORBITA.                                                 Coming right up after these summaries.                                                 The first original paper this week provides novel mechanistic insights that may lead to a new treatment approach for obesity and hypertriglyceridemia. Co-corresponding authors, Drs Xiang and Xia from Central South University of Xiangya in China, looked at Reticulin 3, which is an endoplasmic reticular protein that has previously shown to play a role in neurodegenerative diseases.                                                 In the current paper, the authors show that over-expression of Reticulin 3 in mice induced obesity and a greater accumulation of triglycerides. Remarkably, increased Reticulin 3 expression was also found in patients with obesity and hypertriglyceridemia. They further showed that Reticulin 3 played critical roles in regulating the biosynthesis and storage of triglycerides and in controlling lipid droplet expansion. Thus, these results suggest that inhibiting the expression of Reticulin 3 in fat tissue may be a novel therapeutic approach to treat obesity and hypertriglyceridemia in the future.                                                 The next study provides insights into the genetic determinates of residual cardiovascular risk in patients already receiving statins. First author Dr Wei, corresponding Dr Denny from Vanderbilt University Medical Center and their colleagues performed a genome-wide association study and identified that a variation at the LPA Locus was associated with coronary heart disease events during statin therapy and independent of the extent of LDL cholesterol lowering. The association of the LPA Locus with coronary heart disease events persisted in individuals with an LDL cholesterol less than 70 milligrams per deciliter. These findings, therefore, provide support for exploring strategies targeting circulating concentrations of lipoprotein(a) to reduce coronary heart disease events in patients already receiving statins.                                                 The next paper provides important mechanistic results that help us understand pathways in atherosclerotic plague regression. Co first authors, Drs Mueller and Zhu, corresponding author Dr Fazio from Oregon Health and Science University and their colleagues have previously shown that mice lacking an LDL receptor with beta protein 1 in macrophages undergo accelerated atherosclerotic plague formation. However, in the current study they sought to explore the role of macrophage LDL receptor protein 1 during plague regression. They did this by placing EPO E deficient mice on a high fat diet for 12 weeks, then reconstituting their bone marrow using wall type or macrophage LDL receptor protein 1 deficient mice as donors, and finally switching them back to a chow diet for 10 weeks. The authors found that the lack of LDL receptor protein 1 expression in macrophages unexpectedly caused more atherosclerosis regression. Mice with macrophages lacking LDL receptor protein 1 showed less M1 macrophages in the plague and increased CCR7 dependent egress of macrophages from the plague. Thus, loss of macrophage LDL receptor protein 1 has a dual and opposite effect on plague biogenesis, depending on whether the plague is growing or shrinking.                                                 The next paper highlights the intercalated disc, which is a specialized intercellular junction, coupling cardiomyocyte electrical activity in forced transmission as a mechanosensitive signaling hub for causative mutations in cardiomyopathy. First author Dr Trembley, corresponding author Dr Small from University of Rochester School of Medicine and Dentistry and their colleagues showed that myocardin related transcription factors associated with desmosome proteins of their intercalated disc in both murine and human hearts. Genetic deletion of myocardin related transcription factors in cardiomyocytes led to rapid onset of dilated cardiomyopathy in response to pressure overload hypertrophy. Furthermore, myocardin related transcription factors were required for the maintenance of sacromere and intercalated disc integrity under pathological stress. These findings, therefore, provide a unique link between the intercalated disc and mechanosensitive transcriptional regulations. Since myocardin related transcription factors redistribute from intercalated disc in human heart failure, this may represent a novel signaling complex present in cardiomyopathic characterized by desmosome dysfunction.                                                 The next paper investigated the association of blood pressure with peripheral arterial disease events, using data from the ALLHAT Trial. Co first authors Drs Itoga and Tawfik, corresponding author Dr Chang from Stanford University School of Medicine and their colleagues found that both lower systolic blood pressure of less than 120 and higher systolic blood pressure of above 160 millimeters of mercury were both associated with higher rates of peripheral arterial disease events. Diastolic blood pressure less than 70 and a pulse pressure above 65 millimeters mercury were also associated with increased rates of lower extremity peripheral arterial disease events. Given that the recent revised blood pressure guidelines advocate lower systolic blood pressure targets for overall cardiovascular risk reduction, the authors called for future, further refinement of optimal blood pressure targets, specific for peripheral artery disease.                                                 The final original paper this week provides the first integrated atherosclerotic disease risk calculator to incorporate risk factors including high sensitivity C reactive protein, family history, and coronary artery calcium data. First and corresponding author Dr Khera from UT Southwestern Medical Center and colleagues used 3 population-based cohorts to develop Cox Proportional Hazards Models for the outcome of atherosclerotic cardiovascular disease. The derived Astro-CHARM model incorporated factors like age, sex, systolic blood pressure, total and HDL cholesterol, smoking, diabetes, hypertension treatment, family history of myocardial infarction, high sensitivity c reactive protein, and coronary artery calcium scores. The model performance was validated externally in a 4th cohort, and shown to improve risk prediction compared with traditional risk factor equations, and showed good discrimination in calibration in the validation cohort. A mobile application and web based tool was developed to facilitate the clinical application of this tool, and is available at www.astrocharm.org.                                                 And that brings us to the end of this week's summaries. Now for our featured discussion.                                                 Gosh, I am learning for the first time today that it's terribly inconvenient to lose my voice when I am a podcaster. This is Carolyn Lam and our featured discussion that I am so excited about, but the cool thing is the thing we are talking about is so hot that you don't even need me to say anything. And what we are talking about is the ORBITA Trial. That was greeted with as much hype and hoopla and sensationalism since its publication in 2017. I am so proud to have the first and corresponding author Dr Rasha Al-Lamee from National Heart and Lung Institute Hammersmith Hospital in London. I also have Dr Ajay Kirtane from Columbia University Medical Center in New York Presbyterian Hospital and the Cardiovascular Foundation in New York as the editorialist for the paper. And finally, our associate editor Dr Manos Brilakis from UT Southwestern. Rasha, why don't you just take it away and just tell us, what is your paper focusing on in this week's issue? Dr Rasha Al-Lamee:         The paper that was published in this issue in circulation is basically our second analysis of the ORBITA Trial, a substudy analysis. Essentially, looking at the primary endpoint and the secondary endpoints of ORBITA, and having a look at those patients from ORBITA and seeing whether there was any association between their invasive physiological assessment using FFR and ISR at the pre-randomization stage and seeing whether the level of ischemia on ISR or FSR was associated or predicted in the way in which they performed in terms of their endpoints. To see whether there was any difference in the placebo control efficacy of angioplasty in those patients who have more or less severe ischemia on their invasive physiological assessment. Dr Manos Brilakis:            First off, that's a phenomenal paper, and I think she puts things into perspective. I know Ajay put an excellent tutorial. I think all of us were surprised about the findings. You would expect that the more ischemia, that you might see a little more response. Any thoughts as to why there wasn't such an association? Dr Rasha Al-Lamee:         I think it's so difficult because, of course, as we all know from the primary paper that was published in The Lancet, in terms of the primary endpoint, which would be change in exercise time and the difference between the two groups, the difference is actually much smaller than we expected. And when we have such a small difference in exercise time, the ability to be powered enough to be able to split that endpoint based on stratification of invasive physiology becomes very difficult, and we're perhaps underpowered to be able to do that.                                                 Where we did see a very great effect in terms of the primary assessment in The Lancet paper was in stress echo ischemia. What we saw is those patients who had angioplasty were far more likely to have an improvement, or indeed, a normalization of their ischemia on their stress echo. Where we saw a big difference the two groups we were then clearly powered to be able to stratify those patients based on their invasive physiology, and for that secondary endpoint we saw that, in fact, tied to your stenosis or the lower your ISR or FRR, the more likely you are to have an improvement in stress echo, having had placebo controlled angioplasty. Dr Manos Brilakis:            Ajay, I know you had a lot of things insight into the vision of the tutorial for the ORBITA Trial. What are your thoughts about the findings? Dr Ajay Kirtane:                 I would, first of all, congratulate Rasha and the ORBITA team, there are others, for not only doing the main trial, but for conducting these detailed analyses, which were clearly set up ahead of time, and that's been one of the critiques of the trial is why were patients with normal-ish range FFRs included. Well, part of it was to test this hypothesis, and perhaps to show that there would be a correlation between the change in the FFR, if you will, and the endpoints that were measured.                                                 So, I think that that's the first part, that this is actually a scientific experiment, and a thoughtful one in doing so. I think exactly as Rasha said though, if there is a limited signal, with respect to the overall trial, then further subsetting is less likely to show a significant signal. I think that's exactly what the investigators found. The only other comment I would make though is, I would commend Rasha and the team for producing other analyses that are novel in this manuscript including the freedom from angina analysis, as well as responding to some of the earlier critiques of the trial and not using specific methodologies to adjust the baseline differences improves. Those are also included in this analysis. Dr Manos Brilakis:            Yeah, absolutely, I think that was very enlightening to see, the freedom of angina. And I know there was some questions whether that might change the overall findings from the studies, so there is some quality of life benefit. Rasha, what is your thoughts about this? I mean, you must understand this study better than anyone else. People who have stable angina, should they undergo PCI or not? Dr Rasha Al-Lamee:         I think the freedom from angina signal was very important, and obviously not something that we had pre-specified, so it wasn't reported in the primary analysis. We're obviously much more able now, since we've published that primary analysis to do secondary analyses and look at things that perhaps we haven't pre specified. And it's interesting to see that 20% more patients are free from angina having had angioplasty vs. placebo. Having said that, to me, it's a fantastic finding, but still a little unexpected. Much less than we might expect looking at unblinded data, or our unblinded clinical experience. I would have expected much higher levels from freedom of angina. Dr Rasha Al-Lamee:         I think what we know, and what we've seen both from this paper, very importantly, and also the primary manuscript, is that the efficacy of angioplasty is very tightly linked to the improvement in ischemia. We've actually, in fact, got more papers that are coming out from our group recently. And that you can predictably tell your patients that if I sense a lesion that's causing a reduction in ISR or FFR, and potentially symptoms, then I will improve your ischemic burden.                                                 What I think is more tricky is how much I will relieve your symptoms, or make you feel better. That may be because symptom assessment itself is very tricky, and perhaps that actually just diagnosing cardiac angina is actually a very difficult thing. The easiest way to piece out improvement in symptoms is to find those patients who become free of angina because, of course, that's the binary end point. When we look at grades of symptoms, and whether their angina frequency improves, or whether the level of angina improves in terms of PCI, then I think it becomes much harder, especially in a blinded trial where, of course, when people come back, even with atypical chest pain, it will still be recorded as potentially angina because, of course, both the investigators and the patients have no idea what they've had done, which is quite different from real life where, of course, you are able to think more about whether this chest pain might indeed be from the heart or from other causes. Dr Manos Brilakis:            Perfect, thank you very much. And I would completely agree with you that, the study was perfect. And, as Ajay said, it is something that we needed, and more of them should be done. And I think you are right that this is the best way to piece out the symptom improvement.                                                 Ajay, any final comments? Dr Ajay Kirtane:                 I think that the toughest challenge with trials like this is to really enroll the patients that many of us as interventionists feel would really improve in terms of their symptom class. Even despite these efforts, if one looks at the baseline of anginal frequency in the trial, the means are relatively high, which suggest that the anginal burden, at least in terms of measurements through the anginal questionnaire is not that severe. One could argue that somebody has severe angina that is occurring all the time, that those are types of patients that are hard to randomize in a clinical trial.                                                 I think, at least my overview stepping back perspective of the context of ORBITA within clinical practice, is exactly that. The trial is an important scientific advance, but this does not encompass the answer for every single patient that comes to see us in the office that have a range of symptoms, very severe to less severe. That was something Rasha has been saying all along as well. It's not something that we could over extrapolate this to every patient that we see. So, I think that when the hype dies down, these types of scientific analyses will stand out. They emphasize the need for regular clinical research, and in that way, I think has generated a lot of attention not only to the clinical field here, but also the scientific pursuit of evidence. That's a really magical thing. Dr Rasha Al-Lamee:         I think, if I can add to that Ajay, I think it's probably also sort of the assessment of symptoms is incredibly important. I think many of us, and I'll include myself in this, when we see a very tight stenosis, are happy to essentially correlate any level of symptoms to that tight stenosis. One thing I've learned from all this, I want to see reproducible angina that very much is textbook, cardiac caused chest pain, and the atypical anginas we see, perhaps some of that pain is not from that stenosis, but from somewhere else. Therefore, by fixing that stenosis, we don't necessarily make that pain go away. Dr Manos Brilakis:            Absolutely, and I think you are absolutely, if it is something simple vessel disease, if it's something a little more straightforward, then I think you are right Ajay, that this is much harder, multiple vessel disease especially in people with reduced ejection fraction. Dr Carolyn Lam:                You've been listening to Circulation on the Run! Don't forget to tune in again next week!  

Commentary by Dr. Valentin Fuster

Commentary by Dr. Valentin Fuster

Hi friend – in this episode we talk about how to monitor your blood pressure. It’s not difficult at all once you know how to do it. Then you can do it once in a while to get a sense of whether chronic stress is building up in your body. This is another example of Boundary Testing. Meaning: it won’t give you an indicator of just how good your health is, but it *will* tell you when to be worried. FYI: Those stats are: Diastolic pressure +120 | Systolic pressure +100 | Heart rate +100 beats per minute. ========== Subscribe to Future Skills on: iTunes | Android  | Stitcher | Spotify Join our newsletter for episode summaries and monthly Q&As: www.futureskillspodcast.com  Apply for the Future Skills Program

Commentary by Dr. Valentin Fuster

In this episode, episode 52, I welcome Dr. Todd Dorman to the show.  Dr. Dorman is a professor of anesthesiology here at Johns Hopkins, is the Vice Chair for Critical Care, and is the immediate past president of the Society of Critical Care Medicine (SCCM).  Dr. Dorman and I discuss diastolic heart failure or heart … Continue reading "Episode 52: Diastolic Heart Failure with Todd Dorman"

This episode covers Chapter 81 of Rosen’s Emergency Medicine. This one is mint! Heart failure is one of those must-know-about presentations, you WILL see this in the ED.   Define Cardiac index Preload Afterload Describe: How compliance changes the relationship between end diastolic pressures and volume the Frank-Starling relationship Pousseils Law and LaPlaces Law List 3 CV and 4 Neurohormonal physiologic compensatory mechanisms in CHF List the 5 most common disease processes resulting in HF and briefly describe the contribution of each Describe the different classifications of heart failure: Acute vs. Chronic HF Systolic vs. Diastolic dysfunction Right vs. Left sided HF High-output vs. Low-output HF Describe the NYHA function HF Classes and the Killip Classification List 10 common precipitants of acute HF List 6 historical predictors of acute HF and 6 clinical features of acute HF List 5 CXR and 5 ECG findings of HF What is the role of BNP in HF? Describe the primary management goals in acute HF Describe the mechanism of action of NIPPV in HF. Who needs to be intubated? When is it contraindicated? Describe the pharmacologic treatment strategy for: Acute pulmonary edema + adequate perfusion Acute pulmonary edema + hypotension How do nitrates work in acute pulmonary edema? What is the dose? List 10 treatment options for chronic HF

This episode covers Chapter 81 of Rosen’s Emergency Medicine. This one is mint! Heart failure is one of those must-know-about presentations, you WILL see this in the ED.   Define Cardiac index Preload Afterload Describe: How compliance changes the relationship between end diastolic pressures and volume the Frank-Starling relationship Pousseils Law and LaPlaces Law List 3 CV and 4 Neurohormonal physiologic compensatory mechanisms in CHF List the 5 most common disease processes resulting in HF and briefly describe the contribution of each Describe the different classifications of heart failure: Acute vs. Chronic HF Systolic vs. Diastolic dysfunction Right vs. Left sided HF High-output vs. Low-output HF Describe the NYHA function HF Classes and the Killip Classification List 10 common precipitants of acute HF List 6 historical predictors of acute HF and 6 clinical features of acute HF List 5 CXR and 5 ECG findings of HF What is the role of BNP in HF? Describe the primary management goals in acute HF Describe the mechanism of action of NIPPV in HF. Who needs to be intubated? When is it contraindicated? Describe the pharmacologic treatment strategy for: Acute pulmonary edema + adequate perfusion Acute pulmonary edema + hypotension How do nitrates work in acute pulmonary edema? What is the dose? List 10 treatment options for chronic HF

Diastolic dysfunction

Commentary by Dr. Valentin Fuster

Podcast summary of articles from the October 2016 edition of Journal of Emergency Medicine from the American Academy of Emergency Medicine.  Topics include Pyuria in Renal Stones, Sickle Cell Anemia, CMAC as Direct Laryngoscopy, Wernicke Korsakoff Syndrome, Ultrasound for Diastolic Heart Failure, Diltiazem dosing, and Board Review on Atrial Fibrillation.  Guest speakers are Dr. John Sakles and Dr. Adam Haushalter.

Commentary by Dr. Valentin Fuster

In this video I walk you through a patient who was able to lose 50+ pounds, reverse her diabetes and improve her energy levels within 3 months. This particular patient failed gastric bypass surgery, was suffering from chronic pain, insomnia, fatigue and of course weight gain. After adding the following therapies to her regimen she was able to lose 50+ pounds of weight, reverse her diabetes, remove her chronic pain and increase her energy: - Thyroid hormone replacement: she needed to use NDT + T3 - Testosterone replacement - Physical work - Biofeedback to reduce stress - Supplements - Fasting routine to reverse insulin resistance - Dietary changes - Detox routine with FAR IR sauna I go over her blood work and symptoms in detail and walk you through how to look at lab studies to find and treat the underlying diagnoses which lead to these symptoms. In this patient she was suffering from: - Diabetes mellitus type II - Thyroid resistance - Diastolic heart disease - Low testosterone - Adrenal issues and chronic fatigue - Iron deficiency - Chronic diarrhea with multiple nutrient deficiencies - Vitamin B12 deficiency - Vitamin D deficiency - Hyperlipidemia with hypertriglyceridemia - Hypertension (high blood pressure) She was seen by previous other Doctors and told her lab tests were "normal". Find more about this approach that can lead to long lasting weight loss and reduce your symptoms in this video! More information in the video and the full blog post can be found here: https://www.restartmed.com/weight-loss-hypothyroidism-success/ You can read more on my website here: http://www.restartmed.com/ This video is not intended to be used as medical advice. If you have questions about your health please consult your physician or primary care provider. Dr. Westin Childs goes to great lengths to produce high quality content but this is NOT a substitute for medical care.

Commentary by Dr. Valentin Fuster

Medical Grand Rounds with Arnold Katz MD

Video podcast today!  This one ended up being a lot longer than I had planned.  In this episode I discuss a simple method for learning murmurs and how to identify where the murmur is occurring and exactly what is happening… The post Murmurs | Stenosis, Regurgitation, Systolic, Diastolic appeared first on NURSING.com.

Francesco Loffredo, Brigham and Women's Hospital, Harvard Stem Cell Institute, Cambridge, MA, USA speaks on "GDF11: a novel regulator of cardiac aging and diastolic function?" This seminar has been recorded by ICGEB Trieste

Auscultation of a diastolic sound referred to as tumor plop, resulting from a left atrial myxoma. The sound arises from obstruction to ventricular in-flow. Copyright 2011 by the Texas Heart Institute at St. Luke's Episcopal Hospital.

Learn Why L-Carnitine May Be A Valuable Therapy In Helping Manage Heart Failure Dr. Mohammad Reza Movahed received his MD from Medizinische Hochschule Hannover, Germany. He completed his medical residency at the University of Rochester, New York and his cardiology training at the University of South Carolina, Columbia. His interventional cardiology training was completed at Yale University Hospital, New Haven, Connecticut in 2000. He has been an Assistant Clinical Professor at the University of California, Irvine and in 2007 joined the Southern Arizona VA Health Care System, University of Arizona College of Medicine for his clinical work and as the medical director of heart transplantation. Since July 2010, Dr Movahed has been a tenured Professor of Medicine at the University of Arizona College of Medicine. He has contributed to over150 publications in major peer reviewed medical journals. He recently was a co-author on a paper with lead investigator Dr. Ali Reza Serati MD and colleagues from Modarres Hospital, Tehran, Iran entitled: "L-Carnitine Treatment in Patients with Mild Diastolic Heart Failure is Associated with Improvement in Diastolic Function and Symptoms" in the jounral Cardiology 2010. Download or Open:

In severe hemorrhagic shock, left ventricular (LV) diastolic dysfunction is an early sign of cardiac failure due to compromised myocardial oxygenation. Immediate fluid replacement or, in particular, administration of a hemoglobin-based oxygen carrier (diaspirin cross-linked hemoglobin; DCLHb) improves myocardial oxygenation; therefore, positive effects on LV diastolic function could be expected. The effects of fluid resuscitation from severe hemorrhagic shock with DCLHb were investigated in 20 anesthetized domestic pigs. After generation of a critical left anterior descending coronary artery stenosis (narrowing of the artery until disappearance of reactive hyperemia after a 10-second complete vessel occlusion), hemorrhagic shock (mean arterial blood pressure 45 mm Hg) was induced within 15 min by controlled blood withdrawal and maintained for 60 min. Fluid resuscitation consisted of replacement of the plasma volume withdrawn during hemorrhage by infusion of either 10% DCLHb (DCLHb group, n = 10) or 8% human serum albumin (HSA) oncotically matched to DCLHb (HSA group, n = 10). After completion of resuscitation, an observation period of 60 min elapsed. Measurements of central hemodynamics, myocardial oxygenation, and LV Stolic function were performed at baseline, after induction of critical coronary artery stenosis, after 60 min hemorrhagic shock, immediately after resuscitation, and 60 min later. While 5 out of 10 animals treated with died within the first 20 min after fluid resuscitation from acute LV pump failure, all DCLHb-treated animals survived until the end of the protocol (p < 0.05). Despite superior myocardial oxygenation due to augmentation of the arterial O-2 content as well as of coronary perfusion pressure, no beneficial effects on LV diastolic function were observed after infusion of DCLHb. Peak velocity Of LV pressure decrease (dp/dt(min)) did not reveal significant differences between the two groups. Immediately after completion of fluid resuscitation with DCLHb, the time constant of LV diastolic relaxation (tau) was prolonged when compared with HSA-treated animals (p < 0.05), indicating retardation of early LV diastolic relaxation. Our data suggest that DCLHb fails to improve LV diastolic function after fluid resuscitation from severe hemorrhagic shock. However, positive effects on myocardial perfusion. and oxygenation result in a significant reduction of the mortality of severe hemorrhagic shock. Copyright (C) 2001 S.Karger AG, Basel.