Podcasts about transthoracic

CardioNerds (Amit Goyal) join Dr. Merna Hussien, Dr. Akhil Kallur, Dr. Abhinav Saxena, and Dr. Brody Deb from the MedStar Georgetown - Washington Hospital Center in DC for a stroll around Rock Creek Park as they discuss an unusual case of cobalt cardiomyopathy. Expert commentary is provided by Dr. Nana Afari Armah. Episode audio was edited by CardioNerds Intern Christiana Dangas. The case is of a middle-aged woman with a past medical history of hypertension, hyperlipidemia, and bilateral hip replacements, who presented with subacute progressive exertional dyspnea, orthopnea, and constitutional symptoms and was found to have SCAI Stage C cardiogenic shock. Transthoracic echocardiogram showed severely reduced left ventricular ejection fraction (LVEF, 20-25%) and a moderate pericardial effusion. Cardiac catheterization revealed biventricular failure with elevated filling pressures. A cardiac MRI showed diffuse late gadolinium enhancement (LGE) in the left ventricle. Endomyocardial biopsy showed nonspecific chronic inflammation. However, the evidence of mitochondrial heavy metal toxicity and elevated cobalt levels made the diagnosis of cobalt cardiomyopathy. The patient underwent revision of hip joint implants to ceramic implants and started chelation therapy. However, due to persistent stage D heart failure despite normalization of cobalt levels, she underwent orthotropic heart transplantation. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case MEdia - Cobalt Cardiomyopathy Pearls - Cobalt Cardiomyopathy A good history goes a long way in diagnosing non-ischemic cardiomyopathy (NICM). Common problems can have uncommon presentations requiring a high degree of suspicion for diagnosis. Imaging features can overlap between causes of NICM. History helps in targeting further histological workup and uncovering the root cause. Multidisciplinary effort is essential in making a rare diagnosis. Taken from1 - Singh M, Krishnan M, Ghazzal A, Halushka M, Tozzi JE, Bunning RD, Rodrigo ME, Najjar SS, Molina EJ, Sheikh FH. From Hip to Heart: A Comprehensive Evaluation of an Infiltrative Cardiomyopathy. CJC Open. 2021 Nov 1;3(11):1392–5. Notes - Cobalt Cardiomyopathy How common is cobalt cardiomyopathy? When should it be suspected? Cobalt cardiomyopathy is incredibly rare, with only a handful of reported cases. 2 It is also known as beer drinkers' cardiomyopathy, as cobalt was added to beer for fortification in Quebec 3, where it was first reported. Cobalt cardiomyopathy is characterized by its rapidly progressive nature, the presence of low voltages on EKG, and diffuse infiltration. Patients also complained of a previous history of anorexia and weight loss and were found to have polycythemia and thyroid abnormalities on labs. This syndrome was very similar to wet beriberi except for the absence of a therapeutic response to thiamine. Taken from - 2 Later, this was noted in patients with total metal hip arthroplasty 4–6, especially in patients with metal-on-metal hip arthroplasty, which led to corrosion and leakage of cobalt into the bloodstream. The syndrome in these patients was similar to those in beer drinkers from Quebec. This figure, taken from 2, shows the reports of Cobalt cardiomyopathy after cobalt alloy prostheses. [HX1]  What is the pathophysiology of cobalt cardiomyopathy? Cobalt has a variety of effects on the heart, both microscopically and biochemically.Cobalt may have multiple calcium-mediated cardiac effects and may also interfere with the Krebs cycle and ATP generation by mitochondria. Histology may show modest changes with no inflammatory response o...

CardioNerds, Dr. Richard Ferraro and Dr. Dan ambinder join Dr. Li Pang, Dr. Emily Hendricks, and Dr. Bei Jiang from West Virginia University to discuss the following case that features apical obliteration with biventricular thrombus. Dr. Christopher Bianco provides the Expert CardioNerd Perspectives & Review (E-CPR) for this episode. Audio editing by CardioNerds Academy Intern, student doctor Tina Reddy. A 37-year-old Caucasian man with a history of tobacco smoking and hypertension who presented with chest pain and elevated troponin was admitted for non-ST elevation myocardial infarction (NSTEMI). Ischemic evaluation with an invasive coronary angiogram was negative. He was treated as NSTEMI and scheduled for outpatient cardiac MRI (CMR). The patient came back 2 months later with right arm weakness and confusion and was found to have an embolic stroke. Labs showed positive troponin with a flat trend and hypereosinophilia. Transthoracic echocardiogram (TTE) showed obliteration of LV and RV apex with thrombus and reduced LV systolic function. CMR was consistent with myocarditis with biventricular thrombus. The patient was started on corticosteroids and warfarin. Hypereosinophilia workup was positive for PDGFRA alpha rearrangement. He was diagnosed with primary hypereosinophila syndrome. Imatinib was initiated. The patient was followed up with the hematology clinic, achieved a complete hematologic response with normalized cell count, and remained free from any cardiovascular event at the 8-month follow-up. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media Pearls - Apical Obliteration with Biventricular Thrombus Cardiac MRI is a valuable test for patients presenting with myocardial infarction with non-obstructive coronary arteries (MINOCA). Obliterated apex with apical thrombus on TTE with hypereosinophilia should raise high suspicion for eosinophilic myocarditis. Initiation of corticosteroids is the first-line treatment for eosinophilic myocarditis, which is associated with lower mortality in patients with myocarditis. For other potential complications, such as heart failure, intracardiac thrombus, arrhythmia, and pericardial effusion, the standard of care for each disorder is recommended. Hypereosinophilia can be seen in parasitic infections, vasculitis, asthma, allergy, hematological malignancies, and as a primary disorder. Show Notes - Apical Obliteration with Biventricular Thrombus What is the differential diagnosis for patients with elevated troponin and nonobstructive CAD? The occurrence of acute myocardial infarction (AMI) without significant CAD was reported 80 years ago. However, the term MINOCA (myocardial infarction with non-obstructive coronary arteries) has only been used recently to describe these patients. It involves ischemic and nonischemic etiologies. First, overlooked ischemic etiologies need to be ruled out by reconciling the angiogram images such as spontaneous coronary artery dissection (SCAD) and plaque disruption. Intracoronary imaging, such as intravascular ultrasound (IVUS) or optical coherence tomography (OCT), may be applied to evaluate for SCAD and subtypes of plaque disruption when indicated.  The investigation continues with nonischemic causes such as stress cardiomyopathy, myocarditis, pulmonary embolism, demand ischemia from sepsis, anemia, chest trauma, heart failure exacerbation, arrhythmia, and stroke. The diagnosis of MINOCA is established when it fulfills the following criteria: First, it is AMI by the Fourth Universal Definition; Second, less than 50% of stenotic lesion on angiogram; Third, there is no alternate diagnosis.

"POCUS Spotlight: Advanced Focused Assessment in Transthoracic Echocardiography (FATE) " by Deepak Borde, MD, DNB, FCA, FTEE, Kumar Chidambaram, DA, DNB, PDCC, FTEE, Amit Dikshit, DNB, DA, and Vinayak Desurkar, MD, PDCC, FRCA. From ASRA Pain Medicine News, November 2023. See original article at www.asra.com/november23news for figures and references. This material is copyrighted. Support the show

CardioNerds (Dr. Amit Goyal) join Dr. Anureet Malhotra, Dr. John Fritzlen, and Dr. Tarun Dalia from the University of Kansas School of Medicine for some of Kansas City's famous barbeque. They discuss a case of Hydroxychloroquine induced cardiomyopathy. Notes were drafted by Dr. Anureet Malhotra, Dr. John Fritzlen, and Dr. Tarun Dalia. Expert commentary was provided by Dr. Pradeep Mammen. The episode audio was edited by Dr. Akiva Rosenzveig. Drug-induced cardiomyopathy remains an important and under-recognized etiology of cardiomyopathy and heart failure. Hydroxychloroquine is a disease-modifying antirheumatic drug used for various rheumatological conditions, and its long-term use is well-known to have toxic effects on cardiac muscle cells. Multiple cardiac manifestations of these drugs have been identified, the most prominent being electrophysiological disturbances. In this episode, we discuss a biopsy-proven case of hydroxychloroquine-induced cardiotoxicity with detailed histopathological and imaging findings. We develop a roadmap for the diagnosis of hydroxychloroquine-induced cardiomyopathy and discuss the various differentials of drug-induced cardiomyopathy. We highlight the importance of clinical monitoring and early consideration of drug-induced toxicities as a culprit for heart failure. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - Hydroxychloroquine induced cardiomyopathy Pearls - Hydroxychloroquine induced cardiomyopathy Continued decline in left ventricular systolic function despite appropriate guideline directed medical therapy should prompt a thorough evaluation for unrecognized etiologies and warrants an early referral to advanced heart failure specialists. Transthoracic echocardiogram is a valuable non-invasive screening tool for suspected pulmonary hypertension, but right heart catheterization is required for definitive diagnosis. Cardiac MRI can be used for better characterization of myocardial tissue and can aid in the evaluation of patients with non-ischemic cardiomyopathy. Hydroxychloroquine (HCQ) is a commonly used DMARD that remains an underrecognized etiology of cardiomyopathy and heart failure. In addition to ophthalmological screening, annual ECG, as well as echocardiography screening for patients on long-term HCQ therapy, should be considered in patients at risk for cardiovascular toxicity, including those with pre-existing cardiovascular disease, older age, female sex, longer duration of therapy, and renal impairment. Management of hydroxychloroquine-associated cardiomyopathy consists of discontinuing hydroxychloroquine and standard guideline-directed medical therapy for heart failure.  HCQ cardiomyopathy may persist despite medical therapy, and advanced therapy options may have to be considered in those with refractory heart failure. Show Notes - Hydroxychloroquine induced cardiomyopathy What are the various cardiotoxic effects of hydroxychloroquine (HCQ) and the mechanism of HCQ-mediated cardiomyopathy? One of the most frequently prescribed disease-modifying antirheumatic drugs (DMARDs), HCQ is an immunomodulatory and anti-inflammatory agent that remains an integral part of treatment for a myriad of rheumatological conditions. Its efficacy is linked to inhibiting lysosomal antigen processing, MHC-II antigen presentation, and TLR functions.8 The known cardiac manifestations of HCQ-induced toxicity include conduction abnormalities, ventricular hypertrophy, hypokinesia, and lastly, cardiomyopathy. Conduction Abnormalities - by binding to and inhibiting the human ether-à-go-go-related gene (hERG) voltage-gated potassium channel,

CardioNerds (Dr. Josh Saef and Dr. Sumeet Vaikunth) join Dr. Sheng Fu, Dr. Payton Kendsersky, and Dr. Aniqa Shahrier from the Medical University of South Carolina for some off-shore fishing. They discuss the following featuring a patient with D-TGA and Eisenmenger's syndrome treated with a Heartmate 3. Expert commentary was provided by Dr. Brian Houston. The episode audio was edited by student Dr. Adriana Mares. A 39-year-old woman with a history of D-transposition of the great arteries (D-TGA) with prior atrial switch repair (Mustard) was admitted from the clinic with cardiogenic shock. She underwent right heart catheterization which demonstrated elevated biventricular filling pressures and low cardiac index. An intra-aortic balloon pump was placed, and the patient was evaluated for advanced therapies. A liver biopsy showed grade 3 fibrosis, which, in combination with her shock state, made her a high-risk candidate for isolated heart or combined heart-liver transplantation. After a multi-disciplinary discussion, the patient underwent a Heartmate III left ventricular assist device (LVAD) implant in her systemic right ventricle. Although she did well post-operatively, she was admitted after a month with recurrent cardiogenic shock, with imaging showing her inflow cannula had become perpendicular to the septum.  The patient and family eventually decided to pursue comfort measures, and the patient passed. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - D-TGA and Eisenmenger's syndrome treated with a Heartmate 3 Pearls - D-TGA and Eisenmenger's syndrome treated with a Heartmate 3 Early diagnosis of cyanotic congenital heart disease is paramount for treatment and prevention of future complications. Adult congenital heart disease requires a multi-disciplinary team for management in consultation with an adult congenital cardiology specialist. Eisenmenger syndrome is related to multiple systemic complications and has a high rate of mortality. Advancement in PAH medical management can offer noninvasive treatment options for some patients. Transthoracic echocardiography is the cornerstone for diagnosis. Other modalities (e.g. cardiac CT, cardiac MRI, invasive catheterization) can aid in diagnosis and management. Pearls - D-TGA and Eisenmenger's syndrome treated with a Heartmate 3 While advances in pediatric surgery have allowed many patients born with congenital heart disease to survive into adulthood, adult congenital heart disease (ACHD) patients are complex and prone to numerous adverse sequalae including arrhythmias, heart failure, valvular disease, and non-cardiac organ dysfunction. Heart failure can be a challenging presentation in ACHD patients due to a longstanding history of clinical compensation. Their unique and complex anatomy, as well as highly variable clinical presentation, present unique challenges when it comes to advanced heart failure options such as durable left ventricular assist devices (LVAD) or transplantation. While durable LVAD implantation is possible in patients with systemic right ventricles, anatomic compatibility is paramount and poses ongoing challenges in their management. Goals of care discussions should be had early, as options for treatment may be limited. Show Notes - D-TGA and Eisenmenger's syndrome treated with a Heartmate 3 What are some common sequelae in ACHD patients? ACHD patients are a heterogeneous population, but atrial tachycardias are extremely frequent in this patient population, often due to re-entrant pathways around surgical suture lines. These can often be treated with radiofrequency ablation while paying clos...

CardioNerds (Dr. Josh Saef, Dr. Agnes Koczo) join Dr. Iva Minga, Dr. Kifah Hussain, and Dr. Kevin Lee from the University of Chicago - NorthShore to discuss a case of unrepaired congenital heart disease that involves D-TGA complicated by Eisenmenger syndrome. The ECPR was provided by Dr. Michael Earing. Audio editing by Dr. Akiva Rosenzveig. A 25-year-old woman with an unknown congenital heart disease that was diagnosed in infancy in Pakistan presents to the hospital for abdominal pain and weakness. She is found to be profoundly hypoxemic, and an echocardiogram revealed D-transposition of the great arteries (D-TGA) with a large VSD. As this was not repaired in childhood, she has unfortunately developed Eisenmenger syndrome with elevated pulmonary vascular resistance. She is stabilized and treated medically for her cyanotic heart disease. Unfortunately given the severity and late presentation of her disease, she has limited long-term options for care. CardioNerds discuss the diagnosis of D-TGA and Eisenmenger's syndrome, as well as long-term management and complications associated with this entity. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - Unrepaired Congenital Heart Disease Pearls - Unrepaired Congenital Heart Disease Early diagnosis of cyanotic congenital heart disease is paramount for treatment and prevention of future complications. Adult congenital heart disease requires a multi-disciplinary team for management in consultation with an adult congenital cardiology specialist. Eisenmenger syndrome is related to multiple systemic complications and has a high rate of mortality. Advancement in PAH medical management can offer noninvasive treatment options for some patients. Transthoracic echocardiography is the cornerstone for diagnosis. Other modalities (e.g. cardiac CT, cardiac MRI, invasive catheterization) can aid in diagnosis and management. Show Notes - Unrepaired Congenital Heart Disease Cyanotic congenital heart disease is often diagnosed in infancy and timely treatment is paramount. As these diseases progress over time, pulmonary over-circulation often pulmonary hypertension (PH), elevated pulmonary vascular resistance, and Eisenmenger syndrome will develop, which preclude definitive treatment. For D-TGA, before PH develops, there are surgical options such as the arterial switch procedure that can treat the disease. Unfortunately, once Eisenmenger syndrome develops, there are multiple systemic complications including hyperviscosity, thrombosis, bleeding, kidney disease, iron deficiency, arrhythmias, etc. that can occur. Management requires a multi-disciplinary team including an adult congenital cardiology specialist, but mortality rates remain high, with median survival reduced by 20 years, worse with complex cardiac defects. Bosentan is a first line treatment for patients with Eisenmenger syndrome, with PDE-5 inhibitors as a second line either by themselves or in combination with bosentan. Data are currently limited for latest-generation PH treatments in Eisenmenger syndrome and further study is still underway. References Ferencz C. Transposition of the great vessels. Pathophysiologic considerations based upon a study of the lungs. Circulation. 1966 Feb;33(2):232-41. Arvanitaki A, Gatzoulis MA, Opotowsky AR, Khairy P, Dimopoulos K, Diller GP, Giannakoulas G, Brida M, Griselli M, Grünig E, Montanaro C, Alexander PD, Ameduri R, Mulder BJM, D'Alto M. Eisenmenger Syndrome: JACC State-of-the-Art Review. J Am Coll Cardiol. 2022 Mar 29;79(12):1183-1198. Earing MG, Webb GD. Congenital heart disease and pregnancy: maternal and fetal risks. Clin Perinatol.

The following question refers to Section 7.8 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by Stony Brook University Hospital medicine resident and CardioNerds Intern Dr. Chelsea Tweneboah, answered first by Mayo Clinic Cardiology Fellow and CardioNerds Academy Chief Dr. Teodora Donisan, and then by expert faculty Dr. Michelle Kittleson.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #29 A 69-year-old man was referred to the cardiology clinic after being found to have a reduced left ventricular ejection fraction and left ventricular hypertrophy. For the last several months he has been experiencing progressively worsening fatigue and shortness of breath while getting to the 2nd floor in his house. He has a history of bilateral carpal tunnel syndrome and chronic low back pain. He takes no medications. On exam, his heart rate is 82 bpm, blood pressure is 86/60 mmHg, O2 saturation is 97% breathing ambient air, and BMI is 29 kg/m2. He has a regular rate and rhythm with normal S1 and S2, bibasilar pulmonary rales, and 1+ pitting edema in both legs. EKG shows normal sinus rhythm with a first-degree AV delay and low voltages. Transthoracic echocardiogram shows a moderately depressed LVEF of 35-39%, severe concentric hypertrophy with a left ventricular posterior wall thickness of 1.5 cm and strain imaging showing globally reduced longitudinal strain with apical sparring. There is also biatrial enlargement and a small pericardial effusion. A pharmacologic nuclear stress test did not reveal any perfusion defects. A gammopathy panel including SPEP, UPEP, serum and urine immunofixation studies, and serum free light chains are unrevealing. A 99mTc-Pyrophosphate scan was positive with grade 3 uptake. In addition to starting diuretics, what is the next most appropriate step for managing for this patient? A Start metoprolol succinate B Start sacubitril/valsartan C Perform genetic sequencing of the TTR gene D Perform endomyocardial biopsy Answer #29 Explanation The correct answer is C – perform genetic sequencing of the TTR gene.   This patient has findings which raise suspicion for cardiac amyloidosis. There are both cardiac (low voltages on EKG and echocardiogram showing marked LVH with biatrial enlargement and small pericardial effusion as well as a characteristic strain pattern) and extra-cardiac (bilateral carpal tunnel syndrome and low back pain) features to suggest amyloidosis. The diagnosis of cardiac amyloidosis requires a high index of suspicion and most commonly occurs due to a deposition of monoclonal immunoglobulin light chains (AL-CM) or transthyretin (ATTR-CM). ATTR may cause cardiac amyloidosis as either a pathogenic variant (ATTRv) or as a wild-type protein (ATTRwt).   Patients for whom there is a clinical suspicion for cardiac amyloidosis should have screening for serum and urine monoclonal light chains with serum and urine immunofixation electrophoresis and serum free light chains (Class 1, LOE B-NR). Immunofixation electrophoresis (IFE) is preferred because serum or urine plasma electrophoresis (SPEP or UPEP) are less sensitive. Together, measurement of serum IFE, urine IFE, and serum FLC is >99% sensitive for AL amyloidosis.

CardioNerds (Drs. Amit Goyal and Dan Ambinder) join Dr. Emily Lee (LAC+USC Internal medicine resident) and Dr. Charlie Lin (LAC+USC Cardiology fellow) as the discuss an important case of stimulant-related (methamphetamine) cardiovascular toxicity that manifested in right ventricular dysfunction due to severe pulmonary hypertension. Dr. Jonathan Davis (Director, Heart Failure Program at Zuckerberg San Francisco General Hospital and Trauma Center) provides the ECPR for this episide. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. With the ongoing methamphetamine epidemic, the incidence of stimulant-related cardiovascular toxicity continues to grow. We discuss the following case: A 36-year-old man was hospitalized for evaluation of dyspnea and volume overload in the setting of previously untreated, provoked deep venous thrombosis. Transthoracic echocardiogram revealed severe right ventricular dysfunction as well as signs of pressure and volume overload. Computed tomography demonstrated a prominent main pulmonary artery and ruled out pulmonary embolism. Right heart catheterization confirmed the presence of pre-capillary pulmonary arterial hypertension without demonstrable vasoreactivity. He was prescribed sildenafil to begin management of methamphetamine-associated cardiomyopathy and right ventricular dysfunction manifesting as severe pre-capillary pulmonary hypertension. CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases', with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ). CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - stimulant-related (methamphetamine) cardiovascular toxicity Pearls - stimulant-related (methamphetamine) cardiovascular toxicity 1. Methamphetamine, and stimulants in general, can have a multitude of effects on the cardiovascular and pulmonary systems. Effects of methamphetamine are thought to be due to catecholamine toxicity with direct effects on cardiac and vascular tissues. Acutely, methamphetamine can cause vascular constriction and vasospasm, while chronic exposure is associated with endothelial damage. Over time, methamphetamine can cause pulmonary hypertension, atherosclerosis, cardiac arrhythmias, and dilated cardiomyopathy. 2. Methamphetamines are the second most commonly misused substances worldwide after opiates. Patients with methamphetamine-associated pulmonary arterial hypertension (PAH) have more severe pulmonary vascular disease, more dilated and dysfunctional right ventricles, and worse prognoses when compared to patients with idiopathic PAH. Additionally, patients with methamphetamine-associated cardiomyopathy and PAH have significantly worse outcomes and prognoses when compared to those with structurally normal hearts without evidence of PAH. Management includes multidisciplinary support, complete cessation of methamphetamine use, and guideline-directed treatment of PAH. 3. The diagnosis of pulmonary hypertension (PH) begins with the history and physical, followed by confirmatory testing using echocardiography and invasive hemodynamics (right heart catheterization). Initial serological evaluation may include routine biochemical, hematologic, endocrine, hepatic, and infectious testing. Though PH is traditionally diagnosed and confirmed in a two-step, echocardiogram-followed-by-catheterization model, other diagnostics often include electrocardiography, blood gas analysis, spirometry, ventilation/perfusion assessment,

The normal heart is very robust. Some people are born with abnormalities of the heart structure. Others acquire damage to the heart valves which become too narrow or unable to close properly. The muscle and linings of the heart may be affected by infections, drugs or other inherited or acquired diseases. All of these can cause heart failure or death if not treated.This lecture will consider the prevention and treatment of structural heart disease.A lecture by Sir Chris Whitty recorded on 16 May 2023 at Barnard's Inn Hall, London.The transcript and downloadable versions of the lecture are available from the Gresham College website: https://www.gresham.ac.uk/watch-now/heart-diseasesGresham College has offered free public lectures for over 400 years, thanks to the generosity of our supporters. There are currently over 2,500 lectures free to access. We believe that everyone should have the opportunity to learn from some of the greatest minds. To support Gresham's mission, please consider making a donation: https://gresham.ac.uk/support/Website:  https://gresham.ac.ukTwitter:  https://twitter.com/greshamcollegeFacebook: https://facebook.com/greshamcollegeInstagram: https://instagram.com/greshamcollegeSupport the show

CardioNerds (Daniel Ambinder) join Dr. Tomio Tran, Dr. Vid Yogeswaran, and Dr. Amanda Cai from the University of Washington for a break from the rain at the waterfront near Pike Place Market. They discuss the following case: A 46-year-old woman presents with cardiac arrest and was found to have cor triatriatum sinistrum (CTS). CTS is a rare congenital cardiac malformation in which the left atrium is divided by a fenestrated membrane, which can restrict blood flow and cause symptoms of congestive heart failure. Rarely, the condition can present in adulthood. To date, there have been no cases of sudden cardiac death attributed to CTS. Dr. Jill Steiner provides the E-CPR for this episode. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases', with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ). CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - A Sinister Cause of Sudden Cardiac Death – University of Washington A 40-year-old woman with a history of recurrent exertional syncope had sudden loss of consciousness while kissing her partner. The patient received bystander CPR while 911 was called. EMS arrived within 10 minutes of the call and found the patient apneic and unresponsive. Initial rhythm check showed narrow complex tachycardia at a rate of 136 BPM. ROSC was eventually achieved. A 12-lead ECG showed that the patient was in atrial fibrillation with rapid ventricular rate. The patient was intubated and brought to the emergency department. The patient spontaneously converted to sinus rhythm en route to the hospital. In the emergency department, vital signs were remarkable for hypotension (76/64 mmHg) and sinus tachycardia (110 BPM). The physical exam was remarkable for an inability to follow commands. Laboratory data was remarkable for hypokalemia (2.5 mmol/L), transaminitis (AST 138 units/L, ALT 98 units/L), acidemia (pH 7.12), and hyperlactatemia (11.2 mmol/L). CT scan of the chest revealed a thin membrane within the left atrium. Transthoracic echocardiogram showed normal biventricular size and function, severe tricuspid regurgitation, pulmonary artery systolic pressure of 93 mmHg, and the presence of a membrane within the left atrium with a mean gradient of 25 mmHg between the proximal and distal left atrial chambers. Vasopressors and targeted temperature management were initiated. The patient was able to be re-warmed with eventual discontinuation of vasopressors, however she had ongoing encephalopathy and seizures concerning for hypoxic brain injury. There was discussion with the adult congenital heart disease team about next steps in management, however the patient was too sick to undergo any definitive treatment for the intracardiac membrane within the left atrium. The patient developed ventilator associated pneumonia and antibiotics were initiated. The patient ultimately developed  bradycardia and pulseless electrical activity; ROSC was unable to be achieved, resulting in death. Autopsy was remarkable for the presence of a fenestrated intracardiac membrane within the left atrium and lack of other apparent congenital heart defects. There was right ventricular hypertrophy and pulmonary artery intimal thickening with interstitial fibrosis suggestive of pulmonary hypertension. There were bilateral acute subsegmental pulmonary emboli present. The cause of death was declared to be arrhythmia in the setting of pulmonary hypertension and right s...

CardioNerds join Dr. Samid Muhammad Farooqui, Dr. Hiba Hammad, and Dr. Syed Talal Hussain, from the University of Oklahoma Pulmonary and Critical Care Medicine Fellowship Program, in Oklahoma City. The fellows will take us in a fascinating discussion of a case of rapidly progressing dyspnea and pulmonary hypertension in a patient with metastatic breast cancer. They will then reveal an interesting etiology of pulmonary hypertension, where the secret was on the wedge! University of Oklahoma faculty and expert in pulmonary hypertension and right ventricular physiology, Dr. Roberto J. Bernardo provides the E-CPR for this episode. Audio editing by CardioNerds Academy Intern, Dr. Christian Faaborg-Andersen. A septuagenarian female, with a past medical history of metastatic breast adenocarcinoma, presented to the hospital with worsening dyspnea over a period of 3 weeks. She was found to be in rapidly progressive hypoxic respiratory failure with unremarkable chest x-ray, CTA chest, and V/Q scan. Transthoracic echocardiogram revealed elevated RVSP and a subsequent right heart catheterization showed pre-capillary pulmonary hypertension with a low cardiac index. She was treated for rapidly progressive RV dysfunction with inotropic support and inhaled pulmonary vasodilators until she decided to pursue comfort measures. Wedge cytology came back positive for malignant cells, confirming a diagnosis of Pulmonary Tumoral Thrombotic Microangiopathy (PTTM). CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases', with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ). CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - When Tumors Take Your Breath Away - University of Oklahoma College of Medicine Pearls - When Tumors Take Your Breath Away - University of Oklahoma College of Medicine Pulmonary arterial hypertension (PAH) is a progressive disorder of the pulmonary vasculature, characterized by progressive obliteration and remodeling of the pulmonary circulation, resulting in increased pulmonary vascular resistance and increased right ventricular (RV) wall stress, abnormal right ventricular mechanics, and eventually RV dysfunction and death. Pulmonary hypertension (PH) is divided into pre-capillary and post-capillary profiles, where pre-capillary PH is hemodynamically characterized by a mean pulmonary artery pressure (mPAP) > 20 mmHg, pulmonary artery wedge pressure (PAWP) ≤ 15 mmHg and a pulmonary vascular resistance (PVR) ≥ 3 Woods Units (WU), and post-capillary PH is defined as mPAP > 20 mmHg, PAWP ≥ 15 mmHg, and PVR can be either < 3 WU (isolated post-capillary PH) or ≥ 3 WU (combined pre- and post-capillary PH). Pulmonary arterial hypertension (PAH) falls under the pre-capillary PH profile. Dyspnea on exertion is the most common manifestation of PH, and the most common initial complain. Other symptoms and physical findings such as venous congestion, peripheral edema, signs of RV dysfunction or syncope present later in the disease course. As such, PH has to be considered in the differential diagnosis of dyspnea, especially in cases of undifferentiated or unexplained dyspnea. PAH is a chronic but progressive condition, where symptoms progress over the course of months to years. Subacute or rapidly progressive forms of PH (symptoms rapidly worsening over the course of weeks) should warrant consideration for alternative etiologies (i.e., pulmonary embolism or a different cardiopulmonary disorder as the main d...

The following question refers to Section 7.7 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.  The question is asked by St. George's University medical student and CardioNerds Intern Chelsea Tweneboah, answered first by Baylor College of Medicine Cardiology Fellow and CardioNerds Ambassador Dr. Jamal Mahar, and then by expert faculty Dr. Michelle Kittleson. Dr. Kittleson is Director of Education in Heart Failure and Transplantation, Director of Heart Failure Research, and Professor of Medicine at the Smidt Heart Institute, Cedars-Sinai. She is Deputy Editor of the Journal of Heart and Lung Transplantation, on Guideline Writing Committees for the American College of Cardiology (ACC)/American Heart Association, is the Co Editor-in-Chief for the ACC Heart Failure Self-Assessment Program, and on the Board of Directors for the Heart Failure Society of America. Her Clinician's Guide to the 2022 Heart Failure guidelines, published in the Journal of Cardiac Failure, are a must-read for everyone! The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #10 Ms. Heffpefner is a 54-year-old woman who comes to your office for a routine visit. She does report increased fatigue and dyspnea on exertion without new orthopnea or extremity edema. She was previously diagnosed with type 2 diabetes, morbid obesity, obstructive sleep apnea, and TIA. She is currently prescribed metformin 1000mg twice daily, aspirin 81mg daily, rosuvastatin 40mg nightly, and furosemide 40mg daily. In clinic, her BP is 140/85 mmHg, HR is 110/min (rhythm irregularly irregular, found to be atrial fibrillation on ECG), and BMI is 43 kg/m2. Transthoracic echo shows an LVEF of 60%, moderate LV hypertrophy, moderate LA enlargement, and grade 2 diastolic dysfunction with no significant valvulopathy. What is the best next step? A Provide reassurance B Refer for gastric bypass C Refer for atrial fibrillation ablation D Start metoprolol and apixaban Answer #10 Explanation The correct answer is D – start metoprolol and apixaban. Ms. Hefpeffner has a new diagnosis of atrial fibrillation (AF) and has a significantly elevated risk for embolic stroke based on her CHA2DS2-VASc score of 6 (hypertension, diabetes, heart failure, prior TIA, and female sex). The relationship between AF and HF is complex and they the presence of either worsens the status of the other. Managing AF in patients with HFpEF can lead to symptom improvement (Class 2a, LOR C-EO). However, large, randomized trial data are unavailable to specifically guide therapy in patients with AF and HFpEF. Generally, management of AF involves stroke prevention, rate and/or rhythm control, and lifestyle / risk-factor modification. With regards to stroke prevention, patients with chronic HF with permanent-persistent-paroxysmal AF and a CHA2DS2-VASc score of ≥2 (for men) and ≥3 (for women) should receive chronic anticoagulant therapy (Class 1, LOE A). When anticoagulation is used in chronic HF patients with AF, DOAC is recommended over warfarin in eligible patients (Class 1, LOE A). The decision for rate versus rhythm control should be individualized and reflects both patient symptoms and the likelihood of better ventricular function with sinus rhythm. For patients with HF and symptoms caused by AF, AF ablation is reasonable to improve symptoms and QOL (Class 2a,

Dr. Jonathan M. Coutinho discusses his paper, "Diagnostic Yield of ECG-gated Cardiac CT in the Acute Phase of Ischemic Stroke vs Transthoracic Echocardiography". Show references: https://n.neurology.org/content/early/2022/08/01/WNL.0000000000200995 This podcast is sponsored by argenx. Visit www.vyvgarthcp.com for more information.

Dr. Dan Ackerman talks with Dr. Jonathan Coutinho about ECG-gated cardiac CT in the acute phase of ischemic stroke vs. thransthoracic echocardiography. Read the full article in Neurology. This podcast is sponsored by argenx. Visit www.vyvgarthcp.com for more information.

Lung cancer is one of the most commonly diagnosed type of cancer and so it is fitting that we start the first of our disease-specific oncology series with this diagnosis. This week, we sit down with guest pulmonologist Dr. Greta Dahlberg to discuss how she thinks about and works up lung nodules concerning for malignancy.Lung nodules: * For discussions about incidental lung nodules and lung cancer screening, check out Episode 197 from our friends, The Curbsiders (link: https://thecurbsiders.com/podcast/197) * Nodule vs. mass:** “Micronodule” is

Dr. Arjun Ghosh, Dr. Susannah Stanway and Dr. Rebecca Dobson, co-authors of the new "BSE and BCOS Guideline for Transthoracic Echocardiographic Assessment of Adult Cancer Patients Receiving Anthracyclines and/or Trastuzumab" discuss their work. Read the Guideline here: https://www.jacc.org/doi/pdf/10.1016/j.jaccao.2021.01.011

Full article: https://www.ajronline.org/doi/abs/10.2214/AJR.20.23903  Transthoracic echocardiography (TTE) is the standard of care in cardiac imaging for patients with suspected cardioembolic stroke. In this podcast, Amber Liles, MD discusses how cardiac MRI and cardiac CT angiography perform in comparison to TTE in terms of prediction of stroke recurrence.

A 34-year-old woman is a professional triathlete. Her HR is 35, RR 12, BP 105/60. Transthoracic echocardiography shows biventricular dilatation with normal contractility and a left ventricular ejection fraction of 76%. Which of the following is likely in this patient? Concentric hypertrophy Diastolic dysfunction Dilated cardiomyopathy Eccentric hypertrophy Third-degree heart block

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. Dr Greg Hundley: And I'm Greg Hundley, associate editor, Director of the Pauley Heart Center from VCU Health in Richmond, Virginia. Well, our feature article this week, Carolyn, is really interesting and evaluates management of patients that are suspected to have atrial fibrillation and how we should screen them, what kind of monitoring and the like, very interesting discussion that will be coming up. But before we get to that, how about we start into the papers and would you like to go first? Dr Carolyn Lam: I would love to. And the first one is a basic paper on regenerative therapy, very important topic. Now remember that mammalian adult hearts have limited regenerative capacity. However, a transient regenerative capacity is maintained in the neonatal heart. So co-corresponding authors, Dr Wang and Dr Guo from Nanjing Medical University hypothesize that by analyzing systemic phosphorylation signaling in ischemic neonatal myocardium, they may unlock key pathways involved in heart regeneration. They therefore used quantitative phosphorylation proteomics to analyze the kinase substrate network of regenerative myocardium post MI in neonatal mice. And they found that activated Chk1 kinase was responsible for neonatal regeneration and could enhance cardiac regeneration in adult hearts post MI via activating the mTORC1 P70-S6K axis. Dr Greg Hundley: Wow, Carolyn. Sounds like this could have a lot of clinical application several years down the road. So what are your thoughts on that? Dr Carolyn Lam: I thought you may ask. Well, potentiation of Chk1 kinase, therefore, may be a promising regenerative therapy and authors gave this example that Chk1 injection could for example, in the form of a hydrogel, be injected into the myocardial infarction region and surrounding areas and may even be a novel therapeutic option to promote cardiac regeneration post MI. Dr Greg Hundley: Very good, Carolyn. Well, my paper comes from the PARTNER 3 trial and remember PARTNER 3 is a comparison of transcatheter versus surgical aortic-valve replacement in low risk patients. The corresponding author is Dr Philippe Pibarot from Quebec. The placement of aortic transcatheter valve three or PARTNER 3 trial randomized a thousand patients with severe aortic stenosis and low surgical risk at 71 centers to undergo either transfemoral TAVR with the balloon expandable SAPIEN 3 valve versus undergoing SAVR or surgical aortic valve replacement. Transthoracic echocardiograms were obtained at baseline and at 30 days and one-year post procedure and they were analyzed by a consortium of two echocardiography core labs. The objective of this study is to compare echocardiographic findings in low risk patients with severe aortic stenosis following surgical or transcatheter aortic valve replacement. Dr Carolyn Lam: Important topic, very hot. So what did they find? Dr Greg Hundley: In patients with severe aortic stenosis and low surgical risk, TAVR with the SAPIEN 3 valve was associated with a similar percentage of moderate to severe AR compared with SAVR, but a higher percentage of mild AR with no association between any grade of AR and outcomes. Trans-prosthetic gradients, valve areas and LV mass regression were similar in TAVR versus SAVR. And SAVR was associated with a significant deterioration of RV systolic function and greater tricuspid regurgitation, which persisted at one year. So Carolyn, very interesting results. Another study from PARTNER 3 comparing TAVR versus SAVR for patients with severe aortic stenosis. Dr Carolyn Lam: Nice. So going from PARTNER 3, I want to talk about MESA and this time focusing on coronary artery calcium. Now we know that the recent ACC/AHA primary prevention guidelines recommend considering low dose aspirin therapy only among adults who are at high atherosclerotic cardiovascular risk but not at high risk of bleeding. However, it remains unclear how these patients are best identified. So the current study aimed to assess the value of coronary artery calcium for guiding aspirin allocation in primary prevention using the 2019 aspirin meta-analysis data on cardiovascular disease relative risk reduction and bleeding risk. So corresponding author Dr Cainzos-Achirica from Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease and colleagues studied 6,470 participants from MESA all of whom underwent coronary artery calcium scoring at baseline to assess benefit versus harm. A 12% relative risk reduction in cardiovascular disease events was used for five-year number needed to treat calculations, while a 42% relative risk increase in major bleeding events was used for the five-year number needed to harm estimations. And now here are the results. Only 5% of MESA participants would qualify for aspirin consideration for primary prevention according to the ACC/AHA guidelines and using more than 20% estimated atherosclerotic cardiovascular disease risk to define higher risk. Among the 3,540 aspirin naive participants less than 70 years old and not at high risk of bleeding, the overall number needed to treat in five years with aspirin to prevent one cardiovascular disease event was 476, while the number needed to harm in five years was 355. The numbers needed to treat in five years was also greater than or similar to the numbers needed to harm among estimated ASCVD risk strata by pool cohort equations. Conversely, with a coronary artery calcium score of more than a hundred or more than 400, both these cutoffs identified subgroups in which the number needed to treat in five years was lower than the number needed to harm in five years. Also, coronary calcium score of zero identified subgroups in which the number needed to treat was much higher than the number needed to harm. Dr Greg Hundley: Lots of data. So we're mixing aspirin and MESA coronary calcium scores. What do we take home from this? Dr Carolyn Lam: So here's the take home message. Coronary artery calcium may be superior to the pool cohort equations to inform the allocation of aspirin in primary prevention. Individuals with a coronary artery calcium score above hundred and particularly above 400 may be good candidates for aspirin therapy for primary prevention. Although the net expected benefit will likely be modest. In the presence of zero coronary artery calcium, the risk of bleeding is greater than the potential benefit and aspirin therapy for primary prevention should probably be avoided. Overall, implementation of the current 2019 ACC/AHA guideline recommendations together with the use of coronary artery calcium scoring for further risk assessment may result in a more personalized, safer allocation of aspirin for primary prevention. Although ,of course, confirmation and external settings are required. Dr Greg Hundley: That was really interesting. Combining coronary calcium scores, if you happen to have it, if someone's considering primary prevention with aspirin, it looks like those calcium scores could really be helpful there. Well, I've got a couple other papers to talk about in this week's issue. There's an ECG challenge from Abdulhamied Alfaddagh from Johns Hopkins reviewing the quote unquote de Winter EKG pattern in a truck driver presenting with chest pain. Second, there's an in-depth article from Alexander Fletcher from Edinburgh in the United Kingdom who discusses the metabolic pathways involved in inherited aortopathies trying to move beyond just diameter assessments to predict risk above future dilation and rupture. And then lastly, there's a research letter from Petra Frings-Meuthen from the German Aerospace Center, the reports on how weightlessness shifts intravascular volumes and concentration of natriuretic peptides in astronauts. Dr Carolyn Lam: Huh. And I would like one on my mind by Dr Kowey and it talks about the relentless pursuit of new drugs to treat cardiac arrhythmias. Wow. What a nice issue. Let's move on now to our feature discussion. Dr Greg Hundley: Welcome everyone to our feature discussion. In this particular paper will focus on atrial fibrillation and we're delighted to have Dr Søren Diederichsen from Copenhagen presenting this work and Dr Changsheng Ma, one of our associate editors from Beijing, China to have nice discussion. Søren, I was wondering if we could get started with you. Could you tell us a little bit about what was the background related to this study and perhaps even a little bit about the hypothesis that you wanted to test? Dr Søren Diederichsen:  The background for this study is that, as we all know, atrial fibrillation is actually big and it's a growing health problem throughout the world and we also know that AF is often asymptomatic. So many cases of atrial fibrillation go undetected until complications occur. And, of course, one of the most feared complications from AFib is a disabling stroke. And there's more and more evidence growing that a large proportion of people with risk factors for stroke do have some subclinical atrial fibrillation when they investigated or when they are followed, for instance, with a pacemaker. So there has been a recent meta-analysis that found that the at risk of stroke in patients with subclinical AFib was fairly large compared to the risk of stroke in patients without subclinical AFib. So, in this study, we want to look at the subclinical AFib in patients from the general population using loop recorders to follow these patients. And we want to sort of look at how could we screen the patients to find those with subclinical AFib using different screening scenarios which are less intensive than using a loop recorder for everyone. Dr Greg Hundley: Søren, could you tell us a little bit about your study population and your study design? Dr Søren Diederichsen:  First of all, this study is part of an ongoing randomized control trial called the loop study. And in the loop study we recruited study participants from the general population. The participants had to be at least 70 years old. And besides age as a stroke risk factor, they also had to have at least one additional stroke risk factor, hypertension, diabetes, heart failure or previous stroke. And importantly, they could not have AFib. And the included participants were then randomized to control or screening for AFib using implantable loop recorder with remote monitoring and adjudication of new onset AF episodes. In this particular study, we looked at the first participants in the loop recorder group who had been monitored for the entirety of the device's battery life, which is approximately three and a half years. So for these persons, we know whether or not they actually have AFib and we know exactly when they were in AFib and when they were in sinus rhythm. So we use this data from the loop recorders to reconstruct full heart rhythm histories for each person, including exact time of onset and termination of each episode after exclusion of any clinically detected AF in the patients. And it's a bit complicated study design because we have these heart rhythm histories. Now you can imagine where we have a string of data which is approximately three and a half years long and we know exactly when is AFib present and when a sinus rhythm present in this patient. So we could use that data to simulate that the persons had been invited to an AFib screening by the health care service and had undergone a different type of screening at a random time. And these screenings that we investigated were time-point screening using standard ten second ECG during office hours and intermittent screening using single list devices, for instance, and short term continuous screening using external devices such as Holter or event recorder. So we simulated that the patients had undergone such screenings and we could also assimilate that the patients were screened several times on a monthly or annual basis such as, for instance, taking an ECG every year. And this simulation was then used to evaluate the sensitivity and negative predictive value of various screening regiments using the loop recorders' gold standard. Dr Greg Hundley: What were your study results? Dr Søren Diederichsen:  All of this data comprised, as I told you, the first participant in our trial that had been monitored for the full battery life of the device. So that was 590 participants entering nearly 700,000 days of continuous monitoring. So that was our data. And one third of those participants actually had previously unknown AFib and the number of AF episodes in our data was more than 20,000 AF episodes. The main results were that if we simulate the pseudo-random daytime ECG in those patients, we would have identified only 1.5% of those who had AFib while performing by daily 32nd ECGs during 14 days, we would have identified 8% of those with AFib. And if we took a 72-hour Holter, we would have identified 15% or a longer, for instance, a 30-day event recorder, we would have identified about a third of all those with AFib. So that was actually our main results. We were able to see how many would we have identified of those with AFib if we'd done anything from taking a daytime ECG to performing a rather long event recorder. Dr Greg Hundley: Were you able to put together maybe a combination of other variables along with the more lengthy recordings that could forecast future atrial fibrillation? Dr Søren Diederichsen: One of the things we wanted to do with this study was not only did we want to see what is actually the diagnostic performance of doing an ECG or screening patients at risk with different kinds of screening, we also want to look at specific subgroups of the population who were more likely to maybe benefit from the screening in terms of having their AFib diagnosed. So we looked at some population characteristics, age, sex and NT-proBNP. And we saw that the sensitivity of the screening was consistently higher among those who were older with a cutoff at 75 years, and also among males and among those with a high NT-proBNP. So we could see that if we had screened one of those risk factor groups, age, male sex or high NT-proBNP, we would have been more or less likely to identify if AF was actually present. Dr Greg Hundley: Changsheng, I'd like to turn to you. Can you help us put this results into perspective? How should we use this information in managing patients with atrial fibrillation? Dr Changsheng: The AI for screening is a very important clinical problem and a hot topic issue. The heart rate monitoring is a cornerstone for detecting suspected AF patients. And then emerging new technology make monitoring more convenient than before. But however the best screening strategy for those at higher risk of future AF stroke. And probably the strategy for the general population screening remain undetermined. On the contrary, they evaluated the performance of a large panel of AF screening strategy among the 600 persons with a stroke risk factor that was not known yet. The study used as an implantable loop recorder as a gold standard to assess the detection or difference in simulating a screening model. I've got to say, the method employed in this study is quite exquisite and there's a key finding our clients tried to forward. The time-point screening or the short-term monitoring could only identify a very small fraction of AFIB as compared for long-term loop recording screening. And diagnostic yield increased with duration, number and the dispersion of screenings. So this is done to provide important clinical implications that every relatively intense screening such as even now I knew 30-day monitoring would need more than four in ten with AF. And about one in six which are underlying more than 24 hours episode of AF. So the authors also gave the practical dispersion concept that when screening for AF, three times 24 hour monitoring are superior to one time 72 hour monitoring. So I think this is a very important study to understand the condition, to understand the screening of AF patient for the general population. Dr Greg Hundley: So really, helping us put these results in perspective. Maybe I'll ask each of you Søren first and then Changsheng. What do you think is the next research that needs to be performed after taking your results into account? Dr Søren Diederichsen:  In terms of what we should do next, I agree with Changsheng that there's a lot of attention towards AF screening at the moment, but we still really don't know if widespread screening in the population is actually something that could prevent heart endpoints. So the next thing we need to know is, first of all, if we screen, will we have fewer of those events or will we have more side effects from the screening such as anticoagulant-mediated bleedings? It's very important to keep in mind that we don't yet know if screening is something that would prevent heart endpoints. Second of all, we want to know more about what is actually the relationship between AF burden or amount of AF and risk of stroke. There's some evidences coming up that it's growing. Is it, for instance, from the CERT study that the amount of AF and the pattern of AF that you have might tell us a little bit about what is your risk of stroke? For instance, if you have long AF episodes, your risk of stroke is higher than if you have all the short AF episodes. And so that would be two of the next things I would think we should look at. Dr Greg Hundley: Very good. Changsheng, do you have something to add to that? Dr Changsheng: Yes, I agree with Søren. Now, on the detection, it's important but as a burden, even more important. So in practice in future, wouldn't we need more advanced technology and the patients or the participants frontally the monitoring device, which has the same ability to loop record them. But this is more easy to use because when we use frontal monitoring for the patients, the longer duration of your monitoring period. So worse complains to the patients, not as our study because we have a simulation methodology, that 100% of patient accomplishments. So I think in future, the watch with a diagnostic function of AF differentiation based on not ECG, but only based on the pulse. So, the watch diagnostic function, not by ECG that are by pulse, like a detection of pulse. And then depend on the artificial intelligence, the AI function, to make a diagnosis of atrial fibrillation, not by ECG. That would be the future. Dr Søren Diederichsen:  And if you don't mind, I would like to add to that because I think that Changsheng raises an excellent point here with the smartwatch and how could they contribute to our prevention of stroke and in society. So the current smartwatches work by looking at the pulse by photoplethysmography. And they cannot look at the pulse continuously as we do with the loop recorder looking at the ECG continuously. This like with the photoplethysmography turns on when the patient is at risk and builds up an algorithm to look at what is actually the likelihood that the patient is an AF at this moment or today. So at this point it'll only detect fairly long AF episodes, but in this study, we also looked at the longer AF episodes and the AAF burden. How does that impact the likelihood of detecting AF and of course it's more easy to detect it in patients with long AF episodes. And if we find out in the future that a larger AF burden or longer AF episodes are actually required to increase the risk of stroke, then I believe that technology such as smartwatches could be a very feasible way to screen or to detect that kind of AF in patients at risk. Dr Greg Hundley: Well listeners we've had a wonderful discussion here with Dr Søren Diederichsen from Copenhagen and our associate editor, Changsheng Ma from Beijing, China. And really reviewing some important results related to screening for atrial fibrillation and the three 24-hour monitoring sessions combined with risk factors really help us identify who may be experiencing atrial fibrillation in our patients. And then also, very interesting projections for the future, both using technology to try to identify atrial fibrillation perhaps through watches. And then also how we could incorporate the duration, the time, et cetera of atrial fibrillation occurrences and how they may relate to adverse events. Thank you so much Søren. Thank you Changsheng. And to all our listeners, we wish you a very safe week and look forward to meeting with you next week. Take care. This program is copyright the American Heart Association 2020.  

Echocardiography (Diseases of the Aorta) for the Internist-9 Dr RR Baliga's MUST KNOW FACTS PODCASTS for PHYSICIANS from chapter Echocardiography for the Internist in Baliga's Textbook of Internal Medicine with 1480 MCQs www.MasterMedFacts.com authored by Dennis A Tighe, MD, FACC, FACP, FASE Professor, University of Massachusetts Director, Cardiac Ambulatory Services, UMass Memorial Health Care & Martin St. John Sutton, MBBS, MD, FRCP Emeritus Professor, University of Pennsylvania Recipient of 2016 Lifetime Achievement Award from the American Society of Echocardiography   This podcast is not Medical Advice or Medical Opinion

Echocardiography (Pericardial Disease) for the Internist-8 Dr RR Baliga's MUST KNOW FACTS PODCASTS for PHYSICIANS from chapter Echocardiography for the Internist in Baliga's Textbook of Internal Medicine with 1480 MCQs www.MasterMedFacts.com authored by Dennis A Tighe, MD, FACC, FACP, FASE Professor, University of Massachusetts Director, Cardiac Ambulatory Services, UMass Memorial Health Care & Martin St. John Sutton, MBBS, MD, FRCP Emeritus Professor, University of Pennsylvania Recipient of 2016 Lifetime Achievement Award from the American Society of Echocardiography   This podcast is not Medical Advice or Medical Opinion

Echocardiography (Cardiomyopathy) for the Internist-7 Dr RR Baliga's MUST KNOW FACTS PODCASTS for PHYSICIANS from chapter Echocardiography for the Internist in Baliga's Textbook of Internal Medicine with 1480 MCQs www.MasterMedFacts.com authored by Dennis A Tighe, MD, FACC, FACP, FASE Professor, University of Massachusetts Director, Cardiac Ambulatory Services, UMass Memorial Health Care & Martin St. John Sutton, MBBS, MD, FRCP Emeritus Professor, University of Pennsylvania Recipient of 2016 Lifetime Achievement Award from the American Society of Echocardiography   This podcast is not Medical Advice or Medical Opinion

Echocardiography (TTE) for the Internist -2 + MCQ Dr RR Baliga's MUST KNOW FACTS PODCASTS for PHYSICIANS from chapter Echocardiography for the Internist in Baliga's Textbook of Internal Medicine with 1480 MCQs www.MasterMedFacts.com authored by Dennis A Tighe, MD, FACC, FACP, FASE Professor, University of Massachusetts Director, Cardiac Ambulatory Services, UMass Memorial Health Care & Martin St. John Sutton, MBBS, MD, FRCP Emeritus Professor, University of Pennsylvania Recipient of 2016 Lifetime Achievement Award from the American Society of Echocardiography   This podcast is not Medical Advice or Medical Opinion

Echocardiography (Endocarditis) for the Internist-6 Dr RR Baliga's MUST KNOW FACTS PODCASTS for PHYSICIANS from chapter Echocardiography for the Internist in Baliga's Textbook of Internal Medicine with 1480 MCQs www.MasterMedFacts.com authored by Dennis A Tighe, MD, FACC, FACP, FASE Professor, University of Massachusetts Director, Cardiac Ambulatory Services, UMass Memorial Health Care & Martin St. John Sutton, MBBS, MD, FRCP Emeritus Professor, University of Pennsylvania Recipient of 2016 Lifetime Achievement Award from the American Society of Echocardiography   This podcast is not Medical Advice or Medical Opinion

Echocardiography (Assessment of Heart Valve) for the Internist-5 + MCQ Dr RR Baliga's MUST KNOW FACTS PODCASTS for PHYSICIANS from chapter Echocardiography for the Internist in Baliga's Textbook of Internal Medicine with 1480 MCQs www.MasterMedFacts.com authored by Dennis A Tighe, MD, FACC, FACP, FASE Professor, University of Massachusetts Director, Cardiac Ambulatory Services, UMass Memorial Health Care & Martin St. John Sutton, MBBS, MD, FRCP Emeritus Professor, University of Pennsylvania Recipient of 2016 Lifetime Achievement Award from the American Society of Echocardiography   This podcast is not Medical Advice or Medical Opinion

Echocardiography (Assessment of LV) for the Internist-4 + MCQ Dr RR Baliga's MUST KNOW FACTS PODCASTS for PHYSICIANS from chapter Echocardiography for the Internist in Baliga's Textbook of Internal Medicine with 1480 MCQs www.MasterMedFacts.com authored by Dennis A Tighe, MD, FACC, FACP, FASE Professor, University of Massachusetts Director, Cardiac Ambulatory Services, UMass Memorial Health Care & Martin St. John Sutton, MBBS, MD, FRCP Emeritus Professor, University of Pennsylvania Recipient of 2016 Lifetime Achievement Award from the American Society of Echocardiography   This podcast is not Medical Advice or Medical Opinion

Echocardiography (TEE) for the Internist -3 + MCQ Dr RR Baliga's MUST KNOW FACTS PODCASTS for PHYSICIANS from chapter Echocardiography for the Internist in Baliga's Textbook of Internal Medicine with 1480 MCQs www.MasterMedFacts.com authored by Dennis A Tighe, MD, FACC, FACP, FASE Professor, University of Massachusetts Director, Cardiac Ambulatory Services, UMass Memorial Health Care & Martin St. John Sutton, MBBS, MD, FRCP Emeritus Professor, University of Pennsylvania Recipient of 2016 Lifetime Achievement Award from the American Society of Echocardiography   This podcast is not Medical Advice or Medical Opinion

This week we review a work that aimed to improve the thoughtfulness of echocardiography usage in the postoperative period after congenital heart surgery. Dr. Kelly Cox and colleagues report on the use of a 'checklist' type 'pause' aimed at making certain that the ordering team in the CVICU are making an informed decision regarding the need for a new echocardiogram. How often should postoperative studies be performed? How often did the 'fluid check' actually show fluid? These are amongst the many questions we post to Professor Cox who presently works at Lurie Children's Hospital - Northwestern University. doi: 10.1111/echo.1450

This week we review a work that aimed to improve the thoughtfulness of echocardiography usage in the postoperative period after congenital heart surgery. Dr. Kelly Cox and colleagues report on the use of a 'checklist' type 'pause' aimed at making certain that the ordering team in the CVICU are making an informed decision regarding the need for a new echocardiogram. How often should postoperative studies be performed? How often did the 'fluid check' actually show fluid? These are amongst the many questions we post to Professor Cox who presently works at Lurie Children's Hospital - Northwestern University. doi: 10.1111/echo.1450

(*Hypothetical patient) You are called to review a woman who recently arrived in your hospital and is now a few hours postpartum after a pre-term vaginal delivery at 35 weeks. She tells you that she has felt unwell for the last few days with a little bit of vomiting, diarrhoea and her asthma has been playing up and needing quite a few puffs of her ventolin. She went into preterm labour and delivered quickly 2-3 hours ago. She has received 3-4 litres of crystalloid to treat her "dehydration" and the at times non reassuring CTG over the last 24hours. She isn't febrile, but is tachycardic at 115/min, hypotensive 95/45 and she looks a little short of breath with Sp02 92% on room air and a respiratory rate of 20/min. She can talk in sentences and is walking around her room so you are reassured by this. After taking a history and examining her you decide to have a quick look at her heart and lungs with your USS machine (you have recently completed a point of care ultrasound course so are always looking for an opportunity to put your new skills into practice). To your surprise you discover the apices of both her lungs have a large number of B-lines and then when you throw the probe on her heart and inferior vena cava within a couple of minutes you see she has a large poorly contracting left ventricle and a dilated IVC. You reach over and turn off her iv fluids - this woman doesn't need anymore rehydration! Hi everyone, This week Parvesh and I follow up on our earlier podcast discussing the utility of point of care lung ultrasound with a discussion about the merits of point of care echocardiography. Join us and as we discuss the pros / cons, share some anecdotes and talk about where we are on our journey learning this incredibly useful new technique. B-Lines on Pulmonary Ultrasound = interstitial fluid Mitral Stenosis Links https://www.obsgynaecritcare.org/lung-ultrasound-a-discussion-with-dr-parvesh-verma/ 1. Focused transthoracic echocardiography in obstetrics. Griffiths, S.E. et al. BJA Education , Volume 18 , Issue 9 , 271 - 276 2. Transthoracic echocardiography in the perioperative setting. Jørgensen, Martin Ruben Skoua; Juhl-Olsen, Petera; Frederiksen, Christian Alcarazb; Sloth, Erika Current Opinion in Anaesthesiology: February 2016 - Volume 29 - Issue 1 - p 46–54 These articles are not free open access - they are available through most university / hospital libraries or your medical college (eg ANZCA).

This week we review a recent report from the team at the Kravis Children's Hospital at Mount Sinai - Icahn School of Medicine at Mount Sinai on the use of pentobarbital for oral sedation for transthoracic echocardiography. Associate Professor of Pediatrics Rajesh Shenoy shares with us insights into sedation for this indication, the general approach of the echo lab at Sinai and how decisions are made regarding sedation for this reason. doi: 10.1111/echo.14301

This week we review a recent report from the team at the Kravis Children's Hospital at Mount Sinai - Icahn School of Medicine at Mount Sinai on the use of pentobarbital for oral sedation for transthoracic echocardiography. Associate Professor of Pediatrics Rajesh Shenoy shares with us insights into sedation for this indication, the general approach of the echo lab at Sinai and how decisions are made regarding sedation for this reason. doi: 10.1111/echo.14301

Dr Paul Wang:                   Welcome to the monthly podcast, On the Beat for Circulation: Arrhythmia and Electrophysiology. I'm Dr Paul Wang, Editor-in-Chief, with some of the key highlights from this month's issue. In our first paper this month, Shaan Khurshid and associates determine the frequency of rhythm abnormalities in 502,627 adults in the UK Biobank, a national prospective cohort. They found that 2.35% had a baseline rhythm abnormality. The prevalence increased with age, with 4.84% of individuals aged 65 to 73 years having rhythm abnormalities. During over three million person- years of follow up, nearly 16,000 new rhythm abnormalities were detected. Atrial fibrillation was the most frequent with three per thousand person-years. Bradyarrhythmia with almost one per thousand person-years. Conduction system disease is about one per one thousand years. Supraventricular and ventricular arrhythmias, each about one half per one thousand person-years. Older age was associated with a hazard ratio of 2.35 for each 10 year increase. Male sex, hypertension, chronic kidney disease and heart failure were all associated with new rhythm abnormalities. In our next paper, Fabien Squara and associates evaluated a method of determining the septal or free wall positioning of pacemaker or ICD leads during fluoroscopy. They compared in 50 patients a classical approach using posterior anterior, right anterior oblique 30 degrees, and left anterior oblique 40 degrees fluoroscopic imaging’s to 50 patients undergoing an individualized left anterior oblique or LAO approach. This individualized LAO approach view provided a true view of the interventricular septum. This angle was defined by the degree of LAO that allowed the perfect superimposition of the RV apex, using the tip of the right ventricular lead, temporarily placed at the apex, and one of the superior vena cava, inferior vena cava access using a guide wire. Transthoracic echo was used to confirm position of the right ventricular lead. Septal, or free wall, right ventricular lead positioning was correctly identified in 96% of patients in the individualized group, versus 76% in the classical group. P equals 0.004. For septal lead positioning fluoroscopy had 100% sensitivity, and an 89.5 specificity in an individualized group, versus 91.4% sensitivity, and a 40% specificity in the classical group. In our next paper, Elsayed Soliman and associates examined the lifetime risk of atrial fibrillation based on race and socioeconomic status. In the atherosclerosis risk in communities, ARIC, cohort, of 15,343 participants without atrial fibrillation, patients were recruited in 1987 to 1989, when they were 45 to 64 years of age, and followed through 2014. The authors identify 2,760 atrial fibrillation cases during a mean follow up of 21 years. The authors found that the lifetime risk of atrial fibrillation in the ARIC cohort was approximately one in three among whites, and one in five among African Americans. And, the socioeconomic status was inversely associated with cumulative incidents of atrial fibrillation before the last decades of life. In our next paper, Jonathan Steinberg and associates sought to determine the impact of atrial fibrillation episode duration threshold on atrial fibrillation incidents and burden in pacemaker patients in a prospective registry. In 615 pacemaker patients was device detected atrial fibrillation over a mean follow up of 3.7 years, 599 had one or more atrial fibrillation episodes of 30 seconds duration, with a mean number of 22 episodes. At 12 months, freedom from atrial fibrillation ranged from 25.5% to 73.1%, based on a duration threshold from 30 seconds up to 24 hours. Of patients with a first episode of 30 seconds to two minutes, 35.8% were free from subsequent episodes greater than two minutes at 180 days. The mean atrial fibrillation burden of 0.2% for patients with first episodes between 30 seconds and 3.8 hours, was significantly less than the 9.5% burden for those with greater than 3.8 hours. The authors concluded that small differences in atrial fibrillation episode duration definition can significantly affect the perceived incidents of atrial fibrillation impact reported outcomes, including atrial fibrillation success. An initial atrial fibrillation episode of 30 seconds does not predict clinically meaningful atrial fibrillation burden. In the next paper, Hongwu Chen and Linsheng Shi and associates examined the distinct electrophysiologic features of bundle branch reentrant ventricular tachycardia in patients without structural heart disease. They described nine patients, mean age 29.6 years, with normal left ventricular function and bundle branch reentrant ventricular tachycardia, with a right bundle branch block pattern in one patient, and left bundle branch block patterns in nine patients. In all left bundle branch block pattern ventricular tachycardia, the mean ventricular tachycardia cycling was 329.3 milliseconds, and the median HV interval during tachycardia was longer than that of baseline, 78 versus 71 milliseconds. The H to right bundle interval during ventricular tachycardia was slightly shorter, however, the right bundle to ventricular interval was markedly longer than that during sinus rhythm, 50 versus 30 milliseconds. In six patients with three dimensional mapping of the left ventricle, a slow anterograde, or retrograde conduction over the left His-Purkinje system with normal myocardial voltage was identified. In addition, Purkinje related ventricular tachycardias were also induced in five patients. Ablation was applied to the distal left bundle branch block in patients with baseline left bundle branch block, and in one narrow QRS patient with sustained Purkinje related ventricular tachycardia, while right bundle branch was targeted in other patients. During a mean follow up at 31.4 months, frequent premature ventricular contractions occurred in one patient, and new ventricular tachycardia developed in the other patient. In the next paper, Michel Haissaguerre and associates examined detailed mapping in 24 patients who survived idiopathic ventricular fibrillation. They used multi-electrode body surface recordings to identify the drivers maintaining ventricular fibrillation, and analyze electrograms in the driver regions, using endocardial and epicardial catheter mapping during sinus rhythm. Ventricular fibrillation occurred spontaneous in three patients, and was induced in 16, while VF was non-inducible in five. Ventricular fibrillation mapping demonstrated reentrant and focal activities, 87% and 13% respectively. The activities were dominant in one ventricle in nine patients, while they were biventricular in the others. During sinus rhythm, areas of abnormal electrograms were identified in 15 out of 24 patients, or 62.5%, revealing localized structural alterations, in the right ventricle in 11, the left ventricle in one, in both in three. They covered a limited surface, 13 centimeters squared, representing 5% of the total surface, and recorded predominantly on the epicardium. 76% of these areas were co-located with ventricular fibrillation drivers. In nine patients without structural alterations, the authors observed a high incidence of Purkinje triggers, seven out of nine, versus four out of 15. Catheter ablation resulted in arrhythmia-free outcomes in 15 out of 18 patients at a 17 month follow up. In our next paper, David Spar and associates describe the effectiveness, safety, and compliance of the wearable cardioverter defibrillator in the identification and treatment of life-threatening ventricular arrhythmias in all US pediatric patients who wore a wearable defibrillator from 2009 to 2016, ages less than 18 years. The 455 patients had a median age of 15 years, median duration of wearable cardioverter defibrillator use of 33 days, and median patient wear time of 20.6 hours per day. The study population was divided into two groups, 63 patients with an ICD problem, or 392 patients without an ICD problem. The wear time was greater than 20 hours in both groups. There were seven deaths, or 1.5%. All patients were not wearing the wearable cardioverter defibrillator at the time of death. Eight patients, 1.8%, received at least one wearable cardioverter defibrillator shock treatment. Of the six patients who had appropriate therapy, there were seven episodes of either polymorphic ventricular tachycardia, or ventricular fibrillation, with a total of 13 treatments delivered. All episodes were successfully converted, and the patient survived. In our next paper, Marc Lemoine and associates used human-induced pluripotential stem cell-derived cardiomyocytes to examine differences in repolarization reserve. The authors compared the contribution of IKs and IKr on action potential durations in human left ventricular tissue, and the human induced pluripotential stem cell derived cardiomyocytes, or IPS-derived engineered heart tissue. They found that the IPS-derived heart tissue showed spontaneous diastolic depolarization in action potential duration, which were sensitive to low concentrations of Ivabradine. IKr block by E-4031 prolonged action potential duration 90 with similar EC50 in both the IPS-derived heart tissue and the human left ventricular tissue. But a larger effect size in the IPS-derived heart tissue, 281 milliseconds versus 110 milliseconds, in the human left ventricular tissue. While IKr block alone evoked early after depolarizations, it triggered activity in 50% of the IPS-derived heart tissue. Slow pacing reduced extracellular potassium blocking of IKr, IKs and IK1 were necessary to induce early after depolarizations in human left ventricular tissue. In accordance with their clinical safety, Moxifloxacin and Verapamil did not induce EADs in IPS-derived heart tissue. In both IPS-derived heart tissue and human left ventricular tissue, IKs block by HMR 1556 prolonged action potential duration 90 slightly in the combined presence of E-4031 and isoprenaline. In our next paper, Elizabeth Saarel and associates sought to obtain contemporary digital ECG measurements in healthy children from North America to evaluate the effects of sex and race, and to compare the results to commonly published data sets, using 2400 digital ECGs, collected for children less than 18 years of age with normal electrocardiograms at 19 centers in the pediatric heart network. The authors found that the QTc in lead II was greater for females compared to males for age groups three years or older, for whites compared to African Americans, for ages 12 years or older. The R wave amplitude in V6 was greater for males compared to females for age groups 12 years and greater; for African Americans compared to white or other race categories for age groups three years or greater; and greater compared to commonly used public data set groups for ages 12 years and greater. In our next paper, Pyotr Platonov and associates examined T-wave morphology as a possible predictor of cardiac events in patients with type 2 long QT syndrome mutation carriers with normal QTc intervals. The authors compared 154 LQT2 mutation carriers with QTc less than 360 milliseconds in men, and less than 470 milliseconds in women, with 1007 unaffected family members. Flat, notched, or negative T-waves in leads II or V5 on baseline ECG were considered abnormal. Using Cox regression analysis, the associations between T-wave morphology, the presence in mutations in the poor region of KCNH2, and the risk of cardiac events defined that syncope aborted cardiac arrest, defibrillator therapy, or sudden cardiac arrests were assessed. The authors found that LQT2 female carriers with abnormal T-wave morphology had a threefold increased risk of cardiac events compared to LQT2 female carriers with normal T-waves, while this association was not seen in males. LQT2 males with poor location of mutations had a six-fold increased risk of cardiac events than non-poor location males, while no such association was found in females. In our last paper, Yaniv Bar-Cohen and associates describe a percutaneous pacemaker entirely implanted in the pericardium, using a sheath for sub-xiphoid access to the pericardial space, and a miniaturized camera with fiber optic illumination, the micro-pacemakers were successfully implanted in six pigs. All animals were studied during follow up, survived without symptoms. That's it for this month. We hope that you'll find the Journal to be the go-to place for everyone interested in the field. See you next time!  

Commentary by Dr. Valentin Fuster

Commentary by Dr. Valentin Fuster

Audio Journal of Cardiovascular Medicine Transthoracic Echo: A Wasted Test in Stroke Patients? REFERENCE: Poster 434 NICOLE PAGEAU, Trillium Health Centre, Ontario Stroke patients may be going through pointless tests, according to a poster presented by researchers at the Trillium Health Centre in Ottawa. The Stroke clinic there looked at whether routinely ordered tests, trans thoracic echo and 24 hour rhythm monitoring, actually changed patients' treatment, and found that generally, the results of these tests didn’t change a thing. Helen Morant talked to Nicole Pageau about their findings.