Cardionerds: A Cardiology Podcast

CardioNerds

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!

Episodes

Mentioned books

Sep 27, 2021 • 14min

149. The Evolution Of The Neurohormonal Hypothesis With Dr. Milton Packer: Part 4 – SGLT2 Inhibitors – Under-Promised & Over-Delivered

CardioNerds (Amit Goyal, Daniel Ambinder) and Dr. Mark Belkin, (CardioNerds Correspondent) and Dr. Shirlene Obuobi (CardioNerds Ambassador) from University of Chicago are honored to bring to you the Dr. Milton Packer perspective on the evolution of the neurohormonal hypothesis as part of The CardioNerds Heart Success Series. In part 4, Dr. Packer shares his perspective on the revolutionary SGLT2 inhibors. We discuss the mechanisms of action and the data regarding their role in the care of heart failure patients. This episode is particularly historic in that Dr. Packer shares his thoughts about the EMPEROR-PRESERVED trial well before the data was available. Also see Dr. Mark Belkin’s DocWire News article EMPEROR’s New Groove? Empagliflozin Provides Long-Awaited Treatment for HFpEF where Dr. Packer is quoted as saying “we are pleased to have the first trial in patients with HFpEF that shows an unequivocally positive and clinically important result. We are looking forward to many secondary papers that will provide detailed information about what we have found, and what it means for patients.” Check out the CardioNerds Heart Failure Success Series Page for more heart success episodes and content! This is a non CME episode. Disclosures: Milton Packer reports receiving consulting fees from Abbvie, Actavis, Amgen, Amarin, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Casana, CSL Behring, Cytokinetics, Johnson & Johnson Health Care Systems Inc., Eli Lilly and Company, Moderna, Novartis, ParatusRx, Pfizer, Relypsa, Salamandra, Synthetic Biologics, Teva Pharmaceuticals USA Inc. and Theravance Biopharma Inc. CardioNerds Heart Failure Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! This CardioNerds Heart Failure Success Series was created in memory of Dr. David Taylor. We thank our partners at the Heart Failure Society of America which is a multidisciplinary organization working to improve and expand heart failure care through collaboration, education, research, innovation, and advocacy. Its members include physicians, scientists, nurses, nurse practitioners, and pharmacists. Learn more at hfsa.org.

Sep 20, 2021 • 0sec

148. The Evolution Of The Neurohormonal Hypothesis With Dr. Milton Packer: Part 3 – Neutral Trials, A 2nd Chance, & A Paradigm Shift

CardioNerds (Amit Goyal, Daniel Ambinder) and Dr. Mark Belkin, (CardioNerds Correspondent) and Dr. Shirlene Obuobi (CardioNerds Ambassador) from University of Chicago are honored to bring to you the Dr. Milton Packer perspective on the evolution of the neurohormonal hypothesis as part of The CardioNerds Heart Success Series. In part 3 Dr. Packer reflects on the value of neutral trials and recounts the journey that led to the PARADIGM Trial Check out the CardioNerds Heart Failure Success Series Page for more heart success episodes and content! This is a non CME episode. Disclosures: Milton Packer reports receiving consulting fees from Abbvie, Actavis, Amgen, Amarin, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Casana, CSL Behring, Cytokinetics, Johnson & Johnson Health Care Systems Inc., Eli Lilly and Company, Moderna, Novartis, ParatusRx, Pfizer, Relypsa, Salamandra, Synthetic Biologics, Teva Pharmaceuticals USA Inc. and Theravance Biopharma Inc. CardioNerds Heart Failure Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! This CardioNerds Heart Failure Success Series was created in memory of Dr. David Taylor. We thank our partners at the Heart Failure Society of America which is a multidisciplinary organization working to improve and expand heart failure care through collaboration, education, research, innovation, and advocacy. Its members include physicians, scientists, nurses, nurse practitioners, and pharmacists. Learn more at hfsa.org.

Sep 20, 2021 • 15min

147. The Evolution Of The Neurohormonal Hypothesis With Dr. Milton Packer: Part 2 – The Secret To Happiness, The “Aha” Moment, & The Birth Of The Neurohormonal Hypothesis

CardioNerds (Amit Goyal, Daniel Ambinder) and Dr. Mark Belkin, (CardioNerds Correspondent) and Dr. Shirlene Obuobi (CardioNerds Ambassador) from University of Chicago are honored to bring to you the Dr. Milton Packer perspective on the evolution of the neurohormonal hypothesis as part of The CardioNerds Heart Success Series. In part 2 Dr. Packer shares his journey as the trailing spouse and tells the story of how the neurohormonal hypothesis was developed. Check out the CardioNerds Heart Failure Success Series Page for more heart success episodes and content! This is a non CME episode. Disclosures: Milton Packer reports receiving consulting fees from Abbvie, Actavis, Amgen, Amarin, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Casana, CSL Behring, Cytokinetics, Johnson & Johnson Health Care Systems Inc., Eli Lilly and Company, Moderna, Novartis, ParatusRx, Pfizer, Relypsa, Salamandra, Synthetic Biologics, Teva Pharmaceuticals USA Inc. and Theravance Biopharma Inc. CardioNerds Heart Failure Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! This CardioNerds Heart Failure Success Series was created in memory of Dr. David Taylor. We thank our partners at the Heart Failure Society of America which is a multidisciplinary organization working to improve and expand heart failure care through collaboration, education, research, innovation, and advocacy. Its members include physicians, scientists, nurses, nurse practitioners, and pharmacists. Learn more at hfsa.org.

Sep 19, 2021 • 26min

146. The Evolution Of The Neurohormonal Hypothesis With Dr. Milton Packer: Part 1 – Taking Risks, Upsetting People, & Disrupting The Status Quo

CardioNerds (Amit Goyal, Daniel Ambinder) and Dr. Mark Belkin, (CardioNerds Correspondent) and Dr. Shirlene Obuobi (CardioNerds Ambassador) from University of Chicago are honored to bring to you the Dr. Milton Packer perspective on the evolution of the neurohormonal hypothesis as part of The CardioNerds Heart Success Series. In part 1 Dr. Packer discusses taking risks, upsetting people and the ridiculousness of humanity and how stand-up comedy helped contribute and shape his career in cardiovascular medicine. Dr. Packer also discusses how the study of afterload agents in heart failure and the discovery of tachyphylaxis with prazosin helped inspire a long and prosperous career in academic cardiology by changing the status quo. Check out the CardioNerds Heart Failure Success Series Page for more heart success episodes and content! This is a non CME episode. Disclosures: Milton Packer reports receiving consulting fees from Abbvie, Actavis, Amgen, Amarin, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Casana, CSL Behring, Cytokinetics, Johnson & Johnson Health Care Systems Inc., Eli Lilly and Company, Moderna, Novartis, ParatusRx, Pfizer, Relypsa, Salamandra, Synthetic Biologics, Teva Pharmaceuticals USA Inc. and Theravance Biopharma Inc. CardioNerds Heart Failure Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! This CardioNerds Heart Failure Success Series was created in memory of Dr. David Taylor. We thank our partners at the Heart Failure Society of America which is a multidisciplinary organization working to improve and expand heart failure care through collaboration, education, research, innovation, and advocacy. Its members include physicians, scientists, nurses, nurse practitioners, and pharmacists. Learn more at hfsa.org.

Sep 14, 2021 • 1h 4min

145. ACHD: Pregnancy and Congenital Heart Disease with Dr. Carole Warnes

Sep 5, 2021 • 41min

144. Case Report: A Mother with Shortness of Breath – Pushing Against All Odds – Allegheny General Hospital

CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Kushani Gajjar and Dr. Mitha Naik from the Allegheny Health Network for a walk along the Three Rivers Trail in Pittsburgh. They discuss a case of young woman in her third trimester of pregnancy with a known history of pulmonary arterial hypertension. The management of pulmonary hypertension in pregnancy and RV failure in the context of pregnancy is described. The E-CPR segment is provided by Dr. Nandita Scott, Co-Director Corrigan Women’s Heart Health Program and Cardiovascular Disease and Pregnancy Service at Massachusetts General Hospital. Special cameo appearance by Dr. Dani Crousillat. If you’re a current internal medicine resident, interested in the intersection between medical education, cardiovascular disease and digital media, consider applying to the CardioNerds Academy using this link. The deadline for this application is October 15th 2021. Learn more by visiting the CardioNerds Academy page. Claim free CME just for enjoying this episode! Disclosures: None Jump to: Patient summary – Case media – Case teaching – References 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! Patient Summary – Pulmonary Hypertension in Pregnancy A 33-year-old woman in the third trimester of pregnancy, with a known history of untreated PAH in the setting of TKI therapy, presents with shortness of breath. She is found to have PA pressure greater than systemic pressure with PASP >130. We describe the management of PH and RV failure in the context of a pregnancy. The patient was admitted to the ICU where a multidisciplinary team was mobilized, involving high risk ob-gyn, maternal fetal medicine, critical care, anesthesiology, and advanced heart failure. They began pulmonary vasodilators including treprostinil, tadalafil and inhaled nitric oxide. They also added inotropic and vasopressor support for right ventricular dysfunction with her severe PAH. Fetal heart monitoring was performed. PAH also led to worsening of known chronic thrombocytopenia in the setting of CML. HELLP syndrome was ruled out. The patient had preterm rupture of membranes at 32 weeks of gestation and the team pursued assisted vaginal delivery to prevent vagal response. Following successful delivery, the patient elected to undergo intra-uterine device placement. Post-delivery, vasopressors and inotropes were weaned, and she was discharged on treprostinil, ambrisentan and tadalafil. Thankfully both the mother and baby returned healthy and well at 1 month follow up. Case Media – Pulmonary Hypertension in Pregnancy CMR CXR TTE TTE Click to Enlarge Episode Teaching – Pulmonary Hypertension in Pregnancy Pearls – Pulmonary Hypertension in Pregnancy Pulmonary Hypertension is defined as a mean pulmonary arterial pressure (mPAP) of >20mmHg. There are 5 major types of pulmonary hypertension. Risk modifiers include symptom burden, exercise capacity, presence of pericardial effusion, RV function and hemodynamics. Multidisciplinary care teams are the key to achieving optimal pregnancy outcomes in patients with PH. It is critical to create a team of experts with experience in pulmonary hypertension and plan for constant communication before, during, and after pregnancy. Pregnant women who are already on PAH therapy outpatient should continue them during pregnancy (under the direction of PH experts) except for endothelin receptor blockers which fall in pregnancy category X. PH during pregnancy is associated with up to 38% maternal mortality rate as the right ventricle (RV) is often unable to handle the volume shifts and hemodynamic changes that occur during pregnancy, labor, and delivery. Patients with RV failure leading to low cardiac output and hypotension, like in this case, may benefit from vasopressors with the goal to maintain systemic blood pressure above pulmonary arterial pressures, preserving right coronary blood flow and preventing intracardiac shunting. Swan-guided management may be useful – to titrate inotropes and vasopressors, optimize pulmonary vasodilators and ensure that the patient is being adequately fluid-optimized to maintain a CVP of around 8-10. Notes – Pulmonary Hypertension in Pregnancy 1. What are the different types of pulmonary hypertension (PH)?The WHO separates PH into 5 groups: Group 1 Pulmonary arterial hypertension (e.g., idiopathic, heritable [BMPR2], anorexigen associated, drug or toxin-associated, HIV, connective tissue disease associated, schistosomiasis, portal hypertension, congenital heart disease, etc) Group 2 Pulmonary hypertension due to left sided heart disease (e.g., HFrEF, HFpEF, left-side valvular heart disease) Group 3 Pulmonary hypertension due to lung disease or hypoxia: (e.g., COPD, ILD, OSA, hypoxia without lung disease such as high altitude, developmental lung disorders) Group 4 PH due to pulmonary artery obstructions most commonly Chronic Thromboembolic Pulmonary Hypertension (CTEPH) Group 5 Multifactorial causes such as hematologic disorders (chronic hemolytic anemia, as with myeloproliferative disorders), metabolic disorders (e.g., Gaucher disease, glycogen storage diseases, CKD), and systemic disorders (e.g., pulmonary Langerhans cell histiocytosis, neurofibromatosis, sarcoidosis) 2. What is the role of TTE and RHC in the workup of PH? Tyrosine kinase inhibitors are known to cause PAH and there should be a low threshold to do screening TTEs in these patients when there is concern for the development of PAH. Echocardiogram is essential in the evaluation of PH –for positing the presence of PH, evaluating the left heart and congenital defects for clues to PH etiology, and assessing the structural consequences of PH on the right heart. In addition to estimating the pulmonary artery systolic pressure (PASP) by measuring the tricuspid regurgitant jet, we can characterize RV and RA size, RV function, and RV wall thickness, which may help both support the diagnosis and gauge prognosis for PH. Further, we can evaluate for left-sided heart disease contributing to PH. The presence of a pericardial effusion is a poor prognostic sign in those with pulmonary hypertension. Notably, the PASP is not of prognostic value due both to inaccuracies in measurement and falling values in the context of severe PH with failing RV function; a such PASP should not be used to surveil patients with PH or monitor response to PH therapies. McLaughlin et al suggest using a checklist in the echocardiographic assessment of PH which includes the following1: Checklist Salient points Estimated PASP To calculate mean PAP, usually PA diastolic pressure needs to be assessed which often requires a PR jet which is both difficult to obtain and not often present. Evaluate RV size and function Size: abnormal RV basal diameter >4.2 cm, wall thickness in subcostal view >5 mm Function: TAPSE (abnormal <16cm), RV tissue Doppler S’ velocity(abnormal <10cm/s at base) and RV fractional area change (abnormal <35%). Septal flattening: in systole = RV pressure overload and in diastole = RV volume overload Evaluate severity of TR Features suggestive of severe TR include dense TR jet on continuous-wave Doppler, V-wave cutoff sign; and systolic flow reversal on hepatic vein pulse-wave Doppler imaging Evaluate for causes of PH Left heart disease: look for overt LV systolic dysfunction, grade 2 or worse diastolic dysfunction, severe aortic or mitral valvular disease, and less common abnormalities of the left heart (e.g., hypertrophic cardiomyopathy, cor triatriatum). Shunt lesions: perform agitated saline bubble study Right heart catheterization is necessary to confirm the diagnosis of PH. The updated hemodynamic definition of PH hinges on accurate hemodynamic assessment. In a PH crisis, such as our patient, it is also important to delineate the impact of PH on the RV. Invasive hemodynamic testing is the gold standard for differentiating isolated precapillary, isolated postcapillary and combined pre and post capillary PH (see table below). When we consider the hemodynamic profiles of pulmonary hypertension, we break down PH into isolated pre-capillary, isolated post-capillary, or combined pre-and post-capillary pulmonary hypertension as shows in the table below. Mean Pulmonary Artery Pressure (mmHg) Wedge Pressure (mmHg) Pulmonary Vascular Resistance (Woods Units) WHO Groups Pre-capillary > 20 ≤ 15 ≥ 3 1, 3, 4, 5 Post-capillary > 20 > 15 < 3 2, 5 Combined pre- and post-capillary > 20 > 15 ≥ 3 2, 5, multifactorial Furthermore, we can determine if a patient is “vasodilator responsive.” In the catheterization lab, a positive vasodilator response is defined as a decrease in mPAP ≥ 10 mmHg to an absolute value of ≤ 40 mmHg (without a decrease in cardiac output) with the use of inhaled nitric oxide or IV epoprostenol. If a patient has positive vasodilator test, calcium channel blockers can be initiated, however not all patients will be long term responders. We tend to do vasoreactivity testing in patients with PAH and not for other forms of PH (e.g., Pulmonary Veno-Occlusive Disease or Groups 2, 3, 4, or 5). 3. What are PAH-specific pharmacologic treatments? Remember that PAH is fundamentally a disease of increased pulmonary vascular resistance (PVR) causing elevated pulmonary pressures. The consequence of increased PVR includes increased RV afterload and hypoxemia and the subsequent clinical manifestations of PAH. Normally, the pulmonary vascular bed has a balance between vasodilators and vasoconstrictors that maintain a low-resistance, high-compliance state. This balance is disturbed in PAH and the goal of therapy is to “restore” balance between vasodilation and vasoconstriction. The management of PAH relies on 3 primary medication groups1: Nitric oxide pathway PDE5 inhibitors: Sildenafil and tadalafil. These medications prevent the breakdown of cGMP which mediates the potent vasodilator and inhibitor of platelet aggregation, nitric oxide.Soluble guanylate cyclase (sGC) stimulators: riociguat. These medications stimulate sGC and thus increase sensitivity to NO. Riociguat is primarily used in CTEPH, but can also be used in PAH (PATENT-1 and -2 Trials) including PAH associated with sickle cell disease Endothelin-1 (ET-1) pathway Endothelin receptor antagonists (ERAs): macitentan, bosentan, ambrisentan. Common side effects are lower extremity edema and hepatotoxicity. NOTE: patients should not get pregnant on ERAs because of teratogenicity! Prostacyclin Pathway Prostacyclin analogs: epoprostenol, iloprost, treprostinil. Prostacyclin is a potent endogenous vasodilator and inhibits platelet aggregation. This class of medications have PO, SQ, IV, and inhaled formulations. Common side effects include headache, diarrhea, nausea, and jaw pain.PCA-receptor agonist: selexipag (oral). Also remember calcium channel blockers in vasodilator responsive patients with PAH! Other aspects of pharmacologic PAH treatment not discussed here include diuretics, digoxin, and oral anticoagulation, especially for patients with more advanced disease and on continuous parenteral prostacyclin therapy due to microthrombi in pulmonary arterioles. 4. What is the impact of pregnancy in PH? Prevalence of pulmonary hypertension has been rising due to the number of patient with congenital heart disease living to childbearing age, as well as the emergence of effective pulmonary vascular therapy.2,3 According to one widely quoted systemic analysis, although a publication bias cannot be excluded, overall maternal mortality was significantly lower compared with previous era (25 vs. 38%, P = 0.047). Seventy-eight per cent of deaths occurred within the first month after delivery. Primigravidae and parturients who received general anesthesia were at higher risk of death. Maternal mortality in parturients with PAH remains prohibitively high, despite lower death rates than in previous decades. Early counseling regarding pregnancy risks, including contraception, remains paramount. Women with PAH who become pregnant warrant a multidisciplinary approach with consideration of advanced therapies and discussion of pregnancy termination.3-5 Morbidity and mortality were highest in women with idiopathic PH, and lowest in women with PH due to left sided heart disease. Complications were also higher in patient with severe PH (RVSP >70mmHg).7 A comprehensive study looking at approximately 1500 pregnant women with PH from the national inpatient sample (spanning from 2003-2012) found that the rate of major adverse cardiovascular events was around 24.8%.6 Overall mortality for PH patients during pregnancy is quite high, up to 50%. The majority of patients died within the first month after delivery and major causes of death were heart failure, sudden cardiac death and pulmonary embolism4,5,8 Complications of PH during pregnancy: The normal physiologic changes of pregnancy (increased plasma volume, increased stroke volume, increased cardiac output, decreased systemic vascular resistance), are poorly tolerated in PH due to an inability to decrease pulmonary vascular resistance and accommodate the increased pulmonary flow. This can lead to increased right ventricular overload. Decrease in systemic vascular resistance and associated drop in blood pressure can also lead to decreased RV perfusion leading to RV failure. Pregnancy is both a prothrombotic and a pro-arrhythmic state, and maternal morbidity and mortality may also be related to complications from veous thromboembolism and arrhythmias. Abnormal maternal hemodynamics in PH also contribute to increased fetal and neonatal complications including preterm birth as well as fetal and neonatal death. 5. What are some of the most important delivery considerations to keep in mind for these patients? Delivery timing and location: Consider delivering most patients by 37 weeks of gestation, if not earlier, depending on the stability of the patient. While some women may be followed in obstetric hospitals, delivery should take place in a location with backup of a cardiology, critical care, and advanced heart failure teams. 8 Mode of delivery: If women are stable, assisted vaginal delivery is preferred as it is associated with fewer complications. 8 Monitoring: In conjunction with OB consider the use of an arterial line for invasive blood pressure monitoring, central access for IV medication administration etc. A PA catheter may be necessary to optimize PAH therapy and RV support.8 Be wary of increased vascular fragility and the increased risk of complications of invasive vascular procedures during pregnancy. Anesthesia: Epidural anesthesia with good pain management is preferred (to avoid sympathetic surge from pain), with avoidance of general anesthesia if possible (as GA is associated with greater complications in patients with PH)8 VA-ECMO: If concerns for patient destabilization arise, VA-ECMO should be initiated. 8 Post-partum: The majority of complications occur after delivery, with the first week posing the highest risk period. Close monitoring must be initiated, preferably in a CCU/ICU for several days post-delivery. Early diuresis is paramount, as fluid mobilization after delivery can lead to fluid overload and right heart failure. 8 References 1. McLaughlin, V.V., Shah, S.J., Souza, R. and Humbert, M., 2015. Management of pulmonary arterial hypertension. Journal of the American College of Cardiology, 65(18), pp.1976-1997. 2. Meng, M.L., Landau, R., Viktorsdottir, O., Banayan, J., Grant, T., Bateman, B., Smiley, R. and Reitman, E., 2017. Pulmonary hypertension in pregnancy. Obstetrics & Gynecology, 129(3), pp.511-520. 3. Lima, F.V., Yang, J., Xu, J. and Stergiopoulos, K., 2017. National trends and in-hospital outcomes in pregnant women with heart disease in the United States. The American journal of cardiology, 119(10), pp.1694-1700. 4. Bedard, E., Dimopoulos, K. and Gatzoulis, M.A., 2009. Has there been any progress made on pregnancy outcomes among women with pulmonary arterial hypertension?. European heart journal, 30(3), pp.256-265. 5. Weiss BM, Zemp L, Seifert B, Hess OM. Outcome of pulmonary vascular disease in pregnancy: A systematic overview from 1978 through 1996. J Am Coll Cardiol. Published online 1998. doi:10.1016/S0735-1097(98)00162-4 6. Thomas E, Yang J, Xu J, Lima F V., Stergiopoulos K. Pulmonary hypertension and pregnancy outcomes: Insights from the national inpatient sample. J Am Heart Assoc. Published online 2017. doi:10.1161/JAHA.117.006144 7. Sliwa K, van Hagen IM, Budts W, et al. Pulmonary hypertension and pregnancy outcomes: data from the Registry Of Pregnancy and Cardiac Disease (ROPAC) of the European Society of Cardiology. Eur J Heart Fail. Published online 2016. doi:10.1002/ejhf.594 8. Martin, S.R. and Edwards, A., 2019. Pulmonary hypertension and pregnancy. Obstetrics & Gynecology, 134(5), pp.974-987. CardioNerds Case Report Production Team Karan Desai, MD Amit Goyal, MD Daniel Ambinder, MD

12 snips

Sep 1, 2021 • 36min

143. Lipids: (Non)-Fasting LDL & Furious Lipid Lowering with Dr. Alison Bailey

CardioNerds Dr. Rick Ferraro, Director of the #CardsJC Journal Club and cardiology fellow at Johns Hopkins, and Dr. Tommy Das, Program Director of the CardioNerds Academy and cardiology fellow at Cleveland Clinic, learn all about the clinical application of the ASCVD primary and secondary prevention guidelines in terms of lifestyle modifications and lipid lowering strategies from Dr. Allison Bailey, Editor-in-Chief of the ACCEL Audio Journal and Advanced Heart Failure and Transplant Cardiologist at Centennial Heart. Dr. Baily was a co-author on the 2018 ACC/AHA Guideline on the Management of Blood Cholesterol. In this episode we will learn about the current guidelines for primary prevention of ASCVD, the evidence for specific dietary changes in improving cardiovascular outcomes, the current guidelines for secondary prevention of ASCVD, how successful are clinicians and patients in meeting LDL-C recommendations, and what the recent SAMSON trial teaches us about statin intolerance. If you’re a current internal medicine resident, interested in the intersection between medical education, cardiovascular disease and digital media, consider applying to the CardioNerds Academy using this link. The deadline for this application is October 15th 2021. Learn more by visiting the CardioNerds Academy page. Relevant disclosure: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Lipid Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Qoatables – Lipid Lowering with Dr. Alison Bailey “Lifestyle should be the first step and the last step of everything we do.” Pearls – Lipid Lowering with Dr. Alison Bailey In patients without established clinical ASCVD, the percent reduction in LDL-C is the strongest predictor of cardiovascular benefit. In patients with high LDL-C levels, a 50% reduction in LDL-C levels should be targeted. In high-risk patients with established clinical ASCVD, we should target a 50% reduction in LDL-C levels and an LDL-C level less of than <70mg/dL. Lower LDL-C levels are associated with better ASCVD outcomes, and European guidelines recommend targeting an LDL-C level of <55mg/dL. LDL-C lowering starts with promoting a health-lifestyle with emphasis on regular exercise and heart-healthy diet. Randomized trials support the efficacy of the Mediterranean diet in reducing cardiovascular events. Show notes – Lipid Lowering with Dr. Alison Bailey 1. What are the current guidelines for primary prevention of ASCVD? The 2019 ACC/AHA Guidelines on the primary prevention of Cardiovascular Disease provides the following guidance for clinicians (applicable to those without established clinical ASCVD): For all patients, a heart-healthy lifestyle focused on diet and exercise is the most important way to prevent atherosclerotic disease. For any patient with an LDL-C ≥ 190 mg/dL, a high intensity statin is recommended. Patients aged 40-75 years old who have diabetes mellitus warrant at least a moderate intensity statin, and may benefit from a high-intensity statin based on additional risk factors For patients aged 40-75 years old and with an LDL-C between 70-189 mg/dL without diabetes, the pooled cohort equation can determine 10-year ASCVD risk and guide a patient-centric risk discussion. Percent reduction in LDL-C is the strongest predictor of cardiovascular benefit; a 50% reduction in LDL-C should be targeted for most patients. 2. What evidence exists for specific dietary changes in improving cardiovascular outcomes? A diet emphasizing intake of vegetables, fruits, legumes, nuts, whole grains, and fish is recommended to decrease ASCVD risk factors. Additionally, minimizing intake of processed meats, refined carbohydrates, and sweetened beverages can reduce ASCVD risk. The PREDIMED trial showed that among patients with high cardiovascular risk, a Mediterranean diet supplemented with extra-virgin olive oil or nuts reduced the incidence of major cardiovascular events when compared to a control diet (with advice to reduce dietary fat). In a sub-study analysis of PREDIMED, a Mediterranean diet supplemented with nuts was associated with delayed progression of internal carotid intima-media thickness and plaque height by ultrasound, suggesting a mechanistic cause of the Mediterranean diet’s cardio-protective effect. The Adventist Health Study-2 cohort demonstrated a significant association between vegetarian diets and decreased all-cause mortality and cardiovascular mortality. 3. What are the current guidelines for secondary prevention of ASCVD? Secondary prevention of ASCVD is important for all patients with history of clinical ASCVD (e.g. prior history of ACS, MI, stable or unstable angina, stroke, TIA, or PAD including aortic aneurysm of atherosclerotic origin). In these patients, a healthy lifestyle should be emphasized as the first intervention. In addition, patients should be started on a high intensity statin. For all patients we should target a percent LDL-C reduction of at least 50%. In high-risk patients (those with a history of multiple major ASCVD events or one major ASCVD event and multiple high-risk conditions), we should target a LDL-C level of ≤70 as well. While American guidelines recommend targeting a goal of ≤70 mg/dL, European guidelines recommend a target of ≤55 mg/dL. Most data suggests that lower is better for LDL-C; to learn why, enjoy Episode #132 – LDL Physiology & Function with Dr. Peter Toth)! If LDL-C remains above goal (of 70 mg/dL), ezetimibe should be started for an anticipated extra 20% lipid lowering. If LDL-C remains above goal, a PCSK-9 inhibitor should be considered. Notably, the ACC’s prior authorization tool is designed to collect data on the approval of these medications. 4. How successful are clinicians and patients in meeting LDL-C recommendations? In a recent analysis of the PINNACLE registry (made up of over 2.5 million patients with known ASCVD), 52.7% had no history of being prescribed lipid lowering therapy, and 71.9% did not meet an LDL-C goal of ≤70. In the ISCHEMIA trial, only 41% patient patients were on optimal medical therapy by the end of the trial. Dr. Bailey suggests an approach to patient counseling wherein patients are aware of which medications actively improve their symptoms, and which medications improve longevity. Additionally, polypharmacy should be avoided through careful medication reconciliation. 5. What does the recent SAMSON trial teach us about statin intolerance? In this recent trial, 60 patients with a prior history of statin intolerance were randomized to either atorvastatin 20mg, a placebo, or no treatment. Each patient cycled through all three treatment options. When patients were taking either the statin or placebo, they reported significantly more side effects compared to when they were taking no treatment. Notably, after learning whether they were taking placebo or statin while experiencing symptoms at the completion of the trial, roughly 50% of patients were able to tolerate a statin. References – Lipid Lowering with Dr. Alison Bailey Arnett DK, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [published correction appears in Circulation. 2019 Sep 10;140(11):e649-e650] [published correction appears in Circulation. 2020 Jan 28;141(4):e60] [published correction appears in Circulation. 2020 Apr 21;141(16):e774]. Circulation. 2019;140(11):e596-e646. doi:10.1161/CIR.0000000000000678 Estruch R, Ros E, Salas-Salvadó J, et al. Primary Prevention of Cardiovascular Disease with a Mediterranean Diet Supplemented with Extra-Virgin Olive Oil or Nuts. N Engl J Med. 2018;378(25):e34. doi:10.1056/NEJMoa1800389 Sala-Vila A, Romero-Mamani ES, Gilabert R, et al. Changes in ultrasound-assessed carotid intima-media thickness and plaque with a Mediterranean diet: a substudy of the PREDIMED trial. Arterioscler Thromb Vasc Biol. 2014;34(2):439-445. doi:10.1161/ATVBAHA.113.302327 Orlich MJ, Singh PN, Sabaté J, et al. Vegetarian dietary patterns and mortality in Adventist Health Study 2. JAMA Intern Med. 2013;173(13):1230-1238. doi:10.1001/jamainternmed.2013.6473 Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [published correction appears in Circulation. 2019 Jun 18;139(25):e1182-e1186]. Circulation. 2019;139(25):e1082-e1143. doi:10.1161/CIR.0000000000000625 Authors/Task Force Members; ESC Committee for Practice Guidelines (CPG); ESC National Cardiac Societies. 2019 ESC/EAS guidelines for the management of dyslipidaemias: Lipid modification to reduce cardiovascular risk [published correction appears in Atherosclerosis. 2020 Jan;292:160-162] [published correction appears in Atherosclerosis. 2020 Feb;294:80-82]. Atherosclerosis. 2019;290:140-205. doi:10.1016/j.atherosclerosis.2019.08.014 Wood FA, Howard JP, Finegold JA, et al. N-of-1 Trial of a Statin, Placebo, or No Treatment to Assess Side Effects. N Engl J Med. 2020;383(22):2182-2184. doi:10.1056/NEJMc2031173 O’Keefe JH Jr, Cordain L, Harris WH, Moe RM, Vogel R. Optimal low-density lipoprotein is 50 to 70 mg/dl: lower is better and physiologically normal. J Am Coll Cardiol. 2004;43(11):2142-2146. doi:10.1016/j.jacc.2004.03.046 Guest Profiles Dr. Alison Bailey Alison L. Bailey @a_l_bailey is a General Cardiologist in Chattanooga, TN. She completed her medical training (all of it!) at the University of Kentucky and has been using what she learned there for the last 20 years. She loves ALL of cardiology, but spends most of her clinical time in prevention and heart failure. She believes that Food is Medicine and is passionate about helping her community find healthier ways to live. She has been involved in medical education throughout her career as a chief resident, chief fellow and Cardiology Fellowship program director. She currently serves as the Editor-in-Chief of ACCEL and thinks the most important contribution any of us can make is to elevate medical education. She believes in the mission of CardioNerds wholeheartedly. She enjoys cooking, reality TV and hanging out with Max, her favorite son. CardioNerds Lipids Production Team Tommy Das, MD Dr. Rick Ferraro Amit Goyal, MD Daniel Ambinder, MD

10 snips

Aug 24, 2021 • 1h 9min

142. HF part 11: The Role of the Clinical Examination in Patients With Heart Failure – with Dr. Mark Drazner

Dr. Mark Drazner discusses the clinical examination in heart failure patients, highlighting non-invasive assessment of hemodynamic status and risk stratification. Topics include evaluating JVP, RA:PCWP ratio, and categorizing patients based on pressures to guide management decisions.

Aug 17, 2021 • 1h

141. Narratives in Cardiology: Empowerment & Growing Together as Women in EP with Dr. Kamala Tamirisa – Texas Chapter

In the PA.ACC – CardioNerds Narratives in Cardiology episode, CardioNerd Amit Goyal joins Dr. Miranda Merrill (FIT, Oregon Health & Science University), Dr. Stephanie Fuentes Rojas (FIT, Houston Methodist Hospital), and Dr. Natasha Cuk (FIT, Cedars-Sinai Medical Center) for a discussion with Dr. Kamala Tamirisa (Clinical Cardiac Electrophysiologist, Texas Cardiac Arrhythmia, National ACC Women in Cardiology Leadership Council Member and Co-Chair for ACC Women in Cardiology Advocacy Work Group, and current co-chair of the Texas Chapter ACC EP section) about gender equity and women in cardiology and electrophysiology. This episode focuses on the experiences of women in cardiology across the spectrum of training, from medical school, fellowship, through the procedural field of electrophysiology, to local and national leadership and beyond. Listen to the episode to learn about the factors which have led to Dr. Tamirisa’s success as a private practice electrophysiologist incorporating leadership roles in medical education and national organizations. Closing remarks by Texas ACC chapter governor, Dr. Kenneth Shaffer. Episode script was developed by Dr. Miranda Merrill and episode notes were developed by Dr. Natasha Cuk. 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. Video Version • Notes • References • Production Team Claim free CME just for enjoying this episode! There are no relevant disclosures for this episode. 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 – Women in EP https://youtu.be/e7Cjv4vPXqg Quotables – Women in EP “The exciting part today is to see three women who are interested in EP… like RBG said, when all EP physicians are women, that’s the day we’re going to celebrate” 07:15 “There’s nothing (more) exciting… than EP, just that technology, the marriage between analytical thinking, tactile, touch, with a deductive logic.” 09:18 “Multiple studies have documented sex disparities in cardiovascular care… (Historically) women and minorities did not receive implantable cardioverter defibrillators or even BiV (biventricular) pacers… a potential driver for these disparities in cardiovascular disease is lack of diversity in the workforce. Very simple.” 19:28 “I still want to wear my lipstick. I still want to wear my heels. I want to do my hair. I still want to be a proceduralist and that’s okay. Make room.” 28:00 Show notes – Women in EP While this episode and the following notes are specific to women in electrophysiology, these same basic principles apply to fostering a more inclusive and welcoming environment in other subspecialties for all persons regardless of sex, gender, race, ethnicity, IMG status, and the other factors which make us different from one another and which enrich our workforce. 1. Why choose electrophysiology? An EP career is unique – it combines the biology, physiology, and procedural skills learned in residency and fellowship training with engineering, mathematic, and imaging principles learned and refined in advanced EP fellowship.1 EPs work in a spectrum of settings and with a spectrum of modalities: inpatient, outpatient clinic, EP lab and with fluoroscopy, echocardiography (including intracardiac echo), 3D mapping systems, intracardiac EGMs, surface EKGs. Bedside medicine is still key to this field. Curative procedures performed in EP have a meaningful impact on patients’ quality and quantity of life1 and life saving devices such as implantable cardioverter defibrillators have profound impacts on mortality with a number needed to treat to save one life between 3-27 for both primary and secondary prevention indications from multiple randomized controlled trials.2 If you LOVE EKGs, find yourself dissecting telemetry strips, and bonding with your mentors over EKG analysis, then EP is the field for you! 40% of the 130 clinical cardiac electrophysiology fellowship positions in the U.S. remain unfilled and there is a decline in the number of fellows choosing EP for advanced training over the last 5 years. Early exposure to internal medicine residents and first year cardiology fellows to the field will allow time for exploration and may help direct more trainees with an interest to this career.1 2. What are some opportunities for an electrophysiologist in private practice? Private practice can facilitate a certain level of independence and flexibility including directing choices both large and small such as which devices and tools are used, how the lab is set up, or even the ability to build an entirely new ablation program. Leadership is inherent to private practice, especially in EP – there are opportunities everywhere! Private practice facilitates close, longitudinal relationships with patients. Understanding the finances is important – take time to learn about this from mentors not just in EP but in other fields of medicine or even outside of medicine. Community initiatives can be a fulfilling aspect in addition to procedures, patient care, and leadership opportunities. Dr. Tamirisa earned a Healthcare Heroes Award for Northwest Ohio in 2017 for making an impact on community wellbeing, domestic violence/impact on cardiovascular disease, and health of minority women and was nominated for the Thomas Jefferson Award for the Northwest Ohio region in 2016 for her contribution to women’s empowerment in the community. 3. Why and how should we promote diversity within electrophysiology? Women physicians across subspecialties are more likely to provide patient centered communication and may provide improved outcomes for certain patient populations.3,4 Diversity drives innovation, which is why drawing more women and underrepresented minorities to EP will advance the field.5 Women are “unicorns” in the procedural subspecialties of cardiology.6 Their representation is not growing at the same rate as in other parts of medicine; only 7-10% of EPs currently in practice are women and there remains limited visibility in leadership roles for women at the national level.1,7,8 How can we address barriers to entry into the field? Dr. Tamirisa makes several suggestions in her EP lab digest article and in the podcast.1 Adjust work and training environments so that they are more inclusive to women and URiM. Address sexual harassment and discrimination on the basis of sex, gender, race, ethnicity, and other factors which make us different and enrich our field.9 Advocate for work-life integration for all, including flexible (full- and part-time) work schedules such as 4 day-a-week schedules. Acknowledge and respond to family planning concerns given that childbearing age may overlap with the training period: limit radiation exposure, protect research and family leave time, provide access to lactation areas, and consider reduced or flexible training schedules (such as 2.5 years/30 months of cardiology fellowship and 18 months of EP training). 4. Mentorship in Electrophysiology and Empowering Women to Succeed Mentorship in EP for women can and should be from both women and men! Initiatives such as social media hashtags #HeforShe and #TakeAWomanToTheCathLab and official speaking opportunities eliminating “manels” at national conferences are creating a more inclusive field.10 Tips for mentors: Be kind always. Listen to your mentees – even without offering advice, just listening can lead to profound insights. Show your flaws – shattering the illusion of a perfect career or trajectory can help your foster confidence and the ability to tackle obstacles. Be open, vulnerable, and honest (both as a mentor and mentee!) Be inclusive with your projects. Understand the microaggressions that women and underrepresented minorities face in training and their careers. Help them with tools to address those issues including microresistance response strategies.11,12 Engage and share your creative endeavors! Dr. Tamirisa writes poetry and journals as her outlet.13 References Tamirisa KP. The Importance of Choosing Cardiac Electrophysiology as a Career: Thoughts on the EP Fellow Shortage. EP Lab Digest. 2020;20(2). https://www.hmpgloballearningnetwork.com/site/eplab/importance-choosing-cardiac-electrophysiology-career-thoughts-ep-fellow-shortage 2. Al-Jefairi N, Burri H. Relevance of guideline-based ICD indications to clinical practice. Indian Heart J. 2014;66 Suppl 1:S82-87. https://www.ncbi.nlm.nih.gov/pubmed/24568834 3. Roter DL, Hall JA. Physician gender and patient-centered communication: a critical review of empirical research. Annu Rev Public Health. 2004;25:497-519. https://www.ncbi.nlm.nih.gov/pubmed/15015932 4. Tsugawa Y, Jena AB, Figueroa JF, Orav EJ, Blumenthal DM, Jha AK. Comparison of Hospital Mortality and Readmission Rates for Medicare Patients Treated by Male vs Female Physicians. JAMA Intern Med. 2017;177(2):206-213. https://www.ncbi.nlm.nih.gov/pubmed/27992617 5. Welson-Rossman T. Healthcare Needs More Diverse Experts To Guide Innovation. ForbesWomen. 2021. https://www.forbes.com/sites/traceywelsonrossman/2021/02/09/healthcare-needs-more-diverse-experts-to-guide-innovation/?sh=358d5b2769e6 6. The Unicorns: Women in Cardiac Electrophysiology and Interventional Cardiology [Webinar]2020. https://www.acc.org/education-and-meetings/meetings/meeting-items/2020/04/01/12/41/the-unicorns 7. Burgess S, Shaw E, Ellenberger K, Thomas L, Grines C, Zaman S. Women in Medicine: Addressing the Gender Gap in Interventional Cardiology. J Am Coll Cardiol. 2018;72(21):2663-2667. https://www.ncbi.nlm.nih.gov/pubmed/30466523 8. Yong CM, Balasubramanian S, Douglas PS, et al. Temporal Trends in the Proportion of Women Physician Speakers at Major Cardiovascular Conferences. Circulation. 2021;143(7):755-757. https://www.ncbi.nlm.nih.gov/pubmed/33587663 9. Tamirisa KP, Volgman AS, Parwani P, Lundberg GP. Advocacy to End Sexual Harassment: Voices From Women in Cardiology. JACC Case Rep. 2021;3(6):975-977. https://www.ncbi.nlm.nih.gov/pubmed/34319306 10. Harrington RA. 5 Questions: Robert Harrington on research, health equity and the gender gap in cardiology. 2020. https://med.stanford.edu/news/all-news/2020/02/harrington-on-research-health-equity-and-more.html. Accessed August 5, 2020. Accessed February 19, 2020. 11. POD Diversity Committee White Paper. 2016 POD Network Conference; November 9-13, 2016, 2016; Louisville, Kentucky. https://podnetwork.org/content/uploads/DC-white-paper-2016_Final2.pdf 12. Wheeler DJ, Zapata J, Davis D, Chou C. Twelve tips for responding to microaggressions and overt discrimination: When the patient offends the learner. Medical Teacher. 2019;41(10):1112-1117. https://doi.org/10.1080/0142159X.2018.1506097 13. Tamirisa KP. Poem | Metaphors For a Woman. ACC WIC Section Online. 2020. https://www.acc.org/membership/sections-and-councils/women-in-cardiology-section/section-updates/2020/02/27/12/42/a-poem-metaphors-for-a-woman Production Team Dr. Gurleen Kaur Amit Goyal, MD Daniel Ambinder, MD

16 snips

Jul 30, 2021 • 47min

140. Lipids: LDL, Cardiovascular Events, & Disparities in Care with Dr. Keith Ferdinand

CardioNerds Dr. Rick Ferraro, Director of the #CardsJC Journal Club and cardiology fellow at Johns Hopkins and Dr. Tommy Das, Program Director of the CardioNerds Academy and cardiology fellow at Cleveland Clinic join Academy fellow and episode lead Dr. Julie Power, chief fellow at the University of Minnesota to learn all about the link between LDL-C and cardiovascular events and disparities in care from Dr. Keith Ferdinand, Professor of Medicine and Chair in Preventative Cardiology at Tulane University School of Medicine. As we’ve learned in prior episodes, LDL-C plays a key role in lipid pathophysiology. But how does it lead to cardiovascular events? LDL-C directly leads to plaque expansion and deposition in the arterial intima. Increasing levels of LDL-C are directly related to worsening plaque burden, a principle exhibited powerfully by the dose-dependent nature of coronary atherosclerosis in patients with underlying mutations leading to LDL-C elevation, such as familial hypercholesterolemia. Importantly, the treatment of atherosclerosis and implementation of lipid-lowering therapies are not uniform, with significant disparities throughout the community. The message is clear: Reducing LDL-C is of paramount significance in the prevention and treatment of coronary atherosclerosis and ensuring equitable access to care is critical to addressing the societal burden of cardiovascular disease and improving the health of our communities. There is no CME associated with this episode. To get free CME from other CardioNerds episodes, please visit VCU Health here. Relevant disclosure: Dr. Ferdinand reported severing as a consultant for Medtronic, Amgen, and Novartis. Pearls • Quotables • Notes • References • Guest Profiles • Production Team CardioNerds Lipid Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls – LDL, Cardiovascular Events, & Disparities in Care LDL-C is a major stimulant for the initiation and progression of atherosclerosis. The lower the LDL-C level, the greater the clinical benefit in both primary and secondary ASCVD prevention. Our healthcare systems continue to have major disparities in access to quality care and it is essential to reduce barriers to cardiovascular wellness for all communities. Lowering LDL-C in individuals at high cardiovascular risk, especially in those with familial hypercholesterolemia, prevents ASCVD events. Quotables – LDL, Cardiovascular Events, & Disparities in Care “Empower patients to be partners in their care” Dr. Keith Ferdinand Show notes – LDL, Cardiovascular Events, & Disparities in Care 1. What is the link between LDL-C and cardiovascular events? LDL-C is a major stimulant for the initiation and progression of atherosclerosis. The key events in the initiation of ASCVD are the retention and accumulation of cholesterol-rich lipoproteins within the arterial intima at sites with a predilection for plaque formation. As serum levels of LDL-C increase, the probability of intimal retention of LDL leading to the development of atherosclerotic plaque increases in a dose-dependent manner [4]. The WOSCOPS trial demonstrated genes associated with lower LDL-C levels are also associated with a three-fold reduction in the risk of cardiovascular disease per unit reduction in LDL-C [4]. The Emerging Risk Factors Collaboration (ERFC) and Prospective Studies Collaboration reported plasma LDL-C was associated with increased risk of non-fatal MI or CHD death [4]. Statins uniformly reduce atherosclerotic risk across varying levels of baseline LDL-C and are first line therapy for primary and secondary prevention of ASCVD. In high-risk individuals and secondary prevention populations, AHA/ACC guidelines recommend 50% reductions in LDL-C, regardless of baseline, to < 70 mg/dL, using a combination of statins, ezetimibe, and PCSK9 inhibition [6]. Intravascular ultrasound studies of coronary atherosclerosis involving statin-treated patients demonstrated that progression of coronary atherosclerotic plaque volume can be arrested once an LDL-C of 70 mg/dL is reached [4, 10, 11]. The effect of LDL-C on the risk of ASCVD is both causal and cumulative over time; therefore, lowering the LDL-C level early will lead to greater reductions in the lifetime risk of ASCVD. Each millimole per liter reduction in LDL-C reduces the relative risk of ASCVD events by ∼10% in the first year of treatment and ∼20–25% after 5 years [4]. 2. What is Familial Hypercholesterolemia? Familial hypercholesterolemia (FH) is an autosomal co-dominant disorder that results from a mutation in an LDL receptor gene, ApoB gene, or PCSK9 gene. FH is characterized by markedly elevated levels of LDL-C and premature atherosclerosis. Siblings who inherit an FH mutation have markedly elevated plasma LDL-C levels and a corresponding markedly elevated lifetime risk of ASCVD as compared to their unaffected siblings, providing powerful evidence that LDL causes ASCVD. Heterozygous FH affects between 1:200 and 1:300 people worldwide and when untreated is characterized by LDL-C levels >190. FH should be considered in adults with LDL-C levels > 190 mg/dL or total cholesterol levels > 310 mg/dL [5]. Homozygous FH is a much rarer condition, with an extreme phenotype characterized by untreated plasma LDL-C levels above >400 from birth and almost universal development of ASCVD and xanthomas in childhood or early adolescence. Statins can be started as early as 8-10 years of age. PCSK-9 inhibitors may also be used. LDL apheresis is also a common treatment option [5]. To learn more about personalized ASCVD risk assessment and FH, enjoy CardioNerds Episode #98: Personalized Risk Assessment for Cardiovascular Prevention with Dr. Amit Khera. 3. What is the interaction of LDL-C with other ASCVD risk factors? There are numerous risk factors for ASCVD: hypertension, diabetes mellitus, tobacco smoking, and more. Patients with more risk factors have a higher absolute rate of ASCVD in comparison with persons with fewer risk factors [4]. However, reduction in LDL-C is associated with the same proportional risk reduction of ASCVD, regardless of the presence or absence of these other risk factors [4]. Statin therapy reduces vascular event rates, including major coronary events, stroke, and coronary revascularization by 15-25% for each 1 mmol/L reduction in LDL-C [8]. 4. How do we best support the cholesterol management and cardiovascular health needs of underserved and low-resource communities? We must recognize and work together to address CV health disparities from both the individual and population levels. Reduced adherence to statin therapy among eligible patients is associated with increased mortality. Minority patients, those with low income, and those with barriers to health literacy have been found to be less likely to adhere to statins, signaling important disparities that must be addressed further. The reasons are likely multifactorial and require a multipronged approach to address. Team care delivered in nontraditional locations shows promise, but the cost-effectiveness and sustainability of these approaches need to be studied further [13]. Barriers to treatment in low-resource communities exist at multiple levels: educational opportunities, environment, limited access to healthy food options, access to healthcare providers, transport to healthcare facility organization and practice settings where care occurs, and governmental health policy. Focus is needed on developing cross-sectional partnerships to target multiple barriers [13, 16] Programs need early-stage investigators committed to disparities research to bridge these findings to clinical practice and formulation of health policy. To learn about the use of community based participatory research to meaningfully engage and empower the community in addressing these barriers, enjoy CardioNerds Episode #131 with Dr. LaPrincess Brewer and Dr. Norrisa Haynes. To learn about strategies to engage minority patients in clinical trials, enjoy CardioNerds Episode #135 with Dr. Clyde Yancy. 5. What are some other benefits and consequences of lowering LDL-C? Intensive LDL-C lowering is associated with a greater reduction of all-cause mortality in addition to CV mortality [9]. LDL-C lowering has exhibited protective effects against cerebrovascular events. The ODYSSEY trial in 2019 demonstrated that PCSK-9 therapy decreased the risk of stroke in patients with recent ACS and dyslipidemia; however, this was regardless of LDL-C levels achieved. There is no evidence for an increased risk of cognitive impairment (PROSPER trial) or hemorrhagic stroke with lower LDL-C levels. References – LDL, Cardiovascular Events, & Disparities in Care Baigent C, Blackwell L, Emberson J, et al. Efficacy and Safety of More Intensive Lowering of LDL Cholesterol: A Meta-Analysis of Data from 170,000 Participants in 26 Randomised Trials. Lancet. 2010; 376: 1670–81. Damask A, Steg PG, Schwartz GG et al. Patients With High Genome-Wide Polygenic Risk Scores for Coronary Artery Disease May Receive Greater Clinical Benefit From Alirocumab Treatment in the ODYSSEY OUTCOMES Trial. Circulation. 2020 Feb 25;141(8):624-636. Duran EK, Aday AW, Cook NR, et al. Triglyceride-Rich Lipoprotein Cholesterol, Small Dense LDL Cholesterol, and Incident Cardiovascular Disease. J Am Coll Cardiol. 2020 May 5; 75(17):2122-2135. Ference BA, Yoo W, Alesh I, et al. Effect of Long-Term Exposure to Lower Low-Density Lipoprotein Cholesterol Beginning Early in Life on the Risk of Coronary Heart Disease: a Mendelian Randomization Analysis. Journal of the American College of Cardiology. 2012; 60: 2631-9. Goldberg AC, Hopkins PN, Toth PP, et al. Familial Hypercholesterolemia: Screening, Diagnosis and Management of Pediatric and Adult Patients: Clinical Guidance from the National Lipid Association Expert Panel on Familial Hypercholesterolemia. J Clin Lipidol. 2011; 5:133–40. Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/ AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2019;73: e285–350. Mach F, Baigent C, Catapano AL, et al. 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Eur Heart J. 2020; 41: 111–88. Mihaylova B, Emberson J, Blackwell L, et al. The Effects of Lowering LDL Cholesterol with Statin Therapy in People at Low Risk of Vascular Disease: Meta-analysis of Individual Data from 27 Randomised Trials. Lancet. 2012; 380: 581-90. Navarese EP, Robinson JG, Kowalewski M, et al. Association Between Baseline LDL-C Level and Total and Cardiovascular Mortality after LDL-C Lowering: A Systematic Review and Meta-analysis. JAMA. 2018; 319 (15): 1566-1579. Nicholls SJ, Ballantyne CM, Barter PJ, et al. Effect of Two Intensive Statin Regimens on Progression of Coronary Disease. N Engl J Med. 2011; 365: 2078–2087. Nissen SE, Nicholls SJ, Sipahi I, et al. ASTEROID Investigators. Effect of Very High-intensity Statin Therapy on Regression of Coronary Atherosclerosis: the ASTEROID Trial. JAMA. 2006; 295: 1556–1565. Ridker, PM. LDL Cholesterol: Controversies and Future Therapeutic Directions. Lancet. 2014; 384: 607-617. Schultz WM, Kelli HM, Lisko JC, et al. Socioeconomic Status and Cardiovascular Outcomes: Challenges and Interventions. Circulation. 2018. 137 (20): 2166–2178 Shepherd J, et al. Prevention of Coronary Heart Disease with Pravastatin in Men with Hypercholesterolemia”. The New England Journal of Medicine. 1995. 333 (20): 1301-1308. Valdes-Marquez E, Parish S, Clarke R, et al. Relative Effects of LDL-C on Ischemic Stroke and Coronary Disease: a Mendelian Randomization Study. Neurology. 2019; 92: e1176–87. Whelton PK, Einhorn PT, Muntner P, et al. Research Needs to Improve Hypertension Treatment and Control in African Americans. Hypertension. 2016. Guest Profiles Dr. Keith Ferdinand Keith C Ferdinand, MD, is Professor of Medicine at the Tulane University School of Medicine and the Tulane Heart and Vascular Institute in New Orleans, Louisiana. He was previously Professor of Clinical Pharmacology at Xavier University, New Orleans and Clinical Professor of Medicine at Emory University, Atlanta, Georgia. Dr. Ferdinand received his medical degree from the Howard University College of Medicine in Washington, DC. He is board-certified in internal medicine and cardiovascular disease, certified in the subspecialty of nuclear cardiology, and a specialist in clinical hypertension certified by the American Society of Hypertension. Dr. Juliette Power Dr. Julie Power @JuliettePower44 is a cheif cardiology fellow at the University of Minnesota. She completed medical school at Drexel University in Philadelphia followed by residency training at Allegheny General Hospital in Pittsburgh where she also served a Chief Resident. In addition to a continued involvement in medical education, Julie plans to pursue additional training in interventional cardiology after her general cardiology fellowship. In her free time, she enjoys spending time with family and friends, including exploring Minnesota with her boyfriend, Steve. CardioNerds Cardioobstetrics Production Team Tommy Das, MD Dr. Rick Ferraro Amit Goyal, MD Daniel Ambinder, MD

The AI-powered Podcast Player

Save insights by tapping your headphones, chat with episodes, discover the best highlights - and more!

Get the app