Podcasts about Cardiomyopathy

THE LANCET 2003;362:772-776Background: Angiotensin converting enzyme inhibitors (ACEi) reduce mortality and morbidity in patients with systolic heart failure (see CONSENSUS and SOLVD trials). However, registry data showed that up to 20% of patients with systolic heart failure were not taking ACEi. One of the frequent causes for intolerance to ACEi is cough. Angiotensin converting enzyme inhibitors work by blocking the conversion of angiotensin I to angiotensin II, a key step in the renin–angiotensin–aldosterone system (RAAS). Angiotensin II receptor blockers were tolerated in patients with systolic heart failure who were intolerant to ACEi. However, data on long term effectives as an alternative to ACEi were lacking.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber.The Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity (CHARM)-Alternative trial sough to assess if the angiotensin-receptor blocker (ARB) candesartan, could improve outcomes in patients with systolic heart failure who are intolerant to ACEi.Patients: Eligible patients had left ventricular ejection fraction of 40% or less and NYHA class II, III or IV symptoms of at least 4 weeks duration. Patients had also to be intolerant to ACEi.Exclusion criteria were not provided in the main manuscript.Baseline characteristics: Patients were recruited from 618 centers in 26 countries. The trial randomized 2,028 patients – 1,013 randomized to receive candesartan and 1,015 to receive placebo.The average age of patients was 67 years and 68% were men. The average left ventricular ejection fraction was 30%. Cardiomyopathy was ischemic in 68% of the patients. The NYHA class was II in 48% of the patients, III in 49% and IV in 4%.Approximately 50% had hypertension, 27% had diabetes, 61% had prior myocardial infarction, 9% had stroke, 25% had atrial fibrillation and 14% were current smokers.At the time of enrollment, 85% were taking a diuretic, 46% were taking digoxin, 55% were taking beta-blockers and 24% were taking spironolactone.The most common reasons for ACEi intolerance were cough in 72% of the patients, hypotension in 13%, renal dysfunction in 12% and angioedema or anaphylaxis in 4%.Procedures: The trial was double-blinded. Patients were assigned in a 1:1 ratio to receive candesartan starting at 4 or 8mg once daily or placebo. The treatment was doubled every two weeks to a target dose of 32mg once daily.After randomization, follow up occurred at 2, 4, and 6 weeks, 6 months and every 4 months thereafter.Endpoints: The primary outcome was a composite of cardiovascular death or heart failure hospitalizations. All deaths were classified as cardiovascular unless there was a clear non-cardiac cause.Analysis was performed based on the intention-to-treat principle. The estimated sample size to have 80% power at 5% alpha was 2,000 patients. The sample size calculation assumed 18% relative risk reduction in the primary outcome with candesartan assuming a 15% annual event rate in the placebo arm.Results: The median follow up time was 34 months. The mean candesartan daily dose was 23mg at 6 months.Candesartan reduced the primary endpoint of cardiovascular death or heart failure hospitalizations (33.0% vs 40.0%, adjusted HR: 0.70, 95% CI: 0.60 – 0.81; p< 0.001). Candesartan reduced the individual components of the primary outcome - (21.6% vs 24.8%; p= 0.02) for cardiovascular death and (20.4% vs 28.2%; p< 0.001) for heart failure hospitalizations. All-cause death was also lower with candesartan (26.2% vs 29.2%, adjusted HR: 0.83, 95% CI: 0.70–0.99; p= 0.033). The number of patients who had any hospitalization as well as the total number of hospitalizations were numerically but not statistically significantly lower with candesartan (60.2% with candesartan vs 63.3%; p= 0.16) and (1,718 vs 1,835; p= 0.06).Candesartan was associated with more hypotension (3.7% vs 0.9%), more increase in creatinine (6.1% vs 2.7%) and more hyperkalemia (1.9% vs 0.3%). Angioedema occurred in three patients in the candesartan group and none in the placebo group. Cough occurred in two patients taking candesartan and four taking placebo.Authors reported no significant subgroup interactions, however, a corresponding graph was not provided.Conclusion: In patients with systolic heart failure who are intolerant to ACEi, candesartan reduced the primary composite outcome of cardiovascular death or heart failure hospitalizations with a number needed to treat of approximately of 14 patients over 34 months of follow up. Candesartan also reduced all-cause death with a number needed to treat of approximately 33 patients. Adverse events including hypotension, increase in creatinine and hyperkalemia were more common with candesartan.The reduction in the primary endpoint with candesartan was significant and offers an alternative for patients who are unable to tolerate ACEi. Of note, 72% of the patients enrolled in the trial were intolerant to ACEi due to cough. This trial did not include a head-to-head comparison between ARBs and ACEi, and therefore does not address which agent should be preferred as first-line therapy. Only 24% of participants were receiving spironolactone. The combination of ARBs with spironolactone, may increase the risk of adverse events, particularly hyperkalemia and kidney injury.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber. Get full access to Cardiology Trial's Substack at cardiologytrials.substack.com/subscribe

Send us a textFrom a family vacation that turned tragic to the creation of Pakistan's first specialized children's heart hospital, Ana Tanveer Abdullah's journey illustrates how profound loss can spark transformative change.When Ana's athletic, academically gifted brother Daniel collapsed unexpectedly at age 15, no one suspected a heart condition. Despite receiving a pacemaker after being diagnosed with cardiomyopathy, Danial passed away at 16 while awaiting a heart transplant in India. This devastating loss became the catalyst for an extraordinary mission.Together with her father and Farhan Ahmad (who also lost a child to congenital heart disease), Ana founded the Pakistan Children's Heart Foundation with an ambitious vision: to build the country's first specialized cardiac hospital for children. Through innovative fundraising campaigns inspired by Danial's athletic spirit and tireless advocacy, they've now achieved what once seemed impossible.The Children's Heart Hospital opens in Lahore this April, eliminating the need for Pakistani families to seek expensive treatment abroad. Beyond the physical facility, their "Project by Danial" trains young cardiologists and surgeons specifically in pediatric cardiac care, ensuring sustainable healthcare improvements throughout the country.Ana's story reminds us of the remarkable resilience of the human spirit. "We are trying to find peace in this world," she reflects. "He had already found his peace." Through their foundation's life-saving work, Danial's legacy touches countless families across Pakistan, transforming one family's grief into hope for an entire nation.Join our community and discover how you can support organizations like the Pakistan Children's Heart Foundation that are changing the landscape of pediatric cardiac care worldwide.Link to Global Cardiac Alliance: https://cardiac-alliance.org/Link to the Heart to Heart with Anna episode featuring Farhan Ahmad: https://www.buzzsprout.com/62761/398968-a-miracle-in-pakistanPakistan Children's Heart Foundation (PCHF): https://pchf.org.pk/Project Danial: https://pchf.org.pk/cause/project-danial/Support the showAnna's Buzzsprout Affiliate LinkBaby Blue Sound CollectiveSocial Media Pages:Apple PodcastsFacebookInstagramMeWeTwitterYouTubeWebsite

THE LANCET 2003;362:767-771Background: Angiotensin II which plays a role in ventricular remodeling and progression of heart failure can be produced by pathways independent of angiotensin convening enzyme. Preliminary studies showed that the combination of angiotensin II blockers with angiotensin-converting enzyme inhibitors (ACEi) improves hemodynamics and reduces ventricular remodeling.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber.The Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity (CHARM)-Added trial sough to assess if adding the angiotensin-receptor blocker (ARB), candesartan, to ACEi could improve outcomes in patients with systolic heart failure.Patients: Eligible patients had left ventricular ejection fraction of 40% or less within the previous 6 months, and NYHA class II, III or IV symptoms. Patients with NYHA class II symptoms had to have cardiac-related hospitalization within 6 months. Patients also had to have treatment with ACEi at a constant dose for at least 30 days.Exclusion criteria were not provided in the main manuscript.Baseline characteristics: Patients were recruited from 618 centers in 26 countries. The trial randomized 2,548 patients – 1,276 randomized to receive candesartan and 1,272 to receive placebo.The average age of patients was 64 years and 79% were men. The average left ventricular ejection fraction was 28%. Cardiomyopathy was ischemic in 62% of the patients. The NYHA class was II in 24% of the patients, III in 73% and IV in 3%.Approximately 48% had hypertension, 30% had diabetes, 56% had prior myocardial infarction, 9% had stroke, 27% had atrial fibrillation and 17% were current smokers.At the time of enrollment, 90% were taking a diuretic, 58% were taking digoxin, 55% were taking beta-blockers, 17% were taking spironolactone and all but two patients were taking ACEi.Procedures: The trial was double-blinded. Patients were assigned in a 1:1 ratio to receive candesartan starting at 4 or 8mg once daily or placebo. The treatment was doubled every two weeks to a target dose of 32mg once daily.After randomization, follow up occurred at 2, 4, and 6 weeks, 6 months and every 4 months thereafter.Endpoints: The primary outcome was a composite of cardiovascular death or heart failure hospitalizations. All deaths were classified as cardiovascular unless there was a clear non-cardiac cause.Analysis was performed based on the intention-to-treat principle. The estimated sample size to have 80% power at 5% alpha was 2,300 patients. The sample size calculation assumed 16% relative risk reduction in the primary outcome with candesartan assuming an 18% annual event rate in the placebo arm.Results: The median follow up time was 41 months. The mean candesartan daily dose was 24mg at 6 months.Candesartan reduced the primary endpoint of cardiovascular death or heart failure hospitalizations (37.9% vs 42.3%, adjusted HR: 0.85, 95% CI: 0.75 – 0.96; p= 0.01). Candesartan reduced the individual components of the primary outcome - (23.7% vs 27.3%; p= 0.021) for cardiovascular death and (24.2% vs 28.0%; p= 0.018) for heart failure hospitalizations. There was no significant reduction in all-cause death (29.5% with candesartan vs 32.4%; p= 0.105). The number of patients who had any hospitalization was similar in both groups (66.8% with candesartan vs 67.5%; p= 0.7), however, the total number of hospitalizations was lower with candesartan (2,462 vs 2,798; p= 0.023).Serum creatinine at least doubled in 7% of the patients in the candesartan group vs 6% in the placebo group. In the subset of patients taking spironolactone, serum creatinine at least double in 11% of the patients taking candesartan compared to 4% of the patients taking placebo.Hyperkalemia, defined as serum potassium of 6 mmol/L or higher, occurred in 3% of the patients in the candesartan group vs 1% in the placebo group. In the subset of patients taking spironolactone, hyperkalemia occurred in 4% of the patients taking candesartan compared to 1% of the patients taking placebo.There were two cases of angioedema in the candesartan group and three in the placebo group. All patients were taking an ACEi.There were no significant subgroup interactions, including in patients taking both beta-blockers and ACEi at baseline.Conclusion: In patients with systolic heart failure, adding candesartan to an ACEi reduced the primary composite outcome of cardiovascular death or heart failure hospitalizations with a number needed to treat of approximately of 23 patients over 41 months of follow up. The total number of all-cause hospitalizations was reduced by 336 with candesartan. All-cause death was not significantly reduced with candesartan.While the results of the trial appear impressive, the high number of adverse outcomes with candesartan in patients taking spironolactone is concerning. Spironolactone led to significant reduction in all-cause mortality in patients with systolic heart failure, as seen in the RALES trial, and should be prioritized over adding candesartan. Notably, fewer than 20% of patients in the trial were on spironolactone at baseline; if more had been, the incremental benefit of candesartan would likely have been reduced due to an increased risk of adverse effects from triple neurohormonal blockade (ACEi, ARBs, and mineralocorticoid receptor antagonists). Furthermore, spironolactone acts by blocking the aldosterone receptor, which is downstream in the renin–angiotensin–aldosterone system. Since candesartan blocks angiotensin II upstream in the same pathway, simultaneous inhibition at multiple points may lead to diminishing benefit.Finally, the differences observed in the subgroup of patients on beta-blockers between this trial and Val-HeFT remain unclear and may simply reflect the play of chance. As we previously discussed, patients receiving both an ACEi and beta-blockers had worse outcomes with valsartan in the Val-HeFT trial.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber. Get full access to Cardiology Trial's Substack at cardiologytrials.substack.com/subscribe

N Engl J Med 2001;345:1667-1675Background: Angiotensin II is a peptide hormone that is part of the renin–angiotensin–aldosterone system (RAAS). Angiotensin II is a potent vasoconstrictor and growth-stimulating hormone. Data suggested that it plays a role in ventricular remodeling and progression of heart failure. Although treatment with angiotensin-converting enzyme inhibitors (ACEi) reduce angiotensin II levels, physiologically active levels of angiotensin II may persist despite long-term therapy.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber.The Valsartan Heart Failure Trial (Val-HeFT) sough to assess whether the angiotensin-receptor blocker valsartan, could reduce mortality and morbidity when added to optimal medical therapy in patients with systolic heart failure.Patients: Eligible patients had left ventricular ejection fraction less than 40% and left ventricular dilation, in addition to having clinical heart failure for at least 3 months with NYHA class II, III or IV symptoms. Patient also had to have been receiving a fixed-dose drug regimen for at least two weeks, that could include ACEi, diuretics, digoxin, and beta-blockers.There were many exclusion criteria. We mention some here: Postpartum cardiomyopathy, acute myocardial infarction within 3 months, coronary artery disease likely to require intervention, serum creatinine >2.5 mg/dL and life expectancy less than 5 years.Baseline characteristics: Patients were recruited from 302 centers in 16 countries. The trial randomized 5,010 patients – 2,511 randomized to receive valsartan and 2,499 to receive placebo.The average age of patients was 63 years and 80% were men. The average left ventricular ejection fraction was 27%. Cardiomyopathy was ischemic in 57% of the patients. The NYHA class was II in 62% of the patients, III in 36% of the patients and IV in 2%.Approximately 26% had diabetes and 12% had atrial fibrillation.At the time of enrollment, 86% were taking a diuretic, 67% were taking digoxin, 35% were taking beta-blockers, and 93% were taking ACEi.Procedures: The trial was double-blinded. The trial had an initial run-in period for 2 - 4 weeks where patients received placebo twice daily. This was performed to confirm patients' eligibility, clinical stability and compliance.Patients were assigned in a 1:1 ratio to receive valsartan or placebo. Randomization was stratified according to whether or not they were receiving a beta-blocker.Valsartan was started at a dose of 40 mg twice a day, and the dose was doubled every two weeks to the target dose of 160 mg twice a day. Placebo doses were adjusted in a similar way.Follow up occurred at 2, 4, and 6 months and every 3 months thereafter.Endpoints: The trial had two primary end points. The first was all-cause mortality. The second was the combined end point of mortality and morbidity, which was defined as cardiac arrest with resuscitation, hospitalization for heart failure, or administration of intravenous inotropic or vasodilator drugs for four hours or more without hospitalization.The estimated sample size was 5,000 patients. The sample size calculation assumed 20% relative risk reduction in mortality with valsartan assuming 906 patients would die during the trial. This sample size would provide the trial 90% power at 0.02 alpha. Alpha was 0.02 instead of the traditional 0.05 since the trial had two primary endpoints and to adjust for the interim analyses.Results: The target valsartan dose of 160 mg twice a day was achieved in 84% of the patients. The reduction in systolic blood pressure was greater with valsartan vs placebo – mean of 5.2 ± 15.8 mm with valsartan compared to 1.2 ± 14.8 mm Hg with placebo, at 4 months.All-cause mortality was not different between both groups (19.7% with valsartan vs 19.4% with placebo, RR: 1.02, 95% CI: 0.88 – 1.18; p= 0.80). The second co-primary endpoint was reduced with valsartan (28.8% vs 32.1%, RR: 0.87, 95% CI: 0.77 – 0.97; p= 0.009). This was driven by reduction in hospitalizations for heart failure (13.8% vs 18.2%). Cardiac arrest with resuscitation was 0.6% with valsartan and 1.0% with placebo. All-cause hospitalization was numerically lower with valsartan, however, this was not statistically significance (2,856 vs 3,106; p= 0.14). The mean change in ejection fraction was higher with valsartan (4.0% vs 3.2%; p= 0.001). More patients had improvement in NYHA classification with valsartan (23.1% vs 20.7%; p

Felycin-CA1 [fel-i-sin C-A-1], or sirolimus [si-ro·-li-​mus] delayed release tablets, recently received conditional approval for…

Felycin-CA1 [fel-i-sin C-A-1], or sirolimus [si-ro·-li-​mus] delayed release tablets, recently received conditional approval for the management of ventricular hypertrophy [high-PER-trō-fee] in cats with subclinical hypertrophic cardiomyopathy, or HCM. Cardiomyopathy is...

Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances, discusses a recently published original research paper on Cardiomyopathy Prevalence and Pregnancy-Related Mortality: United States, 2010 to 2020.

Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances, discusses a recently published original research paper on Very Long-Term Outcomes of Cardiac Resynchronization Therapy in Patients With Ischemic and Nonischemic Cardiomyopathy.

Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances, discusses a recently published original research paper on MYH7 Mutations in Restrictive Cardiomyopathy.

Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances, discusses a recently published original research paper on Investigating the Anrep Effect in Hypertrophic Obstructive Cardiomyopathy With Invasive Pressure-Volume Analysis.

Circulation 1999;100:2312-2318Background: The CONSENSUS and SOLVD trials established the effectiveness of angiotensin converting enzyme inhibitors (ACEi) in reducing mortality and morbidity in patients with systolic heart failure. Both trials used enalapril with a target dose of 20mg twice a day (max dose) in the CONSENSUS trial and 10mg twice a day (medium dose) in the SOLVD trials. In real-world settings, ACEi are sometimes prescribed at lower doses, likely reflecting concerns about adverse effects or patients' tolerance. It was unclear whether the benefit from low doses of ACEi is comparable to high doses.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber.The Assessment of Treatment with Lisinopril and Survival (ATLAS) trial sought to assess the efficacy and safety of low vs high doses of ACE inhibition in patients with systolic heart failure.Patients: Eligible patients had left ventricular ejection fraction of 30% or less and had NYHA class II, III or IV despite treatment with diuretics for two or more months.Patients were excluded if they had any of the following: Acute coronary syndrome or revascularization procedure within 2 months, history of sustained or symptomatic ventricular tachycardia, known intolerance to ACEi, serum creatinine >2.5 mg/dL, or any noncardiac condition that could limit survival.Baseline characteristics: The trial randomized 3,164 patients – 1,596 randomized to the low-dose arm and 1,568 to the high dose arm.The average age of patients was 64 years and 80% were men. The average left ventricular ejection fraction was 23%. Cardiomyopathy was ischemic in 65% of the patients. The NYHA class was II in 16% of the patients, III in 77% and IV in 7%.Data on baseline comorbid conditions were not provided in the main manuscript.Procedures: The study was double blinded. At the beginning of the study, all patients received open-label lisinopril for four weeks to assess who is able to tolerate the drug. Patients who were able to tolerate lisinopril 12.5 mg to15 mg daily for two or more weeks were randomized in a 1:1 ratio to receive low-dose or high-dose ACEi. The target dose of lisinopril in the lose dose group was 2.5 to 5.0mg daily and was 32.5 to 35mg daily in the high dose group.All patients received open-label lisinopril 2.5 to 5mg daily. This dose was selected by the investigator. In addition, patients received up to three 10mg tablets of lisinopril or matching placebo.Endpoints: The primary endpoint was all-cause mortality. Secondary end points included cardiovascular mortality, all-cause hospitalization and cardiovascular hospitalizations.Analysis was performed based on the intention-to-treat principle. The estimated sample size was 3,000 patients. This sample size had 90% power at 5% alpha to detect 15% relative risk difference in the mortality between both treatment groups assuming 19% 1-year mortality in the high dose group.Results: Of the 3,793 patients who entered the initial open-label tolerability phase, 83.4% were randomized. A total of 176/3,793 (4.6%) were withdrawn for possible side effects. The median follow-up time was 46 months.Target doses were achieved in 92.7% of the patients in the low-dose group and 91.3% in the high-dose group. Study medication was discontinued by 30.6% of patients in the low-dose group and 27.2% in the high-dose group.All-cause mortality was not significantly different between both treatment groups (44.9% with low dose vs 42.5% with high dose, HR: 0.92, 95% CI: 0.82 – 1.03; p= 0.128). Cardiovascular mortality was numerically lower in the high dose group but this was not statistically significant (37.2% vs 40.2%, HR: 0.90, 95% CI: 0.81 – 1.01; p= 0.073). All-cause hospitalization was lower in the high dose group (3,819 hospitalizations vs 4,397; p= 0.021). Hospitalizations for cardiac causes and hospitalizations for heart failure were also lower in the high dose group (2,456 vs 2,923; p= 0.05) and (1,199 vs 1,576; p= 0.002), respectively.Patients in the high-dose group experienced more dizziness (19% vs 12%), more hypotension (11% vs 7%), more worsening renal function (10% vs 7%), and more hyperkalemia (6% vs 4%), but reported less cough (11% vs 13%) and had less hypokalemia (1% vs 3%).There were no significant subgroup interactions for the primary outcome.Conclusion: In patients with systolic heart failure, high dose ACE inhibition did not significantly reduce mortality compared to low-dose but it led to significantly less hospitalizations. In this trial of 3,164 patients and with a median follow up of 46 months, there were 578 less hospitalizations in the high dose group.Based on these results, we recommend up-titrating ACEi and use higher doses if tolerated. Although, side effects were more common in the high dose group, these can generally be managed with reducing the dose in the outpatient settings.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber. Get full access to Cardiology Trial's Substack at cardiologytrials.substack.com/subscribe

N Engl J Med 1999;341:709-717Background: The renin–angiotensin–aldosterone system (RAAS) is activated in patients with systolic heart failure. While this activation initially helps increase blood volume and maintains blood pressure, chronic activation promotes cardiac fibrosis and remodeling. In patients with systolic heart failure, inhibition of the RAAS with angiotensin-converting enzyme inhibitors (ACEi) significantly reduced mortality and morbidity, as seen in the CONSENSUS and SOLVD trials.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber.Preliminary data suggested that adding the aldosterone-receptor blocker spironolactone to ACEi, reduced the levels of atrial natriuretic peptide and did not lead to serious hyperkalemia.The Randomized Aldactone Evaluation Study (RALES) sought to test the hypothesis that spironolactone would significantly reduce the risk of all-cause death in patients with severe systolic heart failure.Patients: Eligible patients had left ventricular ejection fraction of 35% or less, had NYHA class IV heart failure within the 6 months before enrollment and NYHA class III or IV at the time of enrollment, and were treated with ACEi (if tolerated) and a loop diuretic.Patients were excluded if they had primary operable valvular disease (other than mitral or tricuspid regurgitation), congenital heart disease, unstable angina, primary liver failure, active cancer or any life-threatening condition, other than heart failure, prior heart transplant or awaiting heart transplant, serum creatinine >2.5 mg/dL, or serum potassium > 5.0 mmol/L.Baseline characteristics: Patients were recruited from 195 centers in 15 countries. The trial randomized 1,663 patients – 822 randomized to receive spironolactone and 841 to receive placebo.The average age of patients was 65 years and 73% were men. The average left ventricular ejection fraction was 25%. Cardiomyopathy was ischemic in 55% of the patients and non-ischemic in the rest. The NYHA class was III in 71% of the patients and IV in 29%.Data on baseline comorbid conditions were not provided.At the time of enrollment, 100% were taking loop diuretics, 94% were taking ACEi, 73% were taking digitalis, and 10% were taking beta-blockers. The mean daily dose of ACEi were as following: 63mg for captopril, 15mg for enalapril, and 14mg for lisinopril.Note: Max daily dose is 450mg for captopril, 40mg for enalapril, and 40mg for lisinopril.Procedures: The trial was double-blinded. Patients were assigned in a 1:1 ratio to receive spironolactone 25mg PO daily or placebo.The dose could be increased to 50mg daily after 8 weeks of treatment, If the patient had worsening heart failure and had no evidence of hyperkalemia. In the event of hyperkalemia, the dose could be lowered to 25 mg every other day. Laboratory testing including potassium were performed every 4 weeks for the first 12 weeks, then every 3 months for up to 1 year and every 6 months thereafter until the end of the study.Endpoints: The primary outcome was all-cause death. Secondary end points included death from cardiac causes, hospitalization for cardiac causes and change in the NYHA class.Analysis was performed based on the intention-to-treat principle. The planned sample size was not mentioned in the methods. However, the results mention that recruitment was complete. The sample size calculation assumed 38% mortality rate in the placebo group and that spironolactone would reduce mortality by 17% (relative risk reduction). The power of the study was set at 90% with a two-sided alpha of 5%.Results: Recruitment was complete in Dec, 1996 with follow up planned through Dec, 1999. However, the study was stopped early on Aug, 1998 after interim analysis showed significant reduction in mortality with spironolactone. The mean follow up time was 24 months. After 24 months of follow up, the mean daily dose of spironolactone was 26 mg.Spironolactone reduced all-cause death (35% vs 46%, RR: 0.70, 95% CI: 0.60 - 0.82; p< 0.001). Death from cardiac causes was also reduced with spironolactone (27% vs 37%, RR: 0.69, 95% CI: 0.58 - 0.82; p

In this episode, we review the high-yield topic Restrictive / Obliterative Cardiomyopathy ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠from the Cardiovascular section at ⁠⁠⁠⁠⁠⁠Medbullets.com⁠⁠⁠⁠⁠⁠Follow⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ Medbullets⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ on social media:Facebook: www.facebook.com/medbulletsInstagram: www.instagram.com/medbulletsofficialTwitter: www.twitter.com/medbulletsLinkedin: https://www.linkedin.com/company/medbullets

Interview with Leonoor F. J. M. Wijdeveld, BSc and Sean J. Jurgens, MD, MSc, PhD, authors of Cardiomyopathy-Associated Gene Variants in Atrial Fibrillation. Hosted by Sharlene Day, MD. Related Content: Cardiomyopathy-Associated Gene Variants in Atrial Fibrillation Genetic Testing in Early-Onset Atrial Fibrillation

Interview with Leonoor F. J. M. Wijdeveld, BSc and Sean J. Jurgens, MD, MSc, PhD, authors of Cardiomyopathy-Associated Gene Variants in Atrial Fibrillation. Hosted by Sharlene Day, MD. Related Content: Cardiomyopathy-Associated Gene Variants in Atrial Fibrillation Genetic Testing in Early-Onset Atrial Fibrillation

In this week's episode we'll learn more about how phosphoseryl-tRNA kinase inhibition promotes cell death in acute myeloid leukemia, or AML; APOE gene variants and their association with post-hematopoietic stem cell transplant outcomes in AML; and pathways by which chronic inflammation and oxidative stress may lead to cardiomyopathy in patients with sickle cell disease.Featured Articles:PSTK inhibition activates cGAS-STING, precipitating ferroptotic cell death in leukemic stem cells Common Hereditary Variants of the APOE Gene and Posttransplant Outcome in Acute Myeloid Leukemia 17R-Resolvin D1 Protects Against Sickle Cell Related Inflammatory Cardiomyopathy in Humanized Mice 

With Justyna Sokolska, Institute of Heart Diseases, Wroclaw Medical University, Wroclaw - Poland, and Maja Cikes, University of Zagreb School of Medicine, Head at the Unit for Heart Failure and Mechanical Circulatory Support, Department of Cardiovascular Diseases, University Hospital Center, Zagreb - Croatia. In this episode of HFA CardioTalk, Justyna Sokolska interviews Maja Cikes on the challenges in management of long-term left ventricular assist device in patients with advanced heart failure. The discussion emphasizes the importance of selecting appropriate patients at the optimal time, examines the adverse events and highlights major ongoing clinical trials.  Recommended readings:  Aspirin and Hemocompatibility Events With a Left Ventricular Assist Device in Advanced Heart Failure: The ARIES-HM3 Randomized Clinical Trial, Mehra MR, et al. JAMA. 2023 Dec 12;330(22):2171-81  Trends and Outcomes of Left Ventricular Assist Device Therapy: JACC Focus Seminar, Varshney AS, et al. J Am Coll Cardiol 2022 Mar 22;79(11):1092-1107 Cardiac implantable electronic devices with a defibrillator component and all-cause mortality in left ventricular assist device carriers: results from the PCHF-VAD registry, Cikes M, et al. Eur J Heart Fail 2019 Sep;21(9):1129-41 A Fully Magnetically Levitated Left Ventricular Assist Device — Final Report, Mehra MR, et al. N Engl J Med 2019 Apr 25;380(17):1618-27 This 2025 HFA Cardio Talk podcast series is supported by Bayer AG in the form of an unrestricted financial support. The discussion has not been influenced in any way by its sponsor.

Commentary by Dr. Nowell Fine.

Commentary by Dr. Jian'an Wang.

The experts at Clinical Concepts in Obstetrics pool their decades of experience caring for critically ill pregnant women to discuss the challenges encountered in caring for these vulnerable women. Dr Stephanie Martin is the Medical Director for Clinical Concepts in Obstetrics and a Maternal Fetal Medicine specialist with expertise in critical care obstetrics. Suzanne McMurtry Baird, DNP, RN is the Nursing Director for Clinical Concepts in Obstetrics with many years of experience caring for critically ill pregnant women. Julie Arafeh, RN, MS is the Simulation Director for Clinical Concepts in Obstetrics and a leading expert in simulation.Critical Care Obstetrics Academy: https://www.clinicalconceptsinob.com/Follow us: Instagram: https://www.instagram.com/criticalcareob/Dr Martin's LinkedIn: http://linkedin.com/in/stephanie-martin-65b07112aCCOB LinkedIn: https://www.linkedin.com/company/clinical-concepts-in-obstetrics/Twitter/X: https://twitter.com/OBCriticalCareCCOB Facebook: https://www.facebook.com/clinicalconceptsinobstetricsDr Ma...

With Robert M.A. van der Boon, Erasmus Medical Center, Rotterdam - The Netherlands, and Anuradha Lala, Mount Sinai Fuster Heart Hospital, New York City - USA. In this episode of HFA Cardio talk, we dive into how factors like sex, socio-economics status and ethnicity shape the way heart failure presents and progresses in different populations. We'll discuss why recognizing these differences is critical for accurate diagnosis and effective treatment and highlight practical steps clinicians can take to close the gaps in prevention and care. Papers: https://onlinelibrary.wiley.com/doi/10.1002/ejhf.2534 https://academic.oup.com/eurheartj/article/40/47/3859/5652224?login=true https://www.sciencedirect.com/science/article/pii/S1071916421004322?via%3Dihub https://www.sciencedirect.com/science/article/pii/S0002914922010074?via%3Dihub https://www.sciencedirect.com/science/article/pii/S2468266719301082?via%3Dihub https://journals.lww.com/co-cardiology/fulltext/2021/05000/racial_and_ethnic_disparities_in_heart_failure_.12.aspx https://onlinelibrary.wiley.com/doi/10.1002/ehf2.14986   This 2025 HFA Cardio Talk podcast series is supported by Bayer AG in the form of an unrestricted financial support. The discussion has not been influenced in any way by its sponsor.

Mary Norine Walsh, MD, MACC, JACC: Case Reports Deputy Editor, is joined by author Dena Hayes, MD, discussing this study from Hayes et al presented at ACC.25 and published in JACC: Case Reports. The diagnosis of cardiac sarcoidosis (CS) is often challenging, particularly in atypical cases. The authors describe a case of a previously healthy 33-year-old woman who was found to have a biatrial mass and evidence of a diffuse inflammatory or neoplastic process on multimodality imaging. Percutaneous biopsy of the cardiac mass was performed and histopathology revealed granulomas consistent with CS. This case adds to the growing number of reports of CS presenting as an intracardiac mass.

Andrea Scotti, MD, JACC: Case Reports Deputy Editor, is joined by authors Richard Carrick, MD, PhD and Drew Bidmead, BS discussing this study from Carrick et al presented at ACC.25 and published in JACC: Case Reports. Left atrial dissection is a rare, but potentially serious, complication that most commonly arises following mitral valve surgeries. In this report, we describe an unusual case of left atrial dissection that occurred after multi-valve surgical replacement in a patient with hypertrophic cardiomyopathy. While permanent pacemaker placement was required due to recurrent episodes of complete heart block, the patient was otherwise managed safely using a conservative approach without surgical re-intervention.

Join our expert as they delve into the critical aspects of recognizing and diagnosing peripartum cardiomyopathy (PPCM), a serious heart condition affecting pregnant and postpartum women. This episode will cover guideline-directed medical therapy tailored for PPCM during pregnancy and the postpartum period. Additionally, postpartum care strategies will be explored along with a patient's personal journey to provide a comprehensive understanding of the condition.

In this episode, Dr. Valentin Fuster highlights a groundbreaking study on acoramides, a novel treatment for transthyretin amyloid cardiomyopathy (ATTR), which shows significant reductions in mortality and cardiovascular hospitalizations compared to a placebo. Experts discuss the clinical implications, comparing acoramides to the previously approved tafamidis, noting exciting advancements in treatments for a once-untreatable disease.

CardioNerds Cardiac Amyloidosis Series Chair Dr. Rick Ferraro and Episode Lead Dr. Anna Radakrishnan discuss the biology of transthyretin amyloid cardiomyopathy (ATTR-CM ) with Dr. Daniel Judge.  Notes were drafted by Dr. Anna Radakrishnan. The audio was engineered by student Dr. Julia Marques.  This episode provides a comprehensive overview of transthyretin (ATTR) cardiac amyloidosis, a complex and rapidly evolving disease process. The discussion covers the key red flags for cardiac amyloidosis, the diagnostic pathway, and the implications of hereditary versus wild-type ATTR. Importantly, the episode delves into the current and emerging therapies for ATTR, including stabilizers, gene silencers, and promising treatments like CRISPR-Cas9 and antibody-based approaches. Dr. Judge shares his insights and excitement about the rapidly advancing field, highlighting the need for early diagnosis and the potential to improve long-term outcomes for patients with this condition.  Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey.  US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here.  CardioNerds Cardiac Amyloid PageCardioNerds Episode Page Pearls: - Biology of Transthyretin amyloid cardiomyopathy Maintain a high index of suspicion! Look for subtle (yet telling) signs like ventricular hypertrophy, discordant EKG findings, bilateral carpal tunnel syndrome, and spontaneous biceps tendon rupture.  Utilize the right diagnostic tests. Endomyocardial biopsy remains the gold standard, but non-invasive tools like PYP scan with SPECT imaging and genetic testing are essential for accurate diagnosis.  Differentiating hereditary from wild-type ATTR is critical, as genetic forms may have a more aggressive course and familial implications.  Early diagnosis and intervention significantly improve prognosis, making vigilance in screening and prompt treatment initiation essential.  The future is now! Cutting-edge therapies are transforming the treatment landscape, including TTR stabilizers, gene silencers, and emerging technologies like CRISPR-Cas9 and antibody-based treatments.  Notes - Biology of Transthyretin amyloid cardiomyopathy What is transthyretin amyloid (aTTR) and how is it derived?  Transthyretin (TTR) is a transport protein primarily synthesized by the liver, responsible for carrying thyroid hormones (thyroxine) and retinol (vitamin A) in the blood. It circulates as a tetramer, composed of four identical monomers, which is essential for its stability and function.  In transthyretin amyloid (ATTR) amyloidosis, the TTR protein becomes unstable, leading to its dissociation into monomers. These monomers misfold and aggregate into insoluble amyloid fibrils, which deposit extracellularly in tissues such as the heart, nerves, and gastrointestinal tract. This progressive amyloid deposition leads to organ dysfunction, including restrictive cardiomyopathy and neuropathy.  There are two main forms of ATTR amyloidosis: hereditary (variant) and wild-type (senile) ATTR.  Hereditary ATTR (ATTRv) is caused by mutations in the TTR gene. These mutations destabilize the TTR tetramer, making it more prone to dissociation. This increases misfolding and amyloid fibril formation, resulting in systemic amyloid deposition.   Wild-type ATTR (ATTRwt) occurs without genetic mutations and is primarily age-related. Over time, even normal TTR tetramers can become unstable, leading to gradual misfolding and amyloid deposition, particularly in the heart. ATTRwt is a common but often underdiagnosed cause of heart failure with preserved ejection fraction (HFpEF) in elderly individuals.  How does aTTR lead to deleterious effects in the heart and other organ systems?    Transthyretin amyloidosis leads to organ dysfunction through the deposition of misfolded TTR protein as amyloid fib...

https://professional.heart.org/en/education/role-of-cardiovascular-health-in-maternal-health/#preeclampsiaThe experts at Clinical Concepts in Obstetrics pool their decades of experience caring for critically ill pregnant women to discuss the challenges encountered in caring for these vulnerable women. Dr Stephanie Martin is the Medical Director for Clinical Concepts in Obstetrics and a Maternal Fetal Medicine specialist with expertise in critical care obstetrics. Suzanne McMurtry Baird, DNP, RN is the Nursing Director for Clinical Concepts in Obstetrics with many years of experience caring for critically ill pregnant women. Julie Arafeh, RN, MS is the Simulation Director for Clinical Concepts in Obstetrics and a leading expert in simulation.Critical Care Obstetrics Academy: https://www.clinicalconceptsinob.com/Follow us: Instagram: https://www.instagram.comDr Martin's LinkedIn: http://linkedin.com/in/stephanie-martin-65b07112aCCOB LinkedIn: https://www.linkedin.com/company/clinical-concepts-in-obstetrics/Twitter/X: https://twitter.com/OBCriticalCareCCOB Facebook: https://www.facebook.com/clinicalconceptsinobstetricsDr Martin's Facebook: ...

With Henrique Arfsten, Medical University of Vienna, Vienna - Austria and Alexandre Mebazza, Hospital Lariboisiere, Paris - France.  In this episode of HFA CardioTalk, Henrike Arfsten and  Alexandre Mebazaa discuss the importance of rapid initiation and titration of guideline-directed medical heart failure therapy. A focus will be on data from the STRONG-HF trial, which demonstrated safety and efficacy of rapid up-titration following an acute heart failure event. The trial was even stopped early as the benefits of the intensive treatment strategy were overwhelming. Moreover, specific questions are raised, such as the right time to start therapy and how to deal with possible side effects. Mebazaa A, et al. Lancet 2022 Dec 3;400(10367):1938-52 Biegus J, et al. Heart Fail Rev 2024 Sep;29(5):1065-1077 McDonagh TA, et al. Eur J Heart Fail 2022 Jan;24(1):4-131 McDonagh TA, et al. Eur J Heart Fail 2024 Jan;26(1):5-17 This 2025 HFA Cardio Talk podcast series is supported by Bayer AG in the form of an unrestricted financial support. The discussion has not been influenced in any way by its sponsor.

The study investigates the K210del mutation in genetic cardiomyopathy, which impairs myocardial contractility due to calcium discoordination in the troponin complex. Using a structure-based drug repurposing approach, researchers identified risedronate, an FDA-approved bisphosphonate, as a structural corrector that restores the calcium-binding domain's normal configuration. Experiments with patient-derived iPSC cardiomyocytes and a mouse model demonstrated that risedronate normalized calcium sensitivity, improved contraction velocity, and restored left ventricular function. The findings highlight the potential of repurposing existing drugs to treat genetic cardiomyopathies.

Episode SummaryThis is a replay of a recent episode because February is American Heart Month. Craig and Karey Packard share their inspiring story about facing an unexpected health crisis that forever changed their lives. They recount how the life-saving power of CPR played a critical role in a miraculous outcome. Their story is one of faith and resilience and a good reminder of the power of preparation in the event of the unexpected. About Craig & Karey PackardCraig and Karey Packard live in Londonderry, NH.  They have been married for 36 years and have 4 children and 2 grandchildren.  Craig did his undergraduate work at Tufts University, completed medical school at the Uniformed Services University of the Health Sciences, and later added a Masters in Public Health from Harvard. He served as a doctor in the US Air Force for 26 years before retiring from the military in 2011 after which he worked in the Occupational Medicine field for an additional 10 years before fully retiring. He was board-certified in Family Medicine, Aerospace Medicine, and Occupational Medicine.Karey graduated from Clarion State College with a degree in accounting after which she received an Associates degree in paralegal studies at George Washington University. She had to leave the workforce when their oldest son was diagnosed with leukemia and with the frequent military moves, she never returned to the paid workforce.  Among her numerous volunteer roles, she has worked for the American Heart Association as an advocate for CPR training and heart health for the past decade.From This EpisodeWhat is Cardiomyopathy?“Miracle Girl” Recovers from “Non-Survivable” EventFind CPR Training near youAmerican Heart Month Find and Follow Carole and Wisdom Shared:https://www.caroleblueweiss.com/Subscribe to YouTube channelFollow and send a message on FacebookFollow and send a message on LinkedInFollow on InstagramFollow on TikTokFollow on ThreadsThe Wisdom Shared TeamAudio Engineering by Steve Heatherington of Good Podcasting WorksCo-Producer and Marketing Coordinator: Kayla NelsonProduction Assistant: Becki Leigh

With Novi Yanti Sari, Siloam Hospitals, Jakarta - Indonesia, and Mark Petrie, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow - UK. In this episode of the HFA podcast series, we explore the complex relationship between obesity and heart failure, discussing challenges, management strategies, and the latest therapies, while emphasising the importance of integrated care in improving clinical outcomes. This 2025 HFA Cardio Talk podcast series is supported by Bayer AG in the form of an unrestricted financial support. The discussion has not been influenced in any way by its sponsor.

Summary:  This week on The Genetics Podcast, Patrick is joined by Eric Adler, Chief Medical Officer and Head of Research at Lexeo Therapeutics and Professor of Medicine at University of California San Diego. Eric shares his experience with genetic cardiomyopathy and his work on gene therapy for Danon disease, drawing from both clinical and research perspectives. Additionally, he explores the evolution of the field and the broader challenges faced by cardiovascular patients. Show Notes:  0:00 Intro to The Genetics Podcast 01:00 Welcome to Eric and his efforts in cardiomyopathy at the bench and bedside 03:32 How modeling genetic diseases using pluripotent stem cells lead Eric to studying Danon disease  04:50 Pivoting from basic to translational research using adeno-associated viruses (AAV)-based gene therapy 07:58 Uncovering genetic cardiomyopathies that were misdiagnosed as idiopathic cardiomyopathy 09:55 Treatment, screening, and penetrance of Danon disease 12:30 Recent successes and remaining challenges in cardiovascular disease 19:47 Battling distrust in the medical profession 21:55 Preventative therapy using APOE2 for patients at risk of early Alzheimer's   25:15 Motivations behind and advantages of Eric's patient-centered approach to therapeutics 27:24 Balancing regulatory requirements for protocols versus patient needs 29:49 The importance of committed clinical partners for successful trial execution 36:08 Eric's passion for cooking and how he won a cooking competition 39:02 Closing remarks and Lexeo Therapeutics' aims for 2025 Find out more Lexeo Therapeutics (https://www.lexeotx.com/) Please consider rating and reviewing us on your chosen podcast listening platform!  https://drive.google.com/file/d/1Bp2_wVNSzntTs_zuoizU8bX1dvao4jfj/view?usp=share_link

SHOW NOTES 2:25 – heart transplant at age 29, no previous cardiac issues3:00 – post-partum cardiomyopathy3:30 – placed on a Life Vest and a low ejection fraction4:30 – a 49-day stay in the hospital5:15 – the fear of leaving one's children behind, without a mom6:15 – emergency room, to a two-week stay, to “we've done all we can for you”7:00 – options and prognosis regarding Cassidy's heart8:30 – praying and deciding to move forward with a heart transplant9:45 – ECMO10:15 – shifting one's perspective during and after a heart transplant11:00 – Cassidy's mom, cardiomyopathy, and her heart transplant months after Cassidy's12:00 – the wait for a heart, and testing for the best match, for improved outcomes13:00 – antibodies after pregnancy can affect transplant success14:20 – a ten-hour surgery14:50 – the new heart needs to wake up16:00 – the importance of family and a support system17:30 –Dr. Allene Magill, an influential leader in education, and in Cassidy's life19:00 – Cassidy's decision to change her career path change21:00 – Shifting plans to find the “sweet spot” for one's work22:30 – teaching and learning, equal importance23:00 – organ donors changes lives and save lives25:00 – donor family and recipient interaction25:30 – a donor's organ can be classified as high-risk26:00 – How does life change when you have someone else's heart replace your own?27:15 – Piedmont Cartersville, Piedmont Atlanta, Samsky Heart Failure Clinic28:00 – great teachers…29:15 – Matt Fox, Becky Reynolds30:00 – Cassidy's closing comments LINKSCardiomyopathyECMOEjection FractionLifeVestTM - Cleveland Clinic pageLifeVestTM - Zoll pageLVADOrgan Donation - American Society of TransplantationOrgan Donation - Donate LifeOrgan Donation - UNOSPiedmont CartersvillePiedmont AtlantaSamsky Heart Failure CenterFairmount Elementary SchoolRed Bud Middle SchoolSonoraville High School   Music for Lead. Learn. Change. is Sweet Adrenaline by Delicate BeatsPodcast cover art is a view from Brunnkogel (mountaintop) over the mountains of the Salzkammergut in Austria, courtesy of photographer Simon Berger, published on www.unsplash.com.Professional Association of Georgia EducatorsDavid's LinkedIn pageLead. Learn. Change. the book

Hey Heart Buddies! I welcome Kina Lucombe, who shares her story of cardiomyopathy and complete heart block. Despite leading a healthy lifestyle as a pescatarian, Kina unexpectedly collapsed during yoga in February 2019. Diagnosed with cardiomyopathy and complete heart block, she required an emergency pacemaker surgery. Kina discusses the emotional aftermath and how it led her to found Hearts of Valor, a support organization for heart patients. She emphasizes the importance of sharing health struggles with loved ones and staying hopeful despite a heart diagnosis. Kina's inspiring story underscores the unexpected challenges of heart health and the power of community support.To learn more about Kina and her work, go to: About Our Organization – Hearts of Valor Inc.Join 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

6th AHA 2024: ATTR Cardiomyopathy

Commentary by Dr. Sabahat Bokhari.

Commentary by Dr. Alexander Maass.

Commentary by Dr. Jan Leerink.

This episode covers hypertrophic obstructive cardiomyopathy.Written notes can be found at https://zerotofinals.com/paediatrics/cardiology/hypertrophicobstructivecardiomyopathy/Questions can be found at https://members.zerotofinals.com/Books can be found at https://zerotofinals.com/books/The audio in the episode was expertly edited by Harry Watchman.

Can a broken heart be mended? Perhaps if we are talking about takotsubo cardiomyopathy - also called broken heart syndrome - which is stress-induced damage to the heart muscle. Ninety percent of the people with this heart syndrome are post-menopausal women whose symptoms occur after severe emotional or physical stress. Learn about it in this episode: https://bit.ly/4g9Ma8x In this Episode:03:04 - Obituaries My My Mother Wrote for Me When I was In My 20's07:21 - Feeding a Broken Heart:  Chicken Tetrazzini 09:15 - Takotsubo Cardiomyopathy (TTS) -You Really Can Die from a Broken Heart24:22 - Epitaph by Merrit Maloy25:41 - OutroRelated Content:S4E18: How to Exorcise Depression and Anxiety with ExerciseS3E37: What Can a Mindfulness Practice Offer You?The Tao of IroningS1E23: Support GroupsS2E16: Big Girls Do CryS3E22: Why Do We Fear Death?S1E07: No Mud, No Lotus – What is the New Normal?Support the showGet show notes and resources at our website: every1dies.org. Facebook | Instagram | YouTube | mail@every1dies.org

Episode SummaryCraig and Karey Packard share their inspiring story about facing an unexpected health crisis that forever changed their lives. They recount how the life-saving power of CPR played a critical role in a miraculous outcome. Their story is one of faith and resilience and a good reminder of the power of preparation in the event of the unexpected. About Craig & Karey PackardCraig and Karey Packard live in Londonderry, NH.  They have been married for 36 years and have 4 children and 2 grandchildren.  Craig did his undergraduate work at Tufts University, completed medical school at the Uniformed Services University of the Health Sciences, and later added a Masters in Public Health from Harvard. He served as a doctor in the US Air Force for 26 years before retiring from the military in 2011 after which he worked in the Occupational Medicine field for an additional 10 years before fully retiring. He was board-certified in Family Medicine, Aerospace Medicine, and Occupational Medicine.Karey graduated from Clarion State College with a degree in accounting after which she received an Associates degree in paralegal studies at George Washington University. She had to leave the workforce when their oldest son was diagnosed with leukemia and with the frequent military moves, she never returned to the paid workforce.  Among her numerous volunteer roles, she has worked for the American Heart Association as an advocate for CPR training and heart health for the past decade.From This EpisodeWhat is Cardiomyopathy?“Miracle Girl” Recovers from “Non-Survivable” EventFind CPR Training near you    Find and Follow Carole and Wisdom Shared:https://www.caroleblueweiss.com/Subscribe to YouTube channelFollow and send a message on FacebookFollow and send a message on LinkedInFollow on InstagramFollow on TikTokFollow on ThreadsThe Wisdom Shared TeamAudio Engineering by Steve Heatherington of Good Podcasting WorksCo-Producer and Marketing Coordinator: Kayla NelsonProduction Assistant: Becki Leigh

Are you up to date on the new developments for emerging therapies for your patients with transthyretin amyloid cardiomyopathy (ATTR-CM)? Credit available for this activity expires: 12/16/25 Earn Credit / Learning Objectives & Disclosures: https://www.medscape.org/viewarticle/1002007?ecd=bdc_podcast_libsyn_mscpedu

Charles, a recently retired cardiologist of 53 years, speaks with David Rintell, Head of Patient Advocacy at BridgeBio, and Mandy Rohrig, Director of Patient Advocacy at BridgeBio Gene Therapy, about how his unexpected early diagnosis of ATTR-CM likely impacted the trajectory of his disease. Dr. Jonathan Fox, President and Chief Medical Officer of cardiorenal programs at BridgeBio, explains how ATTR affects the heart and peripheral nervous system, and the importance of early diagnosis.   For years, Charles suffered from numbness and tingling in both wrists and hands. Eventually, when the pain became so severe that operating a mouse for 10 to 15 minutes was difficult, he was referred to a hand surgeon who recommended carpal tunnel surgery. Preparing for the surgery, Charles recalled reading a medical journal article that indicated 10% of people who underwent carpel tunnel surgery had positive tissue biopsy indicative of ATTR-CM. He requested that his surgeon perform a biopsy and shortly thereafter received his diagnosis. The transition from doctor to patient was not easy for Charles. However, he feels fortunate to be a cardiologist, to have read and remembered the article, requested a biopsy, and received the diagnosis more quickly than many others who live with ATTR. “I have three passions: running, traveling, and teaching," Charles shared. The early diagnosis has allowed him to continue to live a full, active life, running nearly daily as he has for the past 45 years. Charles, now 86, continues to serve others, spending his retirement teaching and mentoring health care providers around the country about ATTR and volunteering for amyloidosis advocacy organizations.

In this episode we sit down with Lisa Schwartz—content creator, author, and new mom—as she shares her intense and unexpected experience with postpartum cardiomyopathy. Lisa opens up about the frightening health scare that struck shortly after her daughter's birth, leading to heart failure and an extended hospital stay. Through humor and honesty, she recounts the warning signs she initially dismissed, the importance of self-advocacy in healthcare, and how this life-threatening condition reshaped her approach to motherhood and privacy. This episode offers valuable insights into the realities of postpartum health, patient advocacy, and the need for awareness around lesser-known maternal health issues. Takeaways: Postpartum cardiomyopathy is a rare but serious condition that can occur after childbirth, leading to heart failure and requiring immediate medical attention. Self-advocacy in healthcare is vital; Lisa's persistence helped her receive a proper diagnosis despite initial dismissals of her symptoms as anxiety. Understanding the symptoms of heart failure—such as swelling, shortness of breath, and fluid buildup—is essential for early intervention. The journey of recovery and adapting to new motherhood after a health crisis can be daunting, but Lisa's story highlights resilience and hope. Raising awareness of postpartum health risks helps empower women to seek care and advocate for themselves during and after pregnancy. — Want to Learn About Lisa Schwartz: Instagram: @lisaschwartz  YouTube: youtube.com/lisbug — To Get Tickets to Wife & Death: You can visit Glaucomflecken.com/live  We want to hear YOUR stories (and medical puns)! Shoot us an email and say hi! knockknockhi@human-content.com Can't get enough of us? Shucks. You can support the show on Patreon for early episode access, exclusive bonus shows, livestream hangouts, and much more! – http://www.patreon.com/glaucomflecken  Also, be sure to check out the newsletter: https://glaucomflecken.com/glauc-to-me/ If you are interested in buying a book from one of our guests, check them all out here: https://www.amazon.com/shop/dr.glaucomflecken If you want more information on models I use: Anatomy Warehouse provides for the best, crafting custom anatomical products, medical simulation kits and presentation models that create a lasting educational impact.  For more information go to Anatomy Warehouse DOT com. Link:  Anatomy Warehouse Plus for 15% off use code: Glaucomflecken15 -- A friendly reminder from the G's and Tarsus: If you want to learn more about Demodex Blepharitis, making an appointment with your eye doctor for an eyelid exam can help you know for sure. Visit http://www.EyelidCheck.com for more information.  Today's episode is brought to you by DAX Copilot from Microsoft. DAX Copilot is your AI assistant for automating clinical documentation and workflows helping you be more efficient and reduce the administrative burdens that cause us to feel overwhelmed and burnt out. To learn more about how DAX Copilot can help improve healthcare experiences for both you and your patients visit aka.ms/knockknockhi. Produced by Human Content Learn more about your ad choices. Visit megaphone.fm/adchoices

Did you miss AHA 2024? Listen here to brief discussions of the latest research. Eric Rubin is the Editor-in-Chief of the Journal. Jane Leopold is a Deputy Editor of the Journal. Stephen Morrissey, the interviewer, is the Executive Managing Editor of the Journal. E.J. Rubin, J. Leopold, and S. Morrissey. NEJM at AHA — Phase 1 Study of AAV9.LAMP2B Gene Therapy in Danon Disease. N Engl J Med. DOI: 10.1056/NEJMe2414477.

Did you miss AHA 2024? Listen here to brief discussions of the latest research. Eric Rubin is the Editor-in-Chief of the Journal. Jane Leopold is a Deputy Editor of the Journal. Stephen Morrissey, the interviewer, is the Executive Managing Editor of the Journal. E.J. Rubin, J. Leopold, and S. Morrissey. NEJM at AHA — CRISPR-Cas9 Gene Editing with Nexiguran Ziclumeran for ATTR Cardiomyopathy. N Engl J Med. DOI: 10.1056/NEJMe2414473.

Did you miss AHA 2024? Listen here to brief discussions of the latest research. Eric Rubin is the Editor-in-Chief of the Journal. Jane Leopold is a Deputy Editor of the Journal. Stephen Morrissey, the interviewer, is the Executive Managing Editor of the Journal. E.J. Rubin, J. Leopold, and S. Morrissey. NEJM at AHA — Catheter Ablation or Antiarrhythmic Drugs for Ventricular Tachycardia. N Engl J Med. DOI: 10.1056/NEJMe2414471.

Kaylin, Sharmin, Cheryl, and Jane discuss two cases of volume overload. Kaylin reviews the pathophysiology behind constrictive pericarditis and restrictive cardiomyopathy, normal pericardial and thoracic anatomy and pressure changes with respiration, and the difference in treatments between the two disease processes. Download CPSolvers App here RLRCPSOLVERS

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...