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مشابه لـCardionerds: A Cardiology Podcast
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Cardionerds: A Cardiology Podcast
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المحتوى المقدم من CardioNerds. يتم تحميل جميع محتويات البودكاست بما في ذلك الحلقات والرسومات وأوصاف البودكاست وتقديمها مباشرة بواسطة CardioNerds أو شريك منصة البودكاست الخاص بهم. إذا كنت تعتقد أن شخصًا ما يستخدم عملك المحمي بحقوق الطبع والنشر دون إذنك، فيمكنك اتباع العملية الموضحة هنا https://ar.player.fm/legal.
Welcome to CardioNerds, where we bring you in-depth discussions with leading experts, case reports, and updates on the latest advancements in the world of cardiology. Tune in to expand your knowledge, sharpen your skills, and become a true CardioNerd!
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المحتوى المقدم من CardioNerds. يتم تحميل جميع محتويات البودكاست بما في ذلك الحلقات والرسومات وأوصاف البودكاست وتقديمها مباشرة بواسطة CardioNerds أو شريك منصة البودكاست الخاص بهم. إذا كنت تعتقد أن شخصًا ما يستخدم عملك المحمي بحقوق الطبع والنشر دون إذنك، فيمكنك اتباع العملية الموضحة هنا https://ar.player.fm/legal.
Welcome to CardioNerds, where we bring you in-depth discussions with leading experts, case reports, and updates on the latest advancements in the world of cardiology. Tune in to expand your knowledge, sharpen your skills, and become a true CardioNerd!
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1 412: The Biology of Transthyretin amyloid cardiomyopathy (ATTR-CM) with Dr. Daniel Judge 13:01
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التشغيل لاحقا التشغيل لاحقا قوائم إعجاب احبCardioNerds 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 Page CardioNerds 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 fibrils, which accumulate extracellularly and disrupt normal tissue architecture and function. These deposits cause progressive damage by increasing stiffness, inducing oxidative stress, and impairing normal cellular function. Cardiac manifestations include amyloid deposition in the myocardial interstitium, leading to increased stiffness, diastolic dysfunction, and restrictive cardiomyopathy. As the disease progresses, systolic dysfunction may develop. Amyloid infiltration can also cause arrhythmia, conduction abnormalities such as atrioventricular block and atrial fibrillation, valvular thickening, coronary ischemia, and pericardial effusion. Disruption of transverse tubules in cardiomyocytes contributes to heart failure and arrhythmia. Systemic involvement depends on the culprit amylodogenic protein. AL amyloidosis caused by deposition of immunoglobulin light chains may deposit in and disrupt the function of any tissue/organ except for the central nevous system. ATTR amyloidosis primarily affects the heart, peripheral nerves, and the musculoskeletal system. Peripheral neuropathy can cause sensory loss, pain, and motor weakness, while autonomic dysfunction may lead to orthostatic hypotension, gastroparesis, and urinary retention. Carpal tunnel syndrome is a common early sign. Gastrointestinal amyloid deposits (specifically for AL but not ATTR) can cause gastroparesis, diarrhea, constipation, and malabsorption, leading to weight loss and malnutrition. Renal involvement (specifically for AL but not ATTR), though less common, can present as proteinuria and renal dysfunction. Amyloid deposition in soft tissues and the lungs may lead to hoarseness and musculoskeletal stiffness. As the disease progresses, continued amyloid accumulation leads to worsening organ dysfunction and failure. Early diagnosis and intervention are essential to slowing disease progression and managing symptoms effectively. When and why is aTTR cardiac amyloidosis hereditary versus obtained sporadically? Hereditary aTTR is caused by genetic mutations in the TTR gene, which are often autosomal dominant. Common mutations include V122I (more common in African Americans) and V30M (more common in certain regions like Portugal). Hereditary aTTR typically presents at an earlier age and may have a more aggressive course, with a higher likelihood of neuropathic involvement. Wild-type aTTR, or senile systemic amyloidosis, occurs sporadically and is more common in older individuals, typically without a family history. The exact reasons for the development of wild-type aTTR are not fully understood, but factors like chronic inflammation and exercise may play a role in the misfolding and aggregation of the normal TTR protein. References: Biology of Transthyretin amyloid cardiomyopathy Ruberg FL, Maurer MS. Cardiac Amyloidosis Due to Transthyretin Protein. JAMA. 2024;331(9):778-778. https://doi.org/10.1001/jama.2024.0442 Ruberg FL, Grogan M, Hanna M, Kelly JW, Maurer MS. Transthyretin Amyloid Cardiomyopathy. Journal of the American College of Cardiology. 2019;73(22):2872-2891. https://doi.org/10.1016/j.jacc.2019.04.003 Maurer MS, Bokhari S, Damy T, et al. Expert Consensus Recommendations for the Suspicion and Diagnosis of Transthyretin Cardiac Amyloidosis. Circulation: Heart Failure. 2019;12(9). https://doi.org/10.1161/circheartfailure.119.006075 Griffin JM, Rosenthal JL, Grodin JL, Maurer MS, Grogan M, Cheng RK. ATTR Amyloidosis: Current and Emerging Management Strategies. JACC: CardioOncology. 2021;3(4):488-505. https://doi.org/10.1016/j.jaccao.2021.06.006…
1 411. Journal Club: The VANISH2 Trial with Dr. Jeff Healey and Dr. Roderick Tung 30:05
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التشغيل لاحقا التشغيل لاحقا قوائم إعجاب احبJoin CardioNerds EP Council Chair Dr. Naima Maqsood and Episode Lead Dr. Jeanne De Lavallaz as they discuss the results of the VANISH2 Trial with expert faculty Dr. Jeff Healey and Dr. Roderick Tung. Audio editing by CardioNerds academy intern, Grace Qiu . The VANISH2 trial enrolled 416 patients with ischemic cardiomyopathy, an ICD in place, and recurrent episodes of sustained monomorphic ventricular tachycardia (VT) to receive either first-line VT catheter ablation or antiarrhythmic drug therapy with the primary composite outcome of death from any cause, appropriate ICD shock, ventricular tachycardia storm (meaning at least 3 ventricular tachycardia events within 24hrs) or treated ventricular tachycardia below the detection limit of the ICD. The study population had a mean age of 68 years, with 94% being men and predominantly of white ethnicity. On average, 14 years had elapsed since their last myocardial infarction, with approximately 60% having undergone percutaneous coronary intervention at the time. The mean ejection fraction was 34%. This episode was planned in collaboration with Heart Rhythm TV with mentorship from Dr. Daniel Alyesh and Dr. Mehak Dhande. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Journal Club Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron! References – VANISH2 Trial Sapp, J. L., Tang, A. S. L., Parkash, R., Stevenson, W. G., Healey, J. S., Gula, L. J., Nair, G. M., & the VANISH2 Study Team. (2025). Catheter ablation or antiarrhythmic drugs for ventricular tachycardia. The New England Journal of Medicine, 392 , 737–747.…
1 410. Case Report: A Curious Case of Refractory Ventricular Tachycardia – Rutgers-Robert Wood Johnson 40:13
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التشغيل لاحقا التشغيل لاحقا قوائم إعجاب احب 1 409. Journal Club: The ARREST-AF Trial with Drs. Prashanthan Sanders and Mehak Dhande 36:04
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التشغيل لاحقا التشغيل لاحقا قوائم إعجاب احبJoin CardioNerds EP Council Chair Dr. Naima Maqsood and Episode Lead Dr. Jeanne De Lavallaz as they discuss the results of the ARREST-AF Trial with expert faculty Dr. Prashanthan Sanders and Dr. Mehak Dhande. Audio editing by CardioNerds intern Bhavya Shah. The ARREST-AF trial enrolled 122 patients with a BMI of 27 kg/m 2 or greater and at least one cardiovascular risk factor with either paroxysmal or persistent AF and were scheduled to undergo de novo AF ablation. They were randomized to an intensive risk factor management (RFM) program versus usual care. The RFM program addressed obesity, sleep apnea, HTN, HLD, tobacco, and alcohol abuse, whereas the usual care arm had a discussion of risk factors but without an extensive risk factor modification or follow-up program. The study population had a mean age of 60 years, a mean BMI of 33 kg/m 2 , and 56-60% of patients with persistent AF. A third of the study population was female. The trial showed a significant improvement in the primary endpoint of the percentage of patients free from atrial fibrillation after ablation in those receiving the intensive lifestyle RFM program. At the end of the 12.3-month follow-up period, 66% percent of patients in the RFM group were free from AF compared to 42% in the usual care group (HR 0.53, p = 0.03). The RFM group also showed significant improvement in AF symptom severity, decline in body weight, systolic blood pressure, glycemic control, and exercise capacity. On average, patients in the RFM arm lost 9 kg of weight compared to 1 kg in the control group. Similarly, systolic blood pressure decreased by 13.1 mmHg in the RFM group but increased by four mmHg in the control group. This episode was planned in collaboration with Heart Rhythm TV with mentorship from Dr. Daniel Alyesh and Dr. Mehak Dhande. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Journal Club Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron! References – The SUMMIT Trial Pathak, Rajeev K., et al. “Aggressive Risk Factor Reduction Study for Atrial Fibrillation and Implications for the Outcome of Ablation: The ARREST-AF Cohort Study.” Journal of the American College of Cardiology , vol. 64, no. 21, 2014, pp. 2222–2231.…
1 408. Journal Club: The SUMMIT Trial with Dr. Milton Packer 18:42
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التشغيل لاحقا التشغيل لاحقا قوائم إعجاب احبJoin CardioNerds Heart Failure Section Chair Dr. Jenna Skowronski, episode lead Dr. Merna Hussein, and expert faculty Dr. Milton Packer as they discuss the SUMMIT trial . The SUMMIT trial randomized 731 patients with HFpEF with LVEF ≥ 50% and obesity with BMI ≥ 30 kg/m 2 to receive tirzepatide or placebo for at least 52 weeks. The two co-primary endpoints were a composite of time to cardiovascular death or a worsening heart failure event and quality of life measured by the Kansas City Cardiomyopathy Questionnaire clinical summary score (KCCQ-CSS). Treatment with tirzepatide led to a lower risk of the composite of cardiovascular death or worsening heart failure as well as improved quality of life. This episode was planned in collaboration with the American College of Cardiology Section of the Prevention of Cardiovascular Disease with mentorship from Section Chair Dr. Eugenia Gianos. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Journal Club Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron! References – The SUMMIT Trial Packer, M., Zile, M. R., Kramer, C. M., Baum, S. J., Litwin, S. E., Menon, V., Ge, J., Weerakkody, G. J., Ou, Y., Bunck, M. C., Hurt, K. C., Murakami, M., Borlaug, B. A., & SUMMIT Trial Study Group. (2024). Tirzepatide for Heart Failure with Preserved Ejection Fraction and Obesity. The New England Journal of Medicine . https://doi.org/10.1056/NEJMoa2410027…
1 407. Journal Club: The Nex-Z Trial – A CRISPR-Cas9 Based Treatment for ATTR Cardiac Amyloidosis with Dr. Ronald Witteles 19:23
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التشغيل لاحقا التشغيل لاحقا قوائم إعجاب احبJoin CardioNerds Heart Failure Section Chair Dr. Jenna Skowronski, episode lead Dr. Apoorva Gangavelli, and expert faculty Dr. Ronald Witteles as they discuss the Nex-Z trial . This was a phase 1, open-label trial investigating nex-z, a CRISPR-Cas9-based treatment, in 36 patients with transthyretin amyloidosis with cardiomyopathy (ATTR-CM). The primary objectives were aimed at studying the safety and pharmacodynamics of this novel gene-based treatment modality. This episode dives into the nuances of the data, future directions for investigation, and future clinical implications. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Journal Club Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron! References – The Nex-Z Trial Fontana, M., Solomon, S. D., Kachadourian, J., Walsh, L., Rocha, R., Lebwohl, D., Smith, D., Täubel, J., Gane, E. J., Pilebro, B., Adams, D., Razvi, Y., Olbertz, J., Haagensen, A., Zhu, P., Xu, Y., Leung, A., Sonderfan, A., Gutstein, D. E., & Gillmore, J. D. (2024). CRISPR-Cas9 Gene Editing with Nexiguran Ziclumeran for ATTR Cardiomyopathy. The New England Journal of Medicine . https://doi.org/10.1056/NEJMoa2412309…
1 406. Journal Club: The BPROAD Trial with Dr. Keith Ferdinand 26:41
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التشغيل لاحقا التشغيل لاحقا قوائم إعجاب احبJoin CardioNerds co-founder Dr. Daniel Ambinder, episode lead Dr. Nidhi Patel, and expert faculty Dr. Keith Ferdinand as they discuss the BP ROAD trial . The BP ROAD trial randomized 12,821 patients 50 years of age or older with type 2 diabetes, elevated systolic blood pressure, and an increased risk of cardiovascular disease to receive intensive treatment that targeted a systolic blood pressure of less than 120 mm Hg or standard treatment that targeted a systolic blood pressure of less than 140 mm Hg for up to 5 years. Investigators found a significant reduction of major cardiovascular events with intensive blood pressure lowering. This episode dives into the nuances of the data and clinical implications. This episode was planned in collaboration with the American College of Cardiology Section of the Prevention of Cardiovascular Disease with mentorship from Section Chair Dr. Eugenia Gianos. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Journal Club Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron! References – BPROAD Trial Bi, Y., Li, M., Liu, Y., Li, T., Lu, J., Duan, P., Xu, F., Dong, Q., Wang, A., Wang, T., Zheng, R., Chen, Y., Xu, M., Wang, X., Zhang, X., Niu, Y., Kang, Z., Lu, C., Wang, J., … Wang, W. (2024). Intensive Blood-Pressure Control in Patients with Type 2 Diabetes. New England Journal of Medicine . https://doi.org/10.1056/NEJMoa2412006…
1 405. Case Report: Like Mother, Like Son? Peripartum Cardiomyopathy and Infantile Hypertrophic Cardiomyopathy Lead to a Unifying Diagnosis – Mayo Clinic Arizona 31:47
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التشغيل لاحقا التشغيل لاحقا قوائم إعجاب احبCardioNerds (Dr. Dan Ambinder and guest host, Dr. Pooja Prasad) join Dr. Donny Mattia from Phoenix Children’s pediatric cardiology fellowship, Dr. Sri Nayak from the Mayo Clinic – Arizona adult cardiology fellowship, and Dr. Harrison VanDolah from the University of Arizona College of Medicine – Phoenix Med/Peds program for a sunrise hike of Piestewa Peak, followed by some coffee at Berdena’s in Old Town Scottsdale (before the bachelorette parties arrive), then finally a stroll through the Phoenix Desert Botanical Gardens to discuss a thought-provoking case series full of clinical cardiology pearls. Expert commentary is provided by Dr. Tabitha Moe. Episode audio was edited by Dan Ambinder. They discuss the following case: Cardiology is consulted by the OB team for a 27-year-old female G1, now P1, who has just delivered a healthy baby boy at 34 weeks gestation after going into premature labor. She is experiencing shortness of breath and is found to have a significant past cardiac history, including atrial fibrillation and preexcitation, now with a pacemaker and intracardiac defibrillator. We review the differential diagnosis for peripartum cardiomyopathy (PPCM) and then combine findings from her infant son, who is seen by our pediatric cardiology colleagues and is found to have severe hypertrophic cardiomyopathy (HCM). Genetic testing for both ultimately reveals a LAMP2 mutation consistent with Danon Disease. The case discussion focuses on the differential diagnosis for PPCM, HCM, pearls on Danon Disease and other HCM “phenocopies,” and the importance of good history. “To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all.” – Sir William Osler. CardioNerds thank the patients and their loved ones whose stories teach us the Art of Medicine and support our Mission to Democratize Cardiovascular Medicine. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron! Case Media Pearls Peripartum cardiomyopathy is a diagnosis of exclusion – we must exclude other possible etiologies of heart failure! Be on the lookout for features of non-sarcomeric HCM – as Dr. Michelle Kittleson said in Episode 166 , “LVH plus” states. HCM with preexcitation, heart block, strong family history, or extracardiac symptoms such as peripheral neuropathy, myopathy, or cognitive impairment should be evaluated for infiltrative/inherited cardiomyopathies! As an X-linked dominant disorder, Danon disease will present differently in males vs females, with males having much more severe and earlier onset disease with extracardiac features. Making the diagnosis for genetic disorders such as Danon disease is important for getting the rest of family members tested as well as the opportunity for specialized treatments such as gene therapy Up to 5% of Danon disease cases may be due to copy number variants, which may be missed in genetic testing that does not do targeted deletion/duplication analysis!). Notes What is the differential diagnosis for peripartum cardiomyopathy? Peripartum cardiomyopathy is a diagnosis of exclusion – we must exclude other possible etiologies of heart failure! First, ensure that you are not missing an acute life-threatening etiology of acute decompensated heart failure – pulmonary embolism, amniotic fluid embolism, ACS, and SCAD should all be ruled out. Second, a careful history can identify underlying heart disease or risk factors for the development of heart failure, such as substance use, high-risk behaviors that put one at risk for HIV infection, and family history that suggests an inheritable cardiomyopathy. Lastly, a careful review of echocardiographic imaging may also identify underlying etiologies that warrant a change in management. Diagnosis of peripartum cardiomyopathy is important to consider as within 7 days of onset, patients may be eligible for treatment with bromocriptine – consider referring the patient for enrollment in the ongoing RCT ReBIRTH. Check out Cardionerds Episode 113 and the great article linked below for more details on heart failure in pregnancy and postpartum! What is the differential diagnosis for hypertrophic cardiomyopathy? Though by far the most common differential diagnosis for HCM is simple LVH or athlete’s heart, as Dr. Michelle Kittleson taught us in CardioNerds Episode 166, we should “remain alert for “LVH+” states.” It is helpful to think of them in two buckets – sarcomeric mutations (classic HCM) or non-sarcomeric causes (“phenocopies”). If you see systemic signs like peripheral neuropathy, renal dysfunction, or skin changes – clues towards a systemic pathology (for adult colleagues, first think amyloidosis; for peds, colleagues, think genetic syndromes such as RASopathies like Noonan syndrome, glycogen, and lysosomal storage diseases like Fabry). Additionally, certain additional cardiac findings can point towards a non-sarcomeric HCM – recall way back in CardioNerds Episode 68 when our friends at VCU presented a man in his 60s with a history of WPW/preexcitation and HCM and was found to have a PRKAG2 mutation, which is a similar lysosomal vacuolopathy to Danon disease. Another example was seen in Episode 349 when we saw a patient with HCM and heart block who was found to have Fabry disease. What is Danon disease, and how does it present? Danon disease is a rare X-linked dominant genetic disorder due to deficiency in LAMP2 , a glycoprotein involved in protecting the lysosome from its roles in endocytosis and autophagy When deficiency of LAMP2 occurs, products build up into vacuoles and lead to cardiomyocyte dysfunction and death. Interestingly, autophagy disruption is the suspected mechanism of cardiomyopathies from anthracyclines and hydroxychloroquine – Danon disease severity underscores the importance of this process! Estimated prevalence of Danon disease in adult patients with HCM is 1-4%, however when both HCM and pre-excitation are present, this rises to 17%. It is highly penetrant, meaning most patients with the mutation will show symptoms. There are several extracardiac features such as skeletal myopathy, retinopathy, and cognitive impairment – these correlated with areas in the body where LAMP2 is expressed more! Classic presentations – remember that X-linked inheritance results in differential expression between males and females! Males: young onset with severe LVH/HCM and extracardiac phenotype Females: isolated cardiomyopathy (can be either dilated or hypertrophic) with preexcitation arrhythmias with a family history suggesting X-linked dominant transmission (i.e., males more severely affected than females). When taking a family history, note that male-to-male transmission (can’t happen since males don’t pass on an X chromosome to their male children) or female-to-offspring transmission (suggests mitochondrial disease) should prompt alternate diagnosis. However, an estimated 1/3 of Danon disease cases are de novo mutations! See Episode 300 for a great in-depth overview of the pathophysiology of Danon disease How is Danon disease diagnosed? Though there are some proposed characteristic cardiac MRI findings (diffuse LGE sparing the interventricular septum), diagnosis is genetic with a loss-of-function mutation in LAMP2 paired with characteristic cardiac or extracardiac features (see below diagnostic algorithm from Hong et al. JACC 2023) LAMP2 is now included in most hypertrophic and dilated CM panels – if found, it is crucial to ensure the patient’s family members also undergo testing and potentially cardiac evaluation! (Note: up to 5% of Danon disease cases may be due to copy number variants, which may be missed in genetic testing that does not do targeted deletion/duplication analysis!) Differential Diagnosis Sarcomeric HCM – the “classic” HCM, which has numerous genetic causes, all of which affect the sarcomere with age-related penetrance leading to three peaks in age at onset (infancy <1yr, teenage/early adulthood, and mid-adulthood). Progression towards massive LVH and systolic dysfunction is uncommon (<10%) and should raise suspicion of a rare genocopy such as Danon. EKG is usually mostly normal in these patients, unlike in Danon disease, which often has striking abnormalities. Pompe disease – lysosome storage disease from mutations in acid alpha-glucosidase leading to lysosomal glycogen accumulation. Autosomal recessive. It can be an infantile form with severe LVH/HCM, and the later forms can have classic skeletal myopathy as well, but usually, these patients have less severe cardiac features. RAS-opathies – genetic diseases due to mutations in the RAS/MAPkinase pathway. Classic examples are Noonan syndrome, LEOPARD syndrome, and Costello syndrome. All have classic extracardiac manifestations as well as oftentimes HCM, as well as congenital heart disease such as pulmonary valve stenosis. Fabry disease – also an X-linked recessive lysosomal disorder due to alpha-galactosidase A enzyme deficiency; however, it is rarely prominent in childhood and is usually more characterized by extracardiac manifestations. HCM is a cardiac manifestation presenting in the 30s-40s. Friedrich ataxia – autosomal recessive multisystem disease due to GAA sequence expansion in the FXN gene that encodes frataxin, a mitochondrial protein, which impairs mitochondrial oxidative phosphorylation. “HCM” is a common disease manifestation in addition to the classic severe neurologic presentation. Mitochondrial diseases – heterogenous conditions affecting mitochondrial DNA, transmitted in matrilinear pattern, with cardiac hypertrophy being a classic disease manifestation in addition to preexcitation. These may present with severe cognitive impairment than Danon disease. PRKAG2 mutations – cause dysregulation of adenosine monophosphate kinase, culminating in accumulation of vacuoles within glycogen stores. Early-onset cardiac hypertrophy with preexcitation can be similar to Danon disease. There are no extracardiac features and the inheritance pattern is autosomal dominant. For a great summary, see Table 2 in Hong K et al. International Consensus on Differential Diagnosis and Management of Patients with Danon disease: JACC state-of-the-art Review. JACC 2023 Oct, 82 (16) 1628-1647 . For patients who undergo heart transplantation for a genetic/inherited cause, it is crucial to recall their index diagnosis after transplant – they may have extracardiac disease manifestations! References Davis M et al. Peripartum cardiomyopathy: JACC state-of-the-art review. JACC 2020 Jan, 75 (2) 207-221. https://www.jacc.org/doi/10.1016/j.jacc.2019.11.014 DeFilippis EM et al. Cardio-obstetrics and heart failure: JACC: Heart Failure state-of-the-art review. JACC: HF 2023 Sep, 11(9) 1165-1180. https://www.jacc.org/doi/10.1016/j.jchf.2023.07.009_ga=2.84541658.274573079.1723517623-224546423.1716483762 Hong K et al. International consensus on differential diagnosis and management of patients with Danon disease: JACC state-of-the-art review. JACC 2023 Oct, 82 (16) 1628- 1647. https://www.jacc.org/doi/abs/10.1016/j.jacc.2023.08.014 Miliou A et al. Danon cardiomyopathy: specific imaging signs. JACC: Case Rep 2022 Nov 6;4(22):1496-1500. https://www.sciencedirect.com/science/article/pii/S2666084922006015 Padkins MR, Bell MR. 33-year-old woman with postpartum acute shortness of breath. Mayo Clinic Proceedings 2020;95(9):2000-2004 https://www.mayoclinicproceedings.org/article/S0025-6196(20)30713-8/fulltext Rigolli M et al. Cardiac magnetic resonance imaging in Danon disease cardiomyopathy. JACC: Imaging 2021 Feb, 14 (2) 514-516. https://www.jacc.org/doi/10.1016/j.jcmg.2020.08.011…
1 404. Case Report: A Stressful Case of Cardiogenic Shock – Tufts Medical Center 51:52
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التشغيل لاحقا التشغيل لاحقا قوائم إعجاب احبCardioNerds ( Dr. Dan Ambinder and Dr. Yoav Karpenshif – Chair of the CardioNerds Critical Care Cardiology Council) join Dr. Munim Khan, Dr. Shravani Gangidi, and Dr. Rachel Goodman from Tufts Medical Center’s general cardiology fellowship program for hot pot in China Town in Boston. They discuss a case involving a patient who presented with stress cardiomyopathy leading to cardiogenic shock. Expert commentary is provided by Dr. Michael Faulx from the Cleveland Clinic. Notes were drafted by Dr. Rachel Goodman. Audio editing by Dr. Diane Masket . A young woman presents with de novo heart-failure cardiogenic shock requiring temporary mechanical circulatory support who is found to have basal variant takotsubo cardiomyopathy. We review the definition and natural history of takotsubo cardiomyopathy, discuss initial evaluation and echocardiographic findings, and review theories regarding pathophysiology of the clinical syndrome. We also highlight complications of takotsubo cardiomyopathy, with a focus on left ventricular outflow obstruction, cardiogenic shock, and arrythmias. “To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all.” – Sir William Osler. CardioNerds thank the patients and their loved ones whose stories teach us the Art of Medicine and support our Mission to Democratize Cardiovascular Medicine. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron! Pearls Takotsubo cardiomyopathy is defined as a reversible systolic dysfunction with wall motion abnormalities that do not follow a coronary vascular distribution. Takotsubo cardiomyopathy is a diagnosis of exclusion; patients often undergo coronary angiography to rule out epicardial coronary artery disease given an overlap in presentation and symptoms with acute myocardial infarction. There are multiple echocardiographic variants of takotsubo. Apical ballooning is the classic finding, but mid-ventricular, basal, and biventricular variants exist as well. Patients with takotsubo cardiomyopathy generally recover, but there are important complications to be aware of. These include arrhythmia, left ventricular outflow tract (LVOT) obstruction related to a hyperdynamic base in the context of apical ballooning, and cardiogenic shock. Patients with Impella devices are at risk of clot formation and stroke. Assessing the motor current can be a clue to what is happening at the level of the motor or screw. Notes What is Takotsubo Syndrome (TTS)? TTS is a syndrome characterized by acute heart failure without epicardial CAD with regional wall motion abnormalities seen on echocardiography that do not correspond to a coronary artery territory (see below). 1 TTS classically develops following an acute stressor—this can be an emotional or physical stressor. 1 An important feature of TTS is that the systolic dysfunction is reversible. The time frame of reversibility is variable, though generally hours to weeks. 2 Epidemiologically, TTS has a predilection for post-menopausal women, however anyone can develop this syndrome. 1 TTS is a diagnosis of exclusion. Coronary artery disease (acute coronary syndrome, spontaneous coronary artery dissection, coronary embolus, etc) should be excluded when considering TTS. Myocarditis is on the differential diagnosis. What are the echocardiographic findings of takotsubo cardiomyopathy? The classic echocardiographic findings of TTS is “apical ballooning,” which is a way of descripting basal hyperkinesis with mid- and apical hypokinesis, akinesis, or dyskinesis. 3 There are multiple variants of TTS. The four most common are listed below: 3 (1) Apical ballooning (classic TTS) (2) Mid-ventricular variant (3) Basal variant (4) Focal variant Less common variants include the biventricular variant and the isolated right ventricular variant. 3 Do patients with TTS generally have EKG changes or biomarker elevation? Patients often have elevated troponin, though the severity wall motion abnormalities seen on TTE is generally out of proportion to the degree of troponin elevation. 4 BNP/NTproBNP are typically elevated, especially early in the course. 4 During the acute phase (defined as within the first 12 hours), patients may have ST elevation or depression, T wave inversions, new LBBB, or QT prolongation. 4 What are complications of takotsubo cardiomyopathy? Heart failure 2 LV outflow tract obstruction—if there is an LVOT obstruction, it is important to avoid diuretics, vasodilators such as nitroglycerin, and inotropic agents. 2 Cardiogenic shock. 2 Atrial and ventricular arrhythmias. 2 LV thrombus—this is of particular risk in patients with the classic “apical ballooning” variant of takotsubo due to apical akinesis and therefore stagnant flow. 2 References Lyon AR, Citro R, Schneider B, et al. Pathophysiology of Takotsubo Syndrome. J Am Coll Cardiol . 2021;77(7):902-921. doi:10. 1016/j.jacc.2020.10.060 Singh T, Khan H, Gamble DT, Scally C, Newby DE, Dawson D. Takotsubo Syndrome: Pathophysiology, Emerging Concepts, and Clinical Implications. Circulation . 2022;145(13):1002-1019. doi:10.1161/CIRCULATIONAHA.121.055854 Ghadri JR, Wittstein IS, Prasad A, et al. International Expert Consensus Document on Takotsubo Syndrome (Part I): Clinical Characteristics, Diagnostic Criteria, and Pathophysiology. Eur Heart J . 2018;39(22):2032-2046. doi:10.1093/eurheartj/ehy076 Current state of knowledge on Takotsubo syndrome: a Position Statement from the Taskforce on Takotsubo Syndrome of the Heart Failure Association of the European Society of Cardiology – Lyon – 2016 – European Journal of Heart Failure – Wiley Online Library…
1 403. Cardio-Rheumatology: Treating Inflammation and Real-World Implementation of Therapies with Dr. Brittany Weber and Dr. Michael Garshick 36:39
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التشغيل لاحقا التشغيل لاحقا قوائم إعجاب احبIn this episode, CardioNerds Dr. Gurleen Kaur and Dr. Akiva Rosenzveig are joined by Cardio-Rheumatology experts, Dr. Brittany Weber and Dr. Michael Garshick to discuss treating inflammation, delving into the pathophysiology behind the inflammatory hypothesis of atherosclerotic cardiovascular disease and the evolving data on anti-inflammatory therapies for reducing ASCVD risk, with insights on real-world implementation. Show notes were drafted by. Dr. Akiva Rosenzveig. This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Agepha Pharma. American Heart Association’s Scientific Sessions 2024 As heard in this episode, the American Heart Association’s Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It’s a special year you won’t want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100 th birthday. Registration is now open, secure your spot here! When registering, use code NERDS and if you’re among the first 20 to sign up, you’ll receive a free 1-year AHA Professional Membership! Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Prevention Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron! Pearls – Treating Inflammation Our understanding of the pathophysiology of atherosclerosis has undergone a few iterations from the incrustation hypothesis to the lipid hypothesis to the response-to-injury hypothesis and culminating with our current understanding of the inflammation hypothesis. Both the adaptive and innate immune systems play instrumental roles in the pathogenesis of atherosclerosis. After adequately controlling classic modifiable risk factors such as blood pressure, dyslipidemia, glucose intolerance, and obesity, systemic inflammation as assessed by CRP can be ascertained as CRP is associated with ~1.8-fold increased risk of cardiovascular events Although the most common side effect of colchicine is gastrointestinal intolerance, colchicine can induce lactose intolerance, so a lactose free diet may help ameliorate colchicine-induced GI symptoms. Anti-inflammatory therapeutics have shown promise in reducing cardiovascular risk but much more is to be learned with ongoing and future basic, translational, and clinical research. Show notes – Treating Inflammation What are the origins of the inflammatory hypothesis? The first hypothesis as to the pathogenesis of atherosclerosis was the incrustation hypothesis by Carl Von Rokitansky in 1852. He suggested that atherosclerosis begins in the intima with thrombus deposition.In 1856, Rudolf Virchow suggested the lipid hypothesis whereby high levels of cholesterol in the blood lead to atherosclerosis. He observed inflammatory changes in the arterial walls associated with atherosclerotic plaque growth, called endo-arteritis chronica deformans.In 1977, Russell Ross suggested the response-to-injury hypothesis, that atherosclerosis develops from injury to the arterial wall.In the 1990’s the role of inflammation in ASCVD became more recognized. Both the adaptive and innate immune system are critical in atherosclerosis. Lipids and inflammation are synergistic in that lipid exposure is required but they translocate through damaged endothelium which occurs by way of inflammatory cytokines, namely within the NLRP3 inflammasome (IL-1, IL-6 etc.).Smooth muscle cells are also involved. They migrate to the endothelial region and secrete collagen to create the fibrous cap. They can also transform into macrophage-like cells to take up lipids and become foam cells. T, B, and K cells are also part of this milieu. In fact, neutrophils, macrophages and monocytes make up only a small portion of the cells involved in the atherosclerotic process. What are ways to individually optimize one’s ASCVD risk? Ensure the patient is on appropriate antiplatelet therapy, lipid lowering therapy, blood pressure is well controlled, and the Hemoglobin A1c is well controlled. Smoking cessation is pivotal. If the patient has an elevated Lipoprotein (a), pursue more aggressive lipid lowering therapy. Targeted therapies may become available in the future. Assess the patient’s systemic inflammatory risk as measured by C-Reactive Protein (CRP) What is the evidence for util izing CRP in risk stratification? CRP, initially termed Fraction C (discovered as a c polysaccharide component of the pneumococcal cell wall), was first discovered at Rockefeller University in the 1930’s. It was discovered to be an acute phase reactant in the 1940’s and noted to be synthesized in the liver in the 1960’s. Although it is not causal in atherosclerosis, elevated CRP is associated with elevated rates of cardiovascular disease. This was first noted in the landmark New England Journal of Medicine study by Ridker et al that showed elevated CRP was associated with elevated cardiovascular risk and treating with anti-inflammatory medication (aspirin) lowered CRP and CV risk. The statin trials also showed reduction in CRP levels was associated with better outcomes. High-sensitivity CRP (hsCRP) >3 mg/L has odds ratio of ~1.8 for risk of CV disease. Recent analyses of the PROMINENT, REDUCE-IT, and STRENGTH trials demonstrated that hsCRP was a more powerful determinant of recurrent CV events, CV death, and all-cause mortality than LDL-C. After effectively controlling the previously stated modifiable risk factors, what therapeutic options remain in a patient with an elevated CRP? CANTOS trial was the first proof of concept trial investigating Canakinumab (an IL-1 inhibitor) which showed a ~15% relative risk reduction in cardiovascular events CIRT trial investigated methotrexate in patients without autoimmune disease. It was stopped early due to it being a negative trial. This emphasized the complex role inflammation plays in ASCVD, and that both patient selection and chosen anti-inflammatory therapy are important to consider for ASCVD risk reduction. Colchicine has seen a lot of focus in this space with trials such as COLCOT, COPS, LODOCO, LODOCO 2, LODOCO MI. Overall, it appears that colchicine may be more effective in chronic stable ischemic heart disease. The CLEAR SYNERGY trial investigated colchicine in the peri-MI period and was a negative trial. However, we do not yet have the published data to further analyze it. A review article by Potere et al (referenced below) provides a useful summary of novel therapies and upcoming trials in the inflammation in ASCVD space. How do we approach inflammation in women? We know that immune response differs between men and women. Women have more robust immune response to vaccines and viruses and greater innate and adaptive immune responses. Women have slightly higher CRP than men. Studies have shown that average high sensitivity hsCRP is 1.7 for women and 1.2 for men. In the JUPITER trial, the subgroup of patients with hsCRP>7 mg/L had the highest proportion of women relative to men. Regardless, hsCRP remains a reliable predictor of CV events in both men and women. What are some practical considerations when starting colchicine? It may help with adherence, if you walk patients through what to expect with the medication. Obtain renal and liver function tests as both organs contribute to colchicine metabolism and clearance. Obtain a thorough medication reconciliation as colchicine has some notable drug-drug interactions. The most common side effects is GI intolerance; cytopenias are rare occurrences. Note that colchicine can induce lactose intolerance, a potential mechanism for causing GI intolerance, so a lactose free diet may help with adherence. What do we have to look forward to in the anti-inflammation space in CV disease? There is still a lot to be learned and discovered in this space. Some clinical trials to look out for are the ZEUS , ARTEMIS , and HERMES trials which look at Ziltivekimab, an IL-6 inhibitor, in chronic kidney disease, acute myocardial infarction, and heart failure, respectively. References – Treating Inflammation Nidorf SM, Eikelboom JW, Budgeon CA, Thompson PL. Low-dose colchicine for secondary prevention of cardiovascular disease. J Am Coll Cardiol. 2013;61(4):404-410. doi:10.1016/j.jacc.2012.10.027 Nidorf SM, Fiolet ATL, Mosterd A, et al. Colchicine in Patients with Chronic Coronary Disease. N Engl J Med. 2020;383(19):1838-1847. doi:10.1056/NEJMoa2021372 Tardif JC, Kouz S, Waters DD, et al. Efficacy and Safety of Low-Dose Colchicine after Myocardial Infarction. N Engl J Med. 2019;381(26):2497-2505. doi:10.1056/NEJMoa1912388 Hennessy T, Soh L, Bowman M, et al. The Low Dose Colchicine after Myocardial Infarction (LoDoCo-MI) study: A pilot randomized placebo controlled trial of colchicine following acute myocardial infarction. Am Heart J. 2019;215:62-69. doi:10.1016/j.ahj.2019.06.003 Tong DC, Quinn S, Nasis A, et al. Colchicine in Patients With Acute Coronary Syndrome: The Australian COPS Randomized Clinical Trial. Circulation. 2020;142(20):1890-1900. doi:10.1161/CIRCULATIONAHA.120.050771 Ridker PM, Everett BM, Thuren T, et al. Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease. N Engl J Med. 2017;377(12):1119-1131. doi:10.1056/NEJMoa1707914 Ridker PM, Everett BM, Pradhan A, et al. Low-Dose Methotrexate for the Prevention of Atherosclerotic Events. N Engl J Med. 2019;380(8):752-762. doi:10.1056/NEJMoa1809798 Potere N, Bonaventura A, Abbate A. Novel Therapeutics and Upcoming Clinical Trials Targeting Inflammation in Cardiovascular Diseases. Arterioscler Thromb Vasc Biol. Published online October 10, 2024. doi:10.1161/ATVBAHA.124.319980 Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men [published correction appears in N Engl J Med 1997 Jul 31;337(5):356]. N Engl J Med. 1997;336(14):973-979. doi:10.1056/NEJM199704033361401 Ridker PM, Danielson E, Fonseca FA, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008;359(21):2195-2207. doi:10.1056/NEJMoa0807646 Ridker PM, Bhatt DL, Pradhan AD, et al. Inflammation and cholesterol as predictors of cardiovascular events among patients receiving statin therapy: a collaborative analysis of three randomised trials. Lancet. 2023;401(10384):1293-1301. doi:10.1016/S0140-6736(23)00215-5 Fernandez DM, Rahman AH, Fernandez NF, et al. Single-cell immune landscape of human atherosclerotic plaques. Nat Med. 2019;25(10):1576-1588. doi:10.1038/s41591-019-0590-4 Moran CA, Collins LF, Beydoun N, et al. Cardiovascular Implications of Immune Disorders in Women. Circ Res. 2022;130(4):593-610. doi:10.1161/CIRCRESAHA.121.319877 Kushner I. C-reactive protein – My perspective on its first half century, 1930-1982. Front Immunol. 2023;14:1150103. Published 2023 Mar 2. doi:10.3389/fimmu.2023.1150103…
1 402. Guidelines: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure – Question #39 with Dr. Robert Mentz 8:00
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التشغيل لاحقا التشغيل لاحقا قوائم إعجاب احبThe following question refers to Sections 7.3.3 and 7.3.6 of the 2022 ACC/AHA/HFSA Guideline for the Management of Heart Failure.The question is asked by Palisades Medical Center medicine resident & CardioNerds Academy Fellow Dr. Maryam Barkhordarian, answered first by UTSW AHFT Cardiologist & CardioNerds FIT Ambassador Dr. Natalie Tapaskar, and then by expert faculty Dr. Robert Mentz.Dr. Mentz is associate professor of medicine and section chief for Heart Failure at Duke University, a clinical researcher at the Duke Clinical Research Institute, and editor-in-chief of the Journal of Cardiac Failure. Dr. Mentz has been a mentor for the CardioNerds Clinical Trials Network as lead principal investigator for PARAGLIDE-HF and is a series mentor for this very Decipher the Guidelines Series. For these reasons and many more, he was awarded the Master CardioNerd Award during ACC22.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. American Heart Association’s Scientific Sessions 2024As heard in this episode, the American Heart Association’s Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It’s a special year you won’t want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here!When registering, use code NERDS and if you’re among the first 20 to sign up, you’ll receive a free 1-year AHA Professional Membership! Question #39 Ms. Kay Lotsa is a 48-year-old woman with a history of CKD stage 2 (baseline creatinine ~1.2 mg/dL) & type 2 diabetes mellitus. She has recently noticed progressively reduced exercise tolerance, leg swelling, and trouble lying flat. This prompted a hospital admission with a new diagnosis of decompensated heart failure. A transthoracic echocardiogram reveals LVEF of 35%. Ms. Lotsa is diuresed to euvolemia, and she is started on carvedilol 25mg BID, sacubitril/valsartan 49-51mg BID, and empagliflozin 10mg daily, which she tolerates well. Her eGFR is at her baseline of 55 mL/min/1.73 m2 and serum potassium concentration is 3.9 mEq/L. Your team is anticipating she will be discharged home in the next one to two days and wants to start spironolactone. Which of the following is most important regarding her treatment with mineralocorticoid antagonists?ASpironolactone is contraindicated based on her level of renal impairment and should not be startedBSerum potassium levels and kidney function should be assessed within 1-2 weeks of starting spironolactoneCEplerenone confers a higher risk of gynecomastia than does spironolactoneDThe patient will likely not benefit from initiation of spironolactone if her cardiomyopathy is ischemic in origin Answer #39 ExplanationThe correct answer is B – after starting a mineralocorticoid receptor antagonist (MRA), it is important to closely monitor renal function and serum potassium levels.MRA (also known as aldosterone antagonists or anti-mineralocorticoids) show consistent improvements in all-cause mortality, HF hospitalizations, and SCD across a wide range of patients with HFrEF.…
1 401. Guidelines: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure – Question #38 with Dr. Randall Starling 12:33
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التشغيل لاحقا التشغيل لاحقا قوائم إعجاب احبThe following question refers to Sections 7.4 and 7.5 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by the Director of the CardioNerds Internship Dr. Akiva Rosenzveig, answered first by Vanderbilt AHFT cardiology fellow Dr. Jenna Skowronski, and then by expert faculty Dr. Randall Starling.Dr. Starling is Professor of Medicine and an advanced heart failure and transplant cardiologist at the Cleveland Clinic where he was formerly the Section Head of Heart Failure, Vice Chairman of Cardiovascular Medicine, and member of the Cleveland Clinic Board of Governors. Dr. Starling is also Past President of the Heart Failure Society of America in 2018-2019. Dr. Staring was among the earliest CardioNerds faculty guests and has since been a valuable source of mentorship and inspiration. Dr. Starling’s sponsorship and support was instrumental in the origins of the CardioNerds Clinical Trials Program.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. American Heart Association’s Scientific Sessions 2024As heard in this episode, the American Heart Association’s Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It’s a special year you won’t want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here!When registering, use code NERDS and if you’re among the first 20 to sign up, you’ll receive a free 1-year AHA Professional Membership! Question #38 Mrs. M is a 65-year-old woman with non-ischemic dilated cardiomyopathy (LVEF 40%) and moderate to severe mitral regurgitation (MR) presenting for outpatient follow-up. Despite improvement overall, she continues to experience dyspnea on exertion with two flights of stairs and occasional PND. She reports adherence with her medication regimen of sacubitril-valsartan 97-103mg twice daily, metoprolol succinate 200mg daily, spironolactone 25mg daily, empagliflozin 10mg daily, and furosemide 80mg daily. A transthoracic echocardiogram today shows an LVEF of 35%, an LVESD of 60 mm, severe MR with a regurgitant fraction of 60%, and an estimated right ventricular systolic pressure of 40 mmHg. Her EKG shows normal sinus rhythm at 65 bpm and a QRS complex width of 100 ms. What is the most appropriate recommendation for management of her heart failure?AContinue maximally tolerated GDMT; no other changesBRefer for cardiac resynchronization therapy (CRT)CRefer for transcatheter mitral valve intervention Answer #38 ExplanationChoice C is correct. The 2020 ACC/AHA Guidelines for the management of patients with valvular heart disease outline specific recommendations.In patients with chronic severe secondary MR related to LV systolic dysfunction (LVEF <50%) who have persistent symptoms (NYHA class II, III, or IV) while on optimal GDMT for HF (Stage D), M-TEER is reasonable in patients with appropriate anatomy as defined on TEE and with LVEF between 20% and 50%, LVESD ≤70 mm, and pulmonary artery systolic pressure ≤70 mmHg (Class 2a, LOE B-R).Conversely,…
1 400. Cardio-Rheumatology: Targeting Inflammation for Cardiovascular Risk Reduction with Dr. Paul Ridker 51:13
51:13 التشغيل لاحقا التشغيل لاحقا قوائم إعجاب احب51:13
التشغيل لاحقا التشغيل لاحقا قوائم إعجاب احبIn this episode, Dr. Paul Ridker, a pioneer in the field of cardiovascular inflammation, joins the CardioNerds (Dr. Gurleen Kaur, Dr. Richard Ferraro, and Dr. Nidhi Patel) to discuss the evolving landscape of inflammation as a key factor in cardiovascular risk reduction. The discussion dives into the importance of biomarkers like high-sensitivity C-reactive protein (hs-CRP) in guiding treatment strategies, the insights gleaned from landmark trials like the JUPITER and CANTOS studies, and the future of targeted anti-inflammatory therapies in cardiology. Show notes were drafted by Dr. Nidhi Patel. Audio editing by CardioNerds academy intern, Grace Qiu. This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Lexicon Pharmaceuticals. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Targeting Inflammation for Cardiovascular Risk "If you don’t measure it, you can’t treat it”: Incorporate hs-CRP into routine practice for patients at risk of cardiovascular events, as it provides crucial information for risk stratification and management. Recognize the dual benefits of statins in lowering both LDL and inflammation, particularly in patients with elevated hs-CRP. Encourage patients to adopt heart-healthy habits, as lifestyle changes remain foundational in reducing both cholesterol and inflammatory risk. Reminder that most autoimmune or inflammatory diseases, from psoriasis to Addison’s disease to lupus to scleroderma to inflammatory bowel disease, have been shown to have elevated cardiovascular risk Ongoing randomized trials including ZEUS, HERMES, and ARTEMIS will inform whether novel targeting of IL-6 can safely lower cardiovascular event rates or slow renal progression Show notes - Targeting Inflammation for Cardiovascular Risk Why is it important to measure both LDL and hs-CRP, and what factors increase hs-CRP? Inflammation and hyperlipidemia are synergistic in promoting atherosclerosis. They interact to exacerbate plaque formation and instability, increasing the risk of cardiovascular events. Just like we measure blood pressure and LDL to know what to treat, we should measure hs-CRP to guide targeted therapy. Clinical Example: in Ms. Flame's case, despite achieving target LDL levels with statins, her elevated hs-CRP indicates ongoing inflammation and residual cardiovascular risk that should be assessed. Residual inflammatory risk should be assessed in both primary and secondary prevention. Increased BMI1, smoking2, a sedentary lifestyle3, and genetics4 (such as a higher risk of metabolic disease in South Asians) all raise hs-CRP levels. SGLTi5 and GLP-1 agonists6 have also been shown to decrease hs-CRP levels. What data do we have to support measuring hs-CRP? Women’s Health Study7: an early study showing that hs-CRP predicted risk at least as well as LDL cholesterol and that models incorporating hs-CRP in addition to lipids were significantly better at predicting risk than models based on lipids alone. JUPITER Trial8 (Primary Prevention): Among patients with normal LDL but elevated hs-CRP there was a 44% reduction in major cardiovascular events (>50% in MI and stroke) and a 20% reduction in all-cause mortality in patients treated with statins. These results led to changes in guidelines in recognizing the need to measure and treat inflammation. CANTOS Trial9 (Secondary Prevention): Randomized >10K patients with previous MI and hs-CRP ≥ 2mg/L and found that canakinumab reduced hs-CRP level from baseline in a dose-dependent manner, without reduction in the LDL, ApoB, TG, or blood pressure. What are the guidelines and supportive data on using Colchicine?…
1 399. Guidelines: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure – Question #37 with Dr. Clyde Yancy 8:40
8:40 التشغيل لاحقا التشغيل لاحقا قوائم إعجاب احب8:40
التشغيل لاحقا التشغيل لاحقا قوائم إعجاب احبThe following question refers to Section 7.4 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by the Director of the CardioNerds Internship Dr. Akiva Rosenzveig, answered first by Vanderbilt AHFT cardiology fellow Dr. Jenna Skowronski, and then by expert faculty Dr. Clyde Yancy.Dr. Yancy is Professor of Medicine and Medical Social Sciences, Chief of Cardiology, and Vice Dean for Diversity and Inclusion at Northwestern University, and a member of the ACC/AHA Joint Committee on Clinical Practice Guidelines.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. American Heart Association’s Scientific Sessions 2024As heard in this episode, the American Heart Association’s Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It’s a special year you won’t want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here!When registering, use code NERDS and if you’re among the first 20 to sign up, you’ll receive a free 1-year AHA Professional Membership! Question #37 Mr. S is an 80-year-old man with a history of hypertension, type II diabetes mellitus, and hypothyroidism who had an anterior myocardial infarction (MI) treated with a drug-eluting stent to the left anterior descending artery (LAD) 45 days ago. His course was complicated by a new LVEF reduction to 30%, and left bundle branch block (LBBB) with QRS duration of 152 ms in normal sinus rhythm. He reports he is feeling well and is able to enjoy gardening without symptoms, though he experiences dyspnea while walking to his bedroom on the second floor of his house. Repeat TTE shows persistent LVEF of 30% despite initiation of goal-directed medical therapy (GDMT). What is the best next step in his management?AMonitor for LVEF improvement for a total of 60 days prior to further interventionBImplantation of a dual-chamber ICDCImplantation of a CRT-DDContinue current management as device implantation is contraindicated given his advanced age Answer #37 Explanation Choice C is correct. Implantation of a CRT-D is the best next step. In patients with nonischemic DCM or ischemic heart disease at least 40 days post-MI with LVEF ≤35% and NYHA class II or III symptoms on chronic GDMT, who have reasonable expectation of meaningful survival for >1 year,ICD therapy is recommended for primary prevention of SCD to reduce total mortality (Class 1, LOE A). A transvenous ICD provides high economic value in this setting, particularly when a patient’s risk of death from ventricular arrhythmia is deemed high and the risk of nonarrhythmic death is deemed low. In addition, for patients who have LVEF ≤35%, sinus rhythm, left bundle branch block (LBBB) with a QRS duration ≥150 ms, and NYHA class II, III, orambulatory IV symptoms on GDMT, cardiac resynchronization therapy (CRT) is indicated to reduce total mortality, reduce hospitalizations, and improve symptoms and QOL. Cardiac resynchronization provides high economic value in this setting. Mr.…
1 398. Narratives in Cardiology: Career Flexibility in Cardiology with Dr. Minnow Walsh 35:38
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التشغيل لاحقا التشغيل لاحقا قوائم إعجاب احبIn this episode, Dr. Gurleen Kaur (Cardiology FIT at Brigham and Women’s Hospital and APD of the CardioNerds Academy) and Dr. Diane Masket (Medicine Resident at the University of Chicago Northshore and CardioNerds Academy Intern) discuss with Dr. Minnow Walsh (Medical Director of the Heart Failure and Cardiovascular programs at Ascension St. Vincent Heart Center in Indianapolis) about her personal and professional journey in Cardiology. They discuss Dr. Walsh’s authorship of the recent ACC statement on career flexibility in Cardiology, her involvement with the ACC at both the local and national levels, and her passion for making cardiology a more inclusive and welcoming field for all. Notes were drafted by Dr. Diane Masket and episode audio was engineered by student Dr. Grace Qiu. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Video version - Career Flexibility in Cardiology https://youtu.be/ygNH6fcQ5ek Quoatables - Career Flexibility in Cardiology “You have to learn to live with ambivalence. You can’t do everything. You can’t do everything all at one time” “One of the most important things the College is behind and pushing, is that competency-based evaluation is what should be used in fellowship rather than this sort of cookie cutter approach where you have to do these many months of echo and this much of cath lab. So, I think flexibility moving from volume to competency is one push.” “Fellowship is daunting, and internal medicine residency is too, but I think culture is how we feel every day. And I think the more we increase flexibility the more that culture is going to shift. Notes - Career Flexibility in Cardiology Process of developing ACC Health Policy Statements These documents address issues that require ACC influence and usually involve a variety of institutions, governing bodies, and other stakeholders. ACC comes to an agreement on how they will approach this topic and shares it broadly. Most of the existing ACC health policy statements are disease-based instead of profession-based. The ACC Career Flexibility statement grew out of the diversity, equity, and inclusion task force, which is a standing committee. A variety of authors are included in health policy statements to reflect the perspectives of many different interest groups. All policy statements, including the one about career flexibility, are available online on JACC.org 1 Major Components of the ACC Career Flexibility Health Policy Statement There are 18 principles that highlight the most important aspects regarding career flexibility in cardiology.2 Flexibility allows for deceleration (decrease in work hours, responsibilities, etc.) and acceleration based on the needs of the physician. For example, during childbearing and rearing time periods, there could be a deceleration, which could accelerate when parenthood responsibilities have decreased. It does not only need to be based around parenting; physicians who are not parents also desire flexibility and enjoy spending time on activities other than their careers. These needs will be unique for each person.…
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