Episodes Archives - Cardionerds

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Episodes Archives - Cardionerds episodes

August 18, 2024387. Cardio-Rheumatology: The Role of Inflammation in Cardiovascular Disease with Dr. Antonio Abbate
CardioNerds Cardio-Rheumatology Series Co-Chairs Dr. Rick Ferraro, Dr. Gurleen Kaur, and Episode Lead Dr. Ronaldo Correa discuss “The Role of Inflammation in Cardiovascular Disease” with Dr. Antonio Abbate.
Join the CardioNerds as they kick off the Cardio-Rheumatology series with Dr. Antonio Abbate. In this episode, Dr. Abbate, a leading expert in cardio-immunology, discusses the role of inflammation in cardiovascular disease. We explore the molecular mechanisms linking inflammation to atherosclerosis, the impact of chronic low-grade systemic inflammation on heart disease, and potential therapeutic targets. Dr. Abbate shares insights on how genes and lifestyle factors contribute to inflammation, the use of inflammatory markers in clinical practice, and emerging anti-inflammatory therapies in atherosclerotic cardiovascular disease. Tune in for an enlightening conversation on the intersection of inflammation and cardiovascular health.
Dr. Ronaldo Correa drafted the notes. Episode audio was engineered by Dr. Amit Goyal.
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.
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Pearls – Cardio-Rheumatology: The Role of Inflammation in Cardiovascular Disease
Inflammation is key in the pathogenesis and progression of atherosclerosis. Estimating systemic inflammation is part of a comprehensive preventive assessment (primary/secondary).
Patients with autoimmune inflammatory diseases are at a higher risk for cardiovascular events.
C-reactive protein (CRP) can estimate systemic inflammation and help assess residual inflammatory risk in patients with traditional intermediate/low cardiovascular disease, guiding management consideration with lipid-lowering therapy, aspirin, and colchicine.
The pharmacological management of atherosclerosis is evolving beyond primarily lipid-lowering therapies to focus on targeting the underlying residual inflammatory process. Colchicine (inflammasome blocker as an anti-mitotic drug) is approved for use in chronic stable CVD in selected cases, and interleukin pathway blockers, especially IL-1 and IL-6, are under clinical trial investigation.
First things first! Prioritize treating and optimizing traditional risk factors and comorbidities and emphasize lifestyle modifications to reduce cardiovascular disease (control diabetes and hypertension, reduce or cease smoking/alcohol, lose weight, and engage in regular physical activity). They all impact inflammation directly or indirectly
Show notes – Cardio-Rheumatology: The Role of Inflammation in Cardiovascular Disease
Notes: Notes drafted by Dr. Ronaldo Correa.
What is the link between inflammation and cardiovascular atherosclerosis?
Inflammation is involved both in the pathogenesis and progression of atherosclerosis.
Histopathological coronary atherosclerosis studies have demonstrated the presence of inflammatory mediators as well as a central role of factors of innate immunity such as macrophages and T cells which can interact with vascular smooth muscle cells in the progression of atherosclerotic plaque.
Patients with autoimmune inflammatory conditions have earlier and higher cardiovascular event rates (accelerated atherosclerosis due to residual inflammatory risk).
Elevated inflammatory markers (for example, high CRP) predict cardiovascular events.
How should inflammation be considered in the context of residual cardiovascular risk?
Inflammation may be the inciting factor in atherosclerosis, or it may amplify the process driven primarily by other risk factors. Therefore, treating the comorbidities and traditional CVD contributors is key to reducing the vicious inflammatory cycle.
Assessing residual risk using inflammatory markers can assist in management. C-reactive protein (CRP) can estimate systemic inflammation and help assess residual inflammatory risk in patients with traditional intermediate/low cardiovascular disease, guiding management consideration with lipid-targeting therapies, aspirin, and colchicine.
Optimizing traditional risk factors, emphasizing appropriate treatment for hypertension, diabetes, dyslipidemia, weight loss, obstructive sleep apnea (OSA), depression, underlying inflammatory conditions, and lifestyle modifications such as consuming a Mediterranean diet, alcohol/smoking reduction/cessation, and getting regular physical activity can help directly and indirectly reduce inflammatory contributors.
How does inflammation contribute to thrombosis, and what are the implications for cardiovascular disease?
Inflammation increases the expression of procoagulant factors through the inflammasome pathway, including mediators like IL-6.
Proinflammatory changes in endothelial cells, leukocytes, and platelets promote thrombosis.
The concept of immunothrombosis has emerged, especially highlighted by conditions like COVID-19.
Inflammation-induced thrombosis has significant implications for cardiovascular disease.
What are the key inflammatory pathways involved in atherosclerosis, and what therapeutic targets have emerged?
The inflammatory process is complex, and we still have much to learn about it. Three inflammatory therapeutic targets are highlighted: NLRP3 inflammasome, IL-1, and IL-6.
Colchicine is an NLRP3 inflammasome blocker that is FDA-approved as an add-on medication for secondary ischemic prevention in patients with stable CAD who remain at higher risk despite optimal medical therapy with aspirin and statin.
The CANTOS trial showed a significant reduction in MACE and hsCRP in post-MI patients who received canakinumab (IL-1 inhibitor) as an add-on therapy.
The ZEUS trial is investigating Ziltivekimab (an IL-6 inhibitor) for secondary ASCVD prevention. Rilonacept (an IL-1 inhibitor) is FDA-approved for recurrent pericarditis based on the RHAPSODY trial. Ongoing trials are further exploring inflammation-targeting therapies for the treatment of cardiovascular disease.
References – Cardio-Rheumatology: The Role of Inflammation in Cardiovascular Disease
Engelen SE, Robinson AJB, Zurke YX, Monaco C. Therapeutic strategies targeting inflammation and immunity in atherosclerosis: how to proceed?. Nat Rev Cardiol. 2022;19(8):522-542. doi:10.1038/s41569-021-00668-4
Kong P, Cui ZY, Huang XF, Zhang DD, Guo RJ, Han M. Inflammation and atherosclerosis: signaling pathways and therapeutic intervention. Signal Transduct Target Ther. 2022;7(1):131. Published 2022 Apr 22. doi:10.1038/s41392-022-00955-7
Saigusa R, Winkels H, Ley K. T cell subsets and functions in atherosclerosis. Nat Rev Cardiol. 2020;17(7):387-401. doi:10.1038/s41569-020-0352-5
Sage AP, Tsiantoulas D, Binder CJ, Mallat Z. The role of B cells in atherosclerosis. Nat Rev Cardiol. 2019;16(3):180-196. doi:10.1038/s41569-018-0106-9
Suero-Abreu GA, Zanni MV, Neilan TG. Atherosclerosis With Immune Checkpoint Inhibitor Therapy: Evidence, Diagnosis, and Management: JACC: CardioOncology State-of-the-Art Review. JACC CardioOncol. 2022;4(5):598-615. Published 2022 Dec 20. doi:10.1016/j.jaccao.2022.11.011
Zhao TX, Mallat Z. Targeting the Immune System in Atherosclerosis: JACC State-of-the-Art Review. J Am Coll Cardiol. 2019;73(13):1691-1706. doi:10.1016/j.jacc.2018.12.083
Geovanini GR, Libby P. Atherosclerosis and inflammation: overview and updates. Clin Sci (Lond). 2018;132(12):1243-1252. Published 2018 Jun 21. doi:10.1042/CS20180306
Fragoulis GE, Soulaidopoulos S, Sfikakis PP, Dimitroulas T, D Kitas G. Effect of Biologics on Cardiovascular Inflammation: Mechanistic Insights and Risk Reduction. J Inflamm Res. 2021;14:1915-1931. Published 2021 May 14. doi:10.2147/JIR.S282691
Giles JT, Sattar N, Gabriel S, et al. Cardiovascular Safety of Tocilizumab Versus Etanercept in Rheumatoid Arthritis: A Randomized Controlled Trial. Arthritis Rheumatol. 2020;72(1):31-40. doi:10.1002/art.41095
Del Buono MG, Bonaventura A, Vecchié A, et al. Pathogenic pathways and therapeutic targets of inflammation in heart diseases: A focus on Interleukin-1. Eur J Clin Invest. 2024;54(2):e14110. doi:10.1111/eci.14110
Abbate A, Toldo S, Marchetti C, Kron J, Van Tassell BW, Dinarello CA. Interleukin-1 and the Inflammasome as Therapeutic Targets in Cardiovascular Disease. Circ Res. 2020;126(9):1260-1280. doi:10.1161/CIRCRESAHA.120.315937
Toldo S, Abbate A. The role of the NLRP3 inflammasome and pyroptosis in cardiovascular diseases. Nat Rev Cardiol. 2024;21(4):219-237. doi:10.1038/s41569-023-00946-3
45 min
August 16, 2024386. Beyond the Boards: Cardiomyopathies with Dr. Steve Ommen
CardioNerds (Drs. Teodora Donisan, Jenna Skowronski, and Johnny Hourmozdi) discuss Cardiomyopathies with Dr. Steve Ommen. Through a case-based discussion, we review the diagnostic evaluation of suspected restrictive cardiomyopathy, and Dr. Ommen shares his expertise in the nuances of caring for patients with hypertrophic cardiomyopathy, from counseling to pharmacologic, device, and septal reduction therapies. We cover the foundations of diagnosis and management that will be helpful to CardioNerds preparing to encounter hypertrophic cardiomyopathy on the boards or on the wards.
Dr. Johnny Hourmozdi drafted notes. The audio was engineered by Dr. Atefeh Ghorbanzadeh.
The CardioNerds Beyond the Boards Series was inspired by the Mayo Clinic Cardiovascular Board Review Course and designed in collaboration with the course directors Dr. Amy Pollak, Dr. Jeffrey Geske, and Dr. Michael Cullen.
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.
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Pearls and Quotes – Cardiomyopathies
The presence of an S4 and a rapid y-descent in the jugular venous pulsation on exam should clue you to the presence of a restrictive filling pattern. Restrictive filling doesn’t necessarily mean restrictive cardiomyopathy and is more commonly due to dilated or ischemic cardiomyopathy.
The five main topics of counseling that every hypertrophic cardiomyopathy (HCM) patient should understand: (1) Prognosis, (2) Family Screening, (3) Risk of Sudden Death, (4) Treatments, and (5) Physical Activity.
Remember 1/3: In clinical trials of cardiac myosin inhibitors for HCM (mavacamten), about a third of patients had a tremendous improvement in symptoms, another third had some improvement, and the final third had no improvement or had to discontinue the drug due to negative inotropy.
When counseling patients about septal reduction therapy, consider the patient’s age. For younger patients, surgical myectomy at an experienced center offers a higher success rate and greater durability with lower rates of pacemaker placement when compared to alcohol septal ablation.
Historically, the conclusion that it was higher risk to be an athlete with HCM was unfortunately generalized to mean that it was high risk to exercise for patients with HCM. “And we turned a generation of HCM patients into HCM cardiometabolic syndrome patients, which is actually a worse combination.”
Notes – Cardiomyopathies
What is the initial approach to evaluating a patient with new or suspected cardiomyopathy, including hypertrophic cardiomyopathy (HCM)?
A history and physical exam, including a thorough past medical and family history, is always the first step and helps determine the patient’s risk for potential underlying etiologies, including genetic cardiomyopathies, hypertrophic cardiomyopathy, or those related to treatments of previous cancer.
In terms of ECG findings, pay attention to QRS voltage (high or low) and the presence of any arrhythmias.
TTE should be obtained in all patients and is often sufficient to diagnose many underlying cardiomyopathies, including HCM.
Cardiac MRI (CMR) is helpful as an adjunct when TTE alone is inconclusive or imaging quality is poor. CMR can help provide a better idea of chamber sizes and wall thickness, and late gadolinium contrast enhancement (LGE) can also be helpful if present in a specific pattern, though often HCM patients may have non-specific patterns of LGE.
Invasive hemodynamics assessment is reserved for patients with discordance between non-invasive testing and the clinical impression. It can also be useful to guide the management of heart failure, especially in advanced disease.
How do you treat patients with hypertrophic obstructive cardiomyopathy (HOCM)?
In patients with HCM and LVOT obstruction (defined as a resting peak LVOT gradient >30 mmHg), we want to avoid medications that increase inotropy, reduce preload (diuretics), or reduce afterload (pure vasodilators).
First-line medical therapies for symptomatic HOCM include non-vasodilating beta-blockers (e.g., metoprolol) and/or non-dihydropyridine calcium channel blockers (e.g., diltiazem, verapamil).
For those with symptoms despite the above first-line medications, second-line therapies include the addition of disopyramide or the newer myosin inhibitors (e.g., mavacamten).
In patients who don’t respond to medical therapies, a referral should be made for septal reduction therapy at an experienced center. Surgical myectomy involves open heart surgery and has a success rate of 90-95% with a durable result. Alcohol septal ablation can be done percutaneously and offers a shorter recovery time, but it has a lower success rate of 75-85%. Septal ablation comes with a similar risk of stroke and mortality compared to surgery (<0.5%) and with a higher rate of pacemaker implantation (5-10% vs 3%).
How should patients with HCM be counseled with regard to physical activity and exercise?
Observational studies suggest an increased risk of sudden cardiac death among athletes with HCM as compared to those without HCM. Among patients with HCM, it is less clear whether there is an association between gradations of physical activity and risk for SCD.
For patients with HCM, the safety and benefits of low to moderate-intensity exercise for cardiovascular health and fitness are established. The 2024 HCM guidelines recommend counseling patients to engage in 150-300 minutes of low-moderate intensity exercise per week in keeping with physical activity guidelines for the general population (Class 1, LOE B-R).
For athletes looking to engage in vigorous exercise or competitive sport, shared decision-making with an expert in HCM is recommended. For most patients, universal restriction from this level of exercise is not indicated.
What is the approach to genetic testing and family screening for HCM?
All patients with a clinical diagnosis of HCM should be offered genetic testing with a gene panel test. Genetic testing results can help with family screening and may inform prognosis but do not currently impact therapy decisions for the patient.
In those where a pathogenic or likely pathogenic variant is identified, cascade testing for this variant should be offered to first-degree relatives. If no variant or a variant of unknown significance (VUS) is identified, then periodic echocardiographic screening should be performed instead in all first-degree relatives.
For adults, screening ECG and TTE in first-degree relatives should begin when a family member has been diagnosed with HCM and be repeated every 3-5 years.
For children and adolescents, initiation of screening should be no later than the onset of puberty and be repeated every 1-2 years.
Who should be offered an implantable cardiac defibrillator (ICD) for prevention of sudden cardiac death?
There are “three layers of eligibility” for an ICD among patients with HCM, corresponding with the strength of the guideline recommendation based on indication (Class 1, 2a, and 2b, respectively).
The “top layer” or Class 1 indication where there is broad agreement that every patient should get an ICD is when a patient has had a documented cardiac arrest or sustained ventricular tachycardia.
The “second layer” or Class 2a indication are patients with one or more major risk factors for SCD, in whom it is reasonable to pursue an ICD:
Massive hypertrophy (LVH of 30 mm or greater in any segment)
A history of “scary” syncope that is suspected to be due to arrhythmia
A family history of sudden cardiac death
LV apical aneurysm with transmural scar
LV systolic dysfunction (EF <50%)
The last layer or Class 2b indication where it is of uncertain benefit but may be offered in shared decision-making is when there is extensive LGE present on CMR or frequent nonsustained VT on ambulatory monitoring in the absence of any major clinical risk factor.
Using an HCM risk calculator can be helpful for estimating individual patient risk for SCD by incorporating all of the above risk factors and can help to frame a shared decision-making discussion around ICD placement.
References – Cardiomyopathies
1. Ommen SR, Ho CY, et al. 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR Guideline for the Management of Hypertrophic Cardiomyopathy. Journal of the American College of Cardiology. 2024;83(23):2324-2405. doi:10.1016/j.jacc.2024.02.014
2. Saberi S, Wheeler M, Bragg-Gresham J, et al. Effect of Moderate-Intensity Exercise Training on Peak Oxygen Consumption in Patients With Hypertrophic Cardiomyopathy: A Randomized Clinical Trial. JAMA. 2017;317(13):1349-1357. doi:10.1001/jama.2017.2503
3. Desai MY, Owens A, Wolski K, et al. Mavacamten in Patients With Hypertrophic Cardiomyopathy Referred for Septal Reduction: Week 56 Results From the VALOR-HCM Randomized Clinical Trial. JAMA Cardiology. 2023;8(10):968-977. doi:10.1001/jamacardio.2023.3342
4. Maron BJ, Doerer JJ, Haas TS, Tierney DM, Mueller FO. Sudden Deaths in Young Competitive Athletes. Circulation. 2009;119(8):1085-1092. doi:10.1161/CIRCULATIONAHA.108.804617
38 min
August 09, 2024 385. Guidelines: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure – Question #34 with Dr. Mark Drazner

The following question refers to Sections 6.1 and 7.4 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.
The question is asked by University of Colorado internal medicine resident Dr. Hirsh Elhence, answered first by University of Chicago advanced heart failure cardiologist and Co-Chair for the CardioNerds Critical Care Cardiology Series Dr. Mark Belkin, and then by expert faculty Dr. Mark Drazner.
Dr. Drazner is an advanced heart failure and transplant cardiologist, Professor of Medicine, and Clinical Chief of Cardiology at UT Southwestern. He is the President of the Heart Failure Society of America.
The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #34

Question Stem
A 72-year-old woman with a history of hypertension, type 2 diabetes mellitus, and a recent myocardial infarction is seen in your clinic. Two months previously, she was hospitalized with a myocardial infarction and underwent successful revascularization of the left anterior descending artery with a drug-eluting stent. Following her myocardial infarction, an echocardiogram revealed an ejection fraction of 17%, and she was discharged on metoprolol succinate, lisinopril, spironolactone, and dapagliflozin with escalation to maximal tolerated doses over subsequent visits. A repeat echocardiogram performed today in your clinic reveals an ejection fraction of 26%. An electrocardiogram reveals normal sinus rhythm with a narrow QRS at a heart rate of 65 beats per minute. She is grateful for her cardiac rehabilitation program and reports no ongoing symptoms. Which of the following devices is indicated for placement at this time?
Answer choices
A
Implantable loop recorder
B
ICD
C
CRT-D
D
CRT-P
Answer #34

Explanation

The correct answer is B.
This patient suffered a myocardial infarction more than 40 days ago and has been on appropriate guideline-directed medical therapy since that time. Her left ventricular ejection fraction has improved but remains under 30%. For patients who have suffered a myocardial infarction over 40 days prior with LVEF ≤ 30% and NYHA Class I symptoms while receiving GDMT and have a reasonable expectation of meaningful survival for >1 year, an ICD is recommended for primary prevention of sudden cardiac death to reduce total mortality (Class I, LOE B-R).
The MADIT-II trial enrolled 1,232 patients with a prior myocardial infarction and LVEF ≤ 30% to prophylactic ICD or medical therapy. At a median follow-up of 20 months, the trial was terminated early for reduced all-cause mortality with prophylactic ICD. The DINAMIT trial later investigated the implantation of ICD in patients with MI and an LVEF of ≤ 35% at 6 to 40 days after the initial myocardial infarction. This trial found no differences in all-cause mortality between the two groups. Therefore, the current recommendation is to wait at least 40 days with GDMT prior to re-evaluation of left ventricular ejection fraction before proceeding with ICD implantation.
Cardiac resynchronization therapy entails implanted pacemakers to simultaneously pace both the RV and LV in order to improve electrical synchrony and generally provides benefit in those with systolic dysfunction and a wide left bundle branch block. Specifically, for patients who have LVEF ≤35%, sinus rhythm, left bundle branch block (LBBB) with a QRS duration ≥150 ms, and NYHA class II, III, or ambulatory IV symptoms on GDMT, CRT is indicated to reduce total mortality, reduce hospitalizations, and improve symptoms and QOL (Class I, LOE B-R). CRT implantation provides high economic value in this setting. CRT implantation carries a Class 2a recommendation for those with reduced LVEF (≤35%) and either a non-LBBB pattern with a QRS ≥150 ms or a LBBB with QRS duration 120-149ms. This patient with a narrow QRS does not have indications for CRT placement at this time.
Main Takeaway
ICD implantation is recommended as primary prophylaxis against ventricular arrhythmias for patients with LVEF ≤30% after 40 days following myocardial infarction despite use of GDMT.
Guideline Loc.
Section 6.1 and 7.4

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6 min
August 07, 2024384. Case Report: Little (a), Big Deal – National Lipid Association
CardioNerds Dan Ambinder and Dr. Devesh Rai join cardiology fellows and National Lipid Association lipid scholars Dr. Oby Ibe from Temple University and Dr. Elizabeth Epstein from Scripps Clinic. They discuss a case involving a patient with elevated Lp(a). Dr. Jessica Pena provides expert commentary. Drs. Oby Ibe and Elizabeth Epstein drafted notes. CardioNerds Intern Christiana Dangas engineered episode audio. This episode is part of a case reports series developed in collaboration with the National Lipid Association and their Lipid Scholarship Program, with mentorship from Dr. Daniel Soffer and Dr. Eugenia Gianos.
An asymptomatic 34-year-old female presented to the cardiology clinic for cardiovascular risk assessment. Her past medical history included polycystic ovarian syndrome (PCOS) and depression. Her labs were notable for total cholesterol 189 mg/dL, LDL of 131 mg/dL, HDL 34 mg/dL, triglycerides 134 mg/dL, and Lp(a) 217 nmol/L. Her 10-year ASCVD risk by the PREVENT calculator was 0.5%, and her 30-year risk was 3.5%. She had no carotid plaque. Because her 30-year risk was significantly increased by her elevated Lp(a), intensive risk factor management was emphasized, and she was started on a low-dose statin with a plan to follow the patient to reassess the need for intensification of lipid-lowering and/or initiation of novel Lp(a)-lowering therapies over time.
“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.
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Pearls – Little (a), Big Deal – National Lipid Association
You are never too young to see a preventive cardiologist! The field of preventive cardiology is shifting focus towards the identification of early upstream risk and intervention before the development of clinical ASCVD (1,5). Patients who have a strong family history of cardiovascular disease, a personal history of CVD at an early age, multiple risk factors, or genetic disorders such as familial hypercholesterolemia especially benefit from early cardiovascular risk assessment and reduction.
Female-specific risk factors to incorporate into a young woman’s cardiovascular risk assessment include polycystic ovarian syndrome, hormone contraceptive use, early menarche (age <10 years old), primary ovarian insufficiency, fertility therapy, hypertensive disorders of pregnancy (eclampsia, preeclampsia, gestational hypertension, preterm delivery, gestational diabetes, multi-parity >5 pregnancies), early menopause (age <45 years old), & post-menopausal hormone therapy.
Lp(a) testing for all! The most recent NLA scientific statement on the use of Lp(a) in clinical practice recommends measuring Lp(a) at least once in every adult for risk stratification.
While Lp(a) has not yet been incorporated into our risk calculators, we do know that elevated Lp(a) increases 10-year risk. The European Atherosclerosis Society published a consensus statement on Lp(a), which includes a handy table to quantify the degree to which a patient’s 10-year risk increases as Lp(a) increases.
Lifestyle changes are the first line and can reduce the risk of high Lp(a) by 66%. Next, we can consider the risks and benefits of LDL-lowering in a young patient and monitor closely for the development of plaque over time. Lp(a) lowering drugs such as olpasiran are on the horizon, and we can keep this patient in mind as a potential candidate for therapy in the future.
Notes – Little (a), Big Deal – National Lipid Association
When should patients see a preventive cardiologist?
Strong family history of cardiovascular disease – A positive family history of CVD was defined as a self‐reported diagnosis of CVD in parents, siblings, or children that occurred at 60 years or younger. A positive family history of CVD is an independent predictor of both myocardial infarction and stroke. Among individuals with hypertension, family history of CVD has been shown to be independently associated with mortality by ischemic heart disease and family history of CVD mortality with incidence of overall CVD. Family history of CVD modifies future CVD risk depending on the number and age of affected first-degree relatives. Siblings of patients with CVD have about a 40% risk increase, while offspring of parents with premature CVD have a 60% to 75% risk increase.
Personal history of early CVD – A personal history of cardiovascular disease at an age younger than 60 years. For young and middle-aged adults, increases in heart disease between 2020 and 2021 explain more than 4% of the most recent shortening in life expectancy. In particular, hypertensive heart disease, heart failure, and endocarditis have increased in young adults, particularly among Black individuals, through 2018. Consequently, young adults make up a growing proportion of cardiovascular disease events, with the proportion of premature myocardial infarction among adults younger than 40 years increasing by 2% every year. The increasing event rates observed among younger adults can be attributed to the increasing prevalence and onset of risk factors such as obesity and hypertension at younger ages, which exacerbate cumulative exposure and cardiovascular disease risk over near- and long-term time horizons.
Multiple cardiovascular risk factors – Risk factors include hyperlipidemia, high triglycerides, elevated lp(a), diabetes mellitus, obesity, tobacco use, unhealthy diet, and lack of physical activity. Unadjusted event rates were 8-fold to 30-fold higher in persons with adverse levels of risk factor exposure during young adulthood (age 20–39 years) compared with persons with optimal levels of exposure.
Familial hypercholesterolemia – In primary prevention, patients with FH had incidences of ASCVD and coronary heart disease (CHD) of 14.9/1000 and 5.8/1000 person-years, respectively, compared to 7.1/1000 and 2.1/1000 person-years in the normolipidemic group. FH conferred a hazard ratio (HR) of 7.1 and 16.7 for ASCVD and CHD, respectively, in patients younger than 35 years. In secondary prevention, patients with FH had incidences of ASCVD and CHD of 89.7/1000 and 34.5/1000 person-years, respectively, compared to 90.9/1000 and 28.2/1000 person-years in the normolipidemic group
What are some female-specific risk factors for cardiovascular disease? (7)
PCOS – Polycystic ovarian syndrome (PCOS) is a disorder characterized by hyperandrogenism and menstrual irregularities. Women affected by PCOS have a heightened risk of developing diabetes due to associated insulin resistance, central obesity, and hypertension. This adverse cardiovascular risk profile in women with PCOS may lead to premature atherosclerosis (8,20). Women with PCOS have been shown to have an increased risk for CVD events (21).
Depression — Among 593,616 young adults (aged 18–49 years) from 2017 to 2020, depression was independently associated with CHD and suboptimal cardiovascular health (CVH), with a dose‐response relationship (CVH was determined using 7 cardiovascular risk factors: hypertension, hypercholesterolemia, overweight/obesity, current smoking, diabetes, physical inactivity, and inadequate fruit and vegetable intake) (13). Suboptimal CVH was defined as the presence of ≥2 of these 7 cardiovascular risk factors, whereas optimal CVH was 0 or 1 cardiovascular risk factor.
Early menarche – Results from the Women’s Ischemia Syndrome Evaluation (WISE) study demonstrated that in comparison to women with menarche at age 12 years, there was an approximately 4-fold adjusted increased risk for major adverse cardiac events for menarche ≤ 10 years (15).
African descent – Safford et al. found that among those at the highest CHD risk, Black women’s hyperlipidemia was the least likely to be treated or controlled. Lp(a) is significantly higher among Blacks versus Whites, and in both, increased Lp(a) correlates positively with LDL-C and negatively with triglycerides. Another study based on the MESA population demonstrated that Black participants showed a significant risk of CHD in those with Lp(a) levels ≥ 75 nmol/L as opposed to White and Hispanic participants who had a greater risk with Lp(a) levels ≥125 nmol/L.
Elevated BMI – Obesity and higher measures of central adiposity are associated with significantly higher rates of CAD, CVD mortality, sudden cardiac death, heart failure, and arrhythmias (23). High BMI accounted for 4.0 million deaths in 2015, more than two-thirds of which were caused by cardiovascular disease. Marked increases in obesity prevalence among adolescents over the past 35 years ultimately contribute to CVD risk into young adulthood.
Who should be getting an Lp(a) measured?
Per the most NLA-focused update to the 2019 scientific statement on the use of Lp(a) in clinical practice, we now have sufficient evidence to support measuring Lp(a) at least once in all adults for risk stratification.
What risk calculators would apply to a young adult?
The American Heart Association recently released the PREVENT calculator (c-statistic 0.72) for 10- and 30-year risk estimation of total CVD (composite of atherosclerotic CVD and heart failure) in primary prevention patients (10). This improves upon the prior pooled cohort equation because it is based on newer data from a larger, more diverse sample (6,612,004 US adults 30 to 79 years of age) than the existing tool. The calculator also takes into account other health conditions, such as cardiovascular-kidney-metabolic risk factors, adjusts for competing risk of non-CVD death, and incorporates an indicator of social determinants of health. Race was not included because it is a social construct, not a biological risk factor, and could, therefore, create bias. Three research teams were awarded $150,000 from AHA to further study how the risk calculator performs among people of various ages, racial and ethnic backgrounds, locations, and socioeconomic levels.
A universal calculator (c-statistic 0.747 and 0.691 for patients with and without CAD) was also recently published in JACC. This was unique because it can be used in patients both with and without CAD, doing away with the concepts of primary vs secondary prevention and placing everyone on the same spectrum of risk. The calculator incorporates ASCVD vs no ASCVD, age, diabetes, SBP, HTN treatment, TC, smoking history, CRP, NT Pro-BNP, hs Troponin T and provides a 5- and 10-year risk of MACE. The calculator was able to identify patients without CAD who had a higher risk than those with prior CAD. This calculator is not yet available online, but the authors did publish their formulae, which can be plugged into Excel to create a calculator. Unfortunately, this calculator may not apply to our patient because it was validated in a cohort of patients aged 45-64 years.
QRISK3 (c-statistic 0.75) has been validated in patients aged 25-84 years, so it can be useful in predicting cardiovascular disease in both younger and older patients. It also incorporates a wider variety of risk-enhancing factors than most other calculators, including diagnosis of HIV/AIDS, inflammatory diseases, CKD stage, type 1 and type 2 diabetes, and erectile dysfunction. However, it is important to note that this calculator was validated in a primarily European population, and the risk prediction may not be as accurate in other ethnic groups.
How does elevated Lp(a) influence a patient’s 10-year risk, and can we quantify it?
A recent observational study demonstrated that elevated Lp(a) is associated with long-term MACE in both patients with and without cardiovascular disease. Among patients with ASCVD, individuals in the 71st to 90th percentile group had a 21% increased hazard of MACE (adjusted HR: 1.21; P < 0.001), and among patients without ASCVD, individuals in the 91st to 100th Lp(a) percentile group had the highest relative risk with an adjusted HR of 1.93 (P < 0.001). In patients without ASCVD, there was a linear association between Lp(a) and CV events, whereas in patients with prior ASCVD, the association plateaued between 150-200 nmol/L.
Similarly, the 2019 consensus statement from HEART UK categorized the impact of CV risk associated with Lp(a) as minor, moderate, high, or very high based on the level of Lp(a). The table from this paper is a clinically useful tool to categorize risk from Lp(a).
The European Atherosclerosis Society has published a consensus statement on Lp(a) in the European Heart Journal which includes another useful table to adjust a patient’s 10-year risk based on the Lp(a) level(12).
How do we manage a young patient with elevated Lp(a)? Which patients might benefit from treatment with emerging Lp(a)-lowering therapies?
Given we do not yet have Lp(a) lowering therapies available for clinical use, the mainstay of management for patients with elevated Lp(a) is intensive risk factor management. Beyond the question of LDL lowering, we know that lifestyle change plays a big role in patients with elevated Lp(a) specifically. While it was previously thought that lifestyle has no impact on ASCVD risk associated with elevated Lp(a), in fact, it very much does. It doesn’t lower Lp(a) directly but following the AHA Life’s Simple 8 lowers the risk of Lp(a) by 66%.
There is some newer data suggesting that in patients with coronary artery disease, aggressive LDL lowering down to 50 can reduce the risk of Lp(a) by up to 50% (6). LDL of 50 mg/dL is a pretty aggressive treatment goal, which makes sense in very high-risk patients with existing CAD. However, we still need more data to guide LDL treatment goals in young patients(18).
Novel Lp(a)-lowering therapies such as olpasiran are currently in clinical trials (19). We await the data from these trials in order to understand which patients would benefit most from treatment.
References
Allen N, Wilkins JT. The Urgent Need to Refocus Cardiovascular Disease Prevention Efforts on Young Adults. JAMA. 2023;329(11):886-887. doi:10.1001/jama.2023.2308
https://jamanetwork.com/journals/jama/fullarticle/2802264
Baber, Usman, Roxana Mehran, Samantha Sartori, Mikkel Malby Schoos, Henrik Sillesen, Pieter Muntendam, Mario J. Garcia, et al. 2015. “Prevalence, Impact, and Predictive Value of Detecting Subclinical Coronary and Carotid Atherosclerosis in Asymptomatic Adults: The BioImage Study.” Journal of the American College of Cardiology 65 (11): 1065–74.
https://pubmed.ncbi.nlm.nih.gov/25790876
Bhatia, H. S., Trainor, P., Carlisle, S., Tsai, M. Y., Criqui, M. H., DeFilippis, A., & Tsimikas, S. (2024). Aspirin and Cardiovascular Risk in Individuals With Elevated Lipoprotein (a): The Multi‐Ethnic Study of Atherosclerosis. Journal of the American Heart Association, 13(3), e033562.
https://www.ahajournals.org/doi/10.1161/JAHA.123.033562
Coll, B., Betriu, A., Feinstein, S. B., Valdivielso, J. M., Zamorano, J. L., & Fernandez, E. (2013). The role of carotid ultrasound in assessing carotid atherosclerosis in individuals at low-to-intermediate cardiovascular risk. Revista Española de Cardiología (English Edition), 66(12), 929-934.
https://pubmed.ncbi.nlm.nih.gov/24774105
Devesa, A, Ibanez, B, Malick, W. et al. Primary Prevention of Subclinical Atherosclerosis in Young Adults: JACC Review Topic of the Week. J Am Coll Cardiol. 2023 Nov, 82 (22) 2152–2162.
https://www.jacc.org/doi/10.1016/j.jacc.2023.09.817
Dykun, Iryna, Jürgen Kampf, Tienush Rassaf, and Amir A. Mahabadi. 2023. “Interaction between Elevated Lipoprotein(a) and LDL Cholesterol on Mortality Risk in Patients with Coronary Artery Disease.” European Journal of Preventive Cardiology 30 (13): e64–65.
https://academic.oup.com/eurjpc/article-abstract/30/13/e64/7065497?redirectedFrom=PDF
Elder P, Sharma G, Gulati M, Michos ED. Identification of female-specific risk enhancers throughout the lifespan of women to improve cardiovascular disease prevention. Am J Prev Cardiol. 2020;2:100028. Published 2020 Jun 6. doi:10.1016/j.ajpc.2020.100028
https://www.sciencedirect.com/science/article/pii/S2666667720300283
Glintborg D, Rubin KH, Nybo M, Abrahamsen B, Andersen M. Cardiovascular disease in a nationwide population of Danish women with polycystic ovary syndrome. Cardiovasc Diabetol. 2018;17(1):37. Published 2018 Mar 8. doi:10.1186/s12933-018-0680-5
https://pubmed.ncbi.nlm.nih.gov/29519249
Guan, W., Cao, J., Steffen, B. T., Post, W. S., Stein, J. H., Tattersall, M. C., … & Tsai, M. Y. (2015). Race is a key variable in assigning lipoprotein (a) cutoff values for coronary heart disease risk assessment: the Multi-Ethnic Study of Atherosclerosis. Arteriosclerosis, thrombosis, and vascular biology, 35(4), 996-1001.
https://pubmed.ncbi.nlm.nih.gov/25810300
Khan, S. S., Coresh, J., Pencina, M. J., Ndumele, C. E., Rangaswami, J., Chow, S. L., … & American Heart Association. (2023). Novel prediction equations for absolute risk assessment of total cardiovascular disease incorporating cardiovascular-kidney-metabolic health: a scientific statement from the American Heart Association. Circulation, 148(24), 1982-2004.
https://www.ahajournals.org/doi/10.1161/CIR.0000000000001191
Kolber MR, Scrimshaw C. Family history of cardiovascular disease. Can Fam Physician. 2014;60(11):1016.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4229162/#:~:text=Family%20history%20of%20CVD%20modifies,%25%20to%2075%25%20risk%20increase.
Kronenberg, Florian, Samia Mora, Erik S. G. Stroes, Brian A. Ference, Benoit J. Arsenault, Lars Berglund, Marc R. Dweck, et al. 2022. “Lipoprotein(a) in Atherosclerotic Cardiovascular Disease and Aortic Stenosis: A European Atherosclerosis Society Consensus Statement.” European Heart Journal 43 (39): 3925–46.
https://pubmed.ncbi.nlm.nih.gov/36036785
Kwapong YA, Boakye E, Khan SS, et al. Association of Depression and Poor Mental Health With Cardiovascular Disease and Suboptimal Cardiovascular Health Among Young Adults in the United States. J Am Heart Assoc. 2023;12(3):e028332. doi:10.1161/JAHA.122.028332
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9973664
Lau, F. D., & Giugliano, R. P. (2022). Lipoprotein (a) and its significance in cardiovascular disease: a review. Jama Cardiology.
https://pubmed.ncbi.nlm.nih.gov/35583875
Lee, J. J., Cook‐Wiens, G., Johnson, B. D., Braunstein, G. D., Berga, S. L., Stanczyk, F. Z., … & Shufelt, C. L. (2019). Age at menarche and risk of cardiovascular disease outcomes: findings from the National Heart Lung and Blood Institute‐sponsored Women’s Ischemia Syndrome Evaluation. Journal of the American Heart Association, 8(12), e012406.
https://pubmed.ncbi.nlm.nih.gov/31165670
Masana L, Zamora A, Plana N, et al. Incidence of Cardiovascular Disease in Patients with Familial Hypercholesterolemia Phenotype: Analysis of 5 Years Follow-Up of Real-World Data from More than 1.5 Million Patients. J Clin Med. 2019;8(7):1080. Published 2019 Jul 23. doi:10.3390/jcm8071080
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678686
Mendieta, Guiomar, Stuart Pocock, Virginia Mass, Andrea Moreno, Ruth Owen, Inés García-Lunar, Beatriz López-Melgar, et al. 2023. “Determinants of Progression and Regression of Subclinical Atherosclerosis Over 6 Years.” Journal of the American College of Cardiology 82 (22): 2069–83.
https://pubmed.ncbi.nlm.nih.gov/37993199
Navar, A. M., Fine, L. J., Ambrosius, W. T., Brown, A., Douglas, P. S., Johnson, K., … & Lewis, C. E. (2022). Earlier treatment in adults with high lifetime risk of cardiovascular diseases: what prevention trials are feasible and could change clinical practice? Report of a National Heart, Lung, and Blood Institute (NHLBI) workshop. American journal of preventive cardiology, 12, 100430.
https://pubmed.ncbi.nlm.nih.gov/36439649
O’Donoghue, M. L., Rosenson, R. S., Gencer, B., López, J. A. G., Lepor, N. E., Baum, S. J., … & Sabatine, M. S. (2022). Small interfering RNA to reduce lipoprotein (a) in cardiovascular disease. New England Journal of Medicine, 387(20), 1855-1864.
https://www.nejm.org/doi/full/10.1056/NEJMoa2211023
Orio Jr, F., Palomba, S., Cascella, T., De Simone, B., Di Biase, S., Russo, T., … & Colao, A. (2004). Early impairment of endothelial structure and function in young normal-weight women with polycystic ovary syndrome. The Journal of Clinical Endocrinology & Metabolism, 89(9), 4588-4593.
https://pubmed.ncbi.nlm.nih.gov/15356067
Osibogun O, Ogunmoroti O, Michos ED. Polycystic ovary syndrome and cardiometabolic risk: Opportunities for cardiovascular disease prevention. Trends Cardiovasc Med. 2020;30(7):399-404. doi:10.1016/j.tcm.2019.08.010
https://www.sciencedirect.com/science/article/pii/S1050173819301288?via%3Dihub
Pletcher MJ, Vittinghoff E, Thanataveerat A, Bibbins-Domingo K, Moran AE. Young Adult Exposure to Cardiovascular Risk Factors and Risk of Events Later in Life: The Framingham Offspring Study. PLoS One. 2016;11(5):e0154288. Published 2016 May 3. doi:10.1371/journal.pone.0154288
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4854462
Powell-Wiley, T. M., Poirier, P., Burke, L. E., Després, J. P., Gordon-Larsen, P., Lavie, C. J., … & American Heart Association Council on Lifestyle and Cardiometabolic Health; Council on Cardiovascular and Stroke Nursing; Council on Clinical Cardiology; Council on Epidemiology and Prevention; and Stroke Council. (2021). Obesity and cardiovascular disease: a scientific statement from the American Heart Association. Circulation, 143(21), e984-e1010.
https://pubmed.ncbi.nlm.nih.gov/33882682
Safford, M. M., Gamboa, C. M., Durant, R. W., Brown, T. M., Glasser, S. P., Shikany, J. M., … & Muntner, P. (2015). Race–Sex Differences in the Management of Hyperlipidemia: The REasons for Geographic And Racial Differences in Stroke Study. American journal of preventive medicine, 48(5), 520-527.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4422177
Talbott EO, Zborowski JV, Rager JR, Boudreaux MY, Edmundowicz DA, Guzick DS. Evidence for an association between metabolic cardiovascular syndrome and coronary and aortic calcification among women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2004;89(11):5454-5461. doi:10.1210/jc.2003-032237
https://academic.oup.com/jcem/article/89/11/5454/2844369?login=false
Wilson DP, Jacobson TA, Jones PH, et al. Use of Lipoprotein(a) in clinical practice: A biomarker whose time has come. A scientific statement from the National Lipid Association [published correction appears in J Clin Lipidol. 2022 Sep-Oct;16(5):e77-e95]. J Clin Lipidol. 2019;13(3):374-392. doi:10.1016/j.jacl.2019.04.010
https://www.lipidjournal.com/article/S1933-2874(22)00244-6/fulltext#seccesectitle0006
32 min
July 30, 2024 383. Guidelines: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure – Question #33 with Dr. Biykem Bozkurt

The following question refers to Section 5.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.
The question is asked by University of Colorado internal medicine resident Dr. Hirsh Elhence, answered first by advanced heart failure faculty at the University of Chicago and Co-Chair for the CardioNerds Critical Care Cardiology Series Dr. Mark Belkin, and then by expert faculty Dr. Biykem Bozkurt.
Dr. Bozkurt is the Mary and Gordon Cain Chair, Professor of Medicine, Director of the Winters Center for Heart Failure Research, and an advanced heart failure and transplant cardiologist at Baylor College of Medicine in Houston, TX. She is former President of HFSA, former senior associate editor for Circulation, and current Editor-In-Chief of JACC Heart Failure. Dr. Bozkurt was the Vice Chair of the writing committee for the 2022 Heart Failure 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.

Question #33

A 63-year-old man with a past medical history of hypertension and type 2 diabetes mellitus presents for routine follow-up. He reports feeling in general good health and enjoys 2-mile walks daily. A review of systems is negative for any symptoms. Which of the following laboratory studies may be beneficial for screening?
A
NT-proBNP
B
CK-MB
C
Troponin
D
C-reactive protein
E
None of the above
Answer #33

Explanation
The correct answer is A – NT-proBNP.
This patient is at risk for HF (Stage A) given the presence of risk factors (hypertension and type 2 diabetes mellitus) but the absence of signs or symptoms of heart failure.
Patients at risk for HF screened with BNP or NT-proBNP followed by collaborative care, diagnostic evaluation, and treatment in those with elevated levels can reduce combined rates of LV systolic dysfunction, diastolic dysfunction, and HF.
The STOP-HF (St Vincent’s Screening to Prevent Heart Failure) study was a large single-center trial of patients at risk of HF that showed BNP-based screening reduced the composite endpoint of incident asymptomatic LV dysfunction with or without newly diagnosed HF.
Therefore, for patients at risk of developing HF, natriuretic peptide biomarker-based screening followed by team-based care, including a cardiovascular specialist optimizing GDMT, can be useful to
prevent the development of LV dysfunction (systolic or diastolic) or new-onset HF (Class 2a, LOE B-R).
There is no indication for measuring troponin, CK-MB, or CRP at this time.
Main Takeaway
In patients at risk for HF, screening for pre-HF using natriuretic peptide testing followed by team-based care may be helpful for preventing disease progression.
Guideline Loc.
Section 5.1

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6 min
July 28, 2024382. SGLT Inhibitors: The Data Supporting SGLT Inhibition with Dr. Muthiah Vaduganathan
CardioNerds Dr. Rick Ferraro, Dr. Gurleen Kaur, and Dr. Maryam Barkhordarian discuss the evidence and data supporting SGLT inhibition for cardiovascular and kidney health outcomes with expert faculty Dr. Muthu Vaduganathan. They discuss the role of SGLT inhibitors in different populations, including those with diabetes mellitus, heart failure, CKD, and myocardial infarction. Show notes and audio editing by CardioNerds Academy Fellow Dr. Maryam Barkhordarian.
This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Lexicon Pharmaceuticals.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Pearls – The Data Supporting SGLT Inhibition with Dr. Muthiah Vaduganathan
The benefit of SGLT inhibition extends beyond diabetes, and improves cardiovascular and kidney health outcomes independent of diabetes in appropriate patient populations.
SGLT inhibition decreases cardiovascular mortality and heart failure hospitalization independent of left ventricular ejection fraction.
SGLT inhibitors reduce clinically relevant events such as dialysis and transplantation in CKD patients irrespective of etiology and are now a cornerstone for the prevention of CKD progression.
The introduction of polypills in heart failure can simplify GDMT implementation.
Show notes – The Data Supporting SGLT Inhibition with Dr. Muthiah Vaduganathan
How did SGLT inhibitors transition from “diabetes medication” to guideline-directed cardiovascular medicine?
Most therapies in cardiology were developed for a particular purpose and ended up being indicated for a vastly different reason. The SGLT-2 inhibitors are no different.
Cardiovascular safety concerns about diabetes medications led to a mandate to conduct cardiovascular outcomes trials for all novel diabetes medications. This federal requirement shed light on the cardiovascular benefits of SGLT inhibitors in patients with diabetes.
These initial trials showed that not only are these medications safe but also, surprisingly, proved their role in preventing heart failure and delaying progression of chronic kidney disease.
What are the mechanisms of action of SGLT-2 and SGLT-1/2 inhibitors?
The central mechanism(s) of how these medications confer health outcomes benefits patients is/are not well understood.
The main organ involved in the action of SGLT-2 inhibitors is the kidney at the level of the proximal tubule, impacting the cardiovascular system by handling salt and water and improving kidney efficiency. Conversely, SGLT-1/2 inhibitors also act at the level of the gut, the predominant location of the SGLT-1 cotransporter.
Their effects on the cardiovascular system are secondary, given there is no SGLT-1 or -2 cotransporters in the myocardium. These secondary effects can be impacted through blood pressure reduction, volume regulation, improved glycemic control, etc. to overall improve cardiovascular status.
Whatever the underlying mechanisms, the empirical data for their use is strong and growing.
What is the role of SGLT inhibitors in preventing CKD progression?
RAAS inhibitors (ACE inhibitors and ARBs) have been the cornerstone of CKD management for the past two to three decades.
SGLT inhibitors have been the first add-on to this background therapy.
Four trials, DAPA-CKD, EMPA-CKD, CREDENCE, and the SCORED, investigated the effects of SGLT-2 and SGLT-1/2 inhibitors in patients with CKD with or without diabetes.
The outcomes of these trials include modifying the course of CKD and reducing events such as dialysis initiation and transplantation. These effects were regardless of participants’ diabetic status, CKD etiology, or individual patient profile.
The addition of SGLT-2 inhibitors to ACEI or ARB can be considered as GDMT of CKD.
What is the role of SGLT-2 inhibitors in combination with other medications as polypill?
Polypills have been beneficial in many areas such as cardiometabolic medicine, hypertension, and diabetes mellitus. In addition, a multi-drug regimen is strongly recommended in heart failure with reduced ejection fraction.
Developing polypills in HFrEF has been challenging because adjacent compounds are not available in the armamentarium of sponsored pharmaceutical companies.
Investigations of various polypills are underway for the management of heart failure.
References – The Data Supporting SGLT Inhibition with Dr. Muthiah Vaduganathan
Heerspink HJL, Stefánsson BV, Correa-Rotter R, et al. Dapagliflozin in Patients with Chronic Kidney Disease. N Engl J Med. 2020;383(15):1436-1446. doi:10.1056/NEJMoa2024816
The EMPA-KIDNEY Collaborative Group, Herrington WG, Staplin N, et al. Empagliflozin in Patients with Chronic Kidney Disease. N Engl J Med. 2023;388(2):117-127. doi:10.1056/NEJMoa2204233
Perkovic V, Jardine MJ, Neal B, et al. Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy. N Engl J Med. 2019;380(24):2295-2306. doi:10.1056/NEJMoa1811744
Bhatt DL, Szarek M, Pitt B, et al. Sotagliflozin in Patients with Diabetes and Chronic Kidney Disease. N Engl J Med. 2021;384(2):129-139. doi:10.1056/NEJMoa2030186
25 min
July 19, 2024381. Narratives in Cardiology: Advocacy for Refugee Health and Empowering First-Generation Cardiologists with Dr. Heval Kelli
In this episode, Dr. Gurleen Kaur (Cardiology FIT at Brigham and Women’s Hospital and APD of the CardioNerds Academy) and Dr. Chelsea Amo-Tweneboah (Medicine Resident at Stonybrook and CardioNerds Academy Intern) discuss with Dr. Heval Kelli (Cardiologist at Northside Hospital Cardiovascular Institute) about his personal and professional journey in Cardiology. They discuss Dr. Kelli’s lifelong advocacy for serving those in need including refugee and immigrant communities, his character in the documentary Refuge, and fostering inclusivity within Cardiology. Audio editing and show notes were drafted by Dr. Chelsea Amo-Tweneboah.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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.
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Video version – Advocacy for Refugee Health and Empowering First-Generation Cardiologists
Quoatables – Advocacy for Refugee Health and Empowering First-Generation Cardiologists
“I have always believed that if someone opened the door for you, you have to hold the door for the next generation. Because if you just walk through the door and close it, you just close the door for many people behind you.”
“Instead of making luck a matter of luck, just make an opportunity for everyone else.”
“Hate makes us realize that no matter how privileged you are, you are not protected.”
“It is very hard to hate something you know.”
“Compassion starts with the neighbor next to you, and then you go out to the world and show it.”
“Your best intern wasn’t the smartest intern. Your best intern was the person ready to go for rounds, took care of everything, sharp early in the morning, stays late, and gets the work done.”
“Intelligence is relative. Hard work and dedication [are] the most important thing.”
Notes – Advocacy for Refugee Health and Empowering First-Generation Cardiologists
Advocacy for refugee health and empowering first-generation cardiologists
Focusing on creating professionals from a given community can help increase their chances of returning to that community and helping to address health disparities.
Refugees and immigrants come from countries and communities where, by and large, prevention is lacking. Seeing a healthcare provider is more appropriate in dire situations.
When approaching immigrants, it is important to present medical information in ways in which they can understand and absorb properly.
For many refugee families, there exists a language barrier and the children are most often the advocates for the family because they are most likely to understand the language of the community they live in.
The vast number of students in the US medical school system come from privileged backgrounds; however, this same statistic is not true for the populations they end up serving.
It is important to have health professionals reflect the populations they serve, and one of the methods to achieve this is through introducing as many individuals as possible to the field of medicine; one of the ways to overcome a leaky pipeline is to pack the pipeline. Strategies include encouraging medical students to serve as mentors for those junior to them.
It is important to build more sustainable relationships with communities because it leads to more trust and success.
Advocating for mental health in these communities is very important because they face these issues at an increased level. However, it is unfortunately under-addressed.
Resource avenues such as the CDC provide substantial information regarding different refugee and immigrant profiles and the issues most pertinent to these communities.
Inclusivity in Cardiology
It is important to normalize people feeling comfortable in having a discourse about differences and recognizing the challenges individuals face when pursuing a career in medicine or cardiology in order to promote inclusivity in this field. This is a major goal for the CardioNerds Narratives in Cardiology program.
Within Cardiology, structural racism and hate are present.
It is important to place yourself in a challenging environment or one different from what you are used to and attempt to find common ground with other individuals.
The Bridge Between Social Issues and Cardiology
As a physician, it is important to create boundaries and choose what social issues you wish to engage in.
If groups of people do not see eye to eye, steps should be taken to reach out to one another and establish and try to understand what these differences are.
Physicians are the best advocates in the world because, for the most part, they are trusted by their patients. Recognizing the importance of the influence that physicians have and realizing this influence can extend beyond the medical space.
Humor can be another means by which to make it easier to bring up important conversations that may otherwise be difficult.
Technology to Help Bridge the Gap
Technology can serve as a means of being able to communicate with refugee families because they are likely to have access to a smartphone.
Refugee families most often don’t understand the information given to them in paper or pamphlet form, and often important medical advice can be lost that way.
Technology provides increased access to medicine and allows patients more individuality and control in keeping on top of their health.
Artificial intelligence technology is the direction that health and medicine are heading in; thus, health professionals and patients must learn how to use this technology to their advantage.
21 min
July 12, 2024380. Case Report: Tearing Up My Heart – A Case of Papillary Muscle Rupture – University of Rochester
CardioNerds co-founder Dan Ambinder joins Dr. Lefan He, Dr. Sina Salehi Omran, and Dr. Neil Gupta from the University of Rochester Cardiovascular Disease Fellowship Program for a day sailing on Lake Ontario. Expert commentary is provided by Dr. Jeffrey Bruckel, and CV Fellowship Program Director Dr. Burr Hall shares insights on the University of Rochester fellowship. The episode audio was edited by CardioNerds intern Dr. Atefeh Ghorbanzadeh. They discuss the following case involving a patient with papillary muscle rupture.
This is a 63-year-old man with hypertension, hyperlipidemia, and active tobacco smoking who presented with acute dyspnea. He was tachycardic but otherwise initially hemodynamically stable. The physical exam demonstrated warm extremities with no murmurs or peripheral edema. Chest X-ray revealed diffuse pulmonary edema, and the ECG showed sinus tachycardia with T-wave inversions in the inferior leads. A bedside echocardiogram revealed a flail anterior mitral valve leaflet. The patient was taken for cardiac catheterization that revealed nonobstructive mid-RCA atheroma with a distal RCA occlusion, which was felt to reflect embolic occlusion from recanalized plaque. PCI was not performed. Right heart catheterization then demonstrated a low cardiac index as well as elevated PCWP and PA pressures. An intra-aortic balloon pump was placed at that time. A TEE was performed soon after which showed the posteromedial papillary muscle was ruptured with flail segments of the anterior mitral leaflet as well as severe posteriorly directed mitral regurgitation. The patient ultimately underwent a successful tissue mitral valve replacement and CABG.
“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.
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case Media
Pearls – A Case of Papillary Muscle Rupture
Most cases of papillary muscle rupture demonstrate only small areas of ischemia with preserved ventricular function, thus causing high shear force on the ischemic papillary muscle.
The posteromedial papillary muscle has a single blood supply from the posterior descending artery, while the anterolateral papillary muscle has a dual blood supply from the LAD and the circumflex. Therefore, the posteromedial papillary muscle is more vulnerable to ischemia and, hence, rupture.
A murmur may be absent in cases of papillary muscle rupture due to the rapid equalization of left atrial and left ventricular pressures caused by the acuteness of the severe MR. Papillary muscle rupture should always be on the differential for acute dyspnea when ACS is suspected.
While mostly associated with STEMIs, mechanical complications of acute myocardial infarctions can also occur after NSTEMIs. Always auscultate patients carefully after a myocardial infarction!
When evaluating patients with chest pain presenting with acute or rapidly progressive heart failure and a hypercontractile LVEF should raise suspicion for mechanical complications of MI.
Once a papillary muscle rupture is diagnosed, cardiac surgery should be immediately contacted. Temporizing measures prior to surgery include positive pressure ventilation, IV nitroglycerin/nitroprusside, and temporary mechanical circulatory support.
Notes – A Case of Papillary Muscle Rupture
What is the clinical presentation of acute mitral regurgitation from papillary muscle rupture?
Patients typically present 3-5 days after a transmural infarct. Roughly half of these patients present with pulmonary edema that may quickly progress to cardiogenic shock.
Most cases are associated with STEMIs, but papillary muscle rupture is also possible with an NSTEMI.
The classic murmur is a mid-, late-, or holosystolic murmur. However, due to the rapid equalization of pressures between the LA and LV, many patients may not present with a murmur!
What is the pathophysiology of papillary muscle rupture?
The most common etiology is acute occlusion of the RCA causing infarct of the posteromedial papillary muscle, which then leads to a partial or complete tear 2-7 days later.
The posteromedial papillary muscle has a single blood supply from the posterior descending artery, while the anterolateral papillary muscle has a dual blood supply from the LAD and the circumflex. Therefore, the posteromedial papillary muscle is more vulnerable to ischemia and, hence, rupture.
What are the echocardiographic features of acute mitral regurgitation?
Typically, acute mitral regurgitation is caused by acute insult to the mitral valve or mitral valve apparatus. Examples include endocarditis with leaflet perforation, acute flail leaflet in the setting of mitral valve prolapse, and infarct-related papillary muscle rupture. Also, the LVEF can be hypercontractile.
Left ventricular and left atrial dimensions tend to be normal in acute MR as the heart has not had time to remodel. This also leads to rapid equalization of the LV-LA pressure during systole, blunting both the Doppler signal and the audible murmur which may under-appreciate acute severe mitral regurgitation.
Severe mitral regurgitation typically has a regurgitant volume of ≥60 mL or a regurgitant fraction of at least 50%. Additionally, an effective regurgitant orifice area of 0.4 cm^2 is typically indicative of severe mitral regurgitation. A complete multiparametric assessment is more important than any single parameter.
Systolic flow reversal in the pulmonary veins is pathognomonic for severe mitral regurgitation. This may not be apparent in all pulmonary veins if the MR is eccentric, as is usually the case of papillary muscle or acute leaflet flail.
How should acute mitral regurgitation due to papillary muscle rupture be managed?
Afterload reduction may help, but this may be limited by hypotension in the acute setting.
Temporary mechanical circulatory support may be necessary, often with an intra-aortic balloon pump which can be effective in improving forward flow.
The ultimate and definitive treatment is urgent cardiac surgery along with concomitant bypass grafting as appropriate. Transcatheter edge-to-edge repair may be considered sparingly when surgery is deemed very high risk.
What are the other mechanical complications of acute myocardial infarction?
Ventricular septal rupture typically occur 3-5 days after an infarct but there is a bimodal distribution. The presentation can vary from an isolated systolic murmur all the way to cardiogenic shock. Echocardiography will show a left to right shunt and right heart cath will show a step-up in oxygenation between the RA and PA as well as an elevated Qp/Qs. VSRs require urgent surgical or percutaneous repair.
Ventricular free wall rupture also occurs 3-5 days after an infarct and presents with elevated jugular venous distension, muffled heart sounds, and pulsus paradoxus. As blood irritates the pericardium, the patient’s ECG can show new ST-elevations. Management is emergent surgery.
Pseudoaneurysms present weeks to years after an infarct. These occur when a cardiac rupture is contained by pericardial adhesions and typically involve the inferior or lateral walls. Patients may be asymptomatic, but once diagnosed, pseudoaneurysms should be urgently repaired, lest they expand or become unstable.
References
Damluji AA, van Diepen S, Katz JN, Menon V, Tamis-Holland JE, Bakitas M, Cohen MG, Balsam LB, Chikwe J; on behalf of the American Heart Association Council on Clinical Cardiology; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular Surgery and Anesthesia; and Council on Cardiovascular and Stroke Nursing. Mechanical complications of acute myocardial infarction: a scientific statement from the American Heart Association. Circulation. 2021;144:e16–e35. doi: 10.1161/CIR.0000000000000985
Chang C et al. Transcatheter Edge-to-Edge Repair for Acute Mitral Regurgitation due to Postinfarction Papillary Muscle Rupture. JSCAI (2022) 100431.
Kilic A et al. Mitral Valve Surgery for Papillary Muscle Rupture: Outcomes in 1342 Patients From The Society of Thoracic Surgeons Database. The Annals of Thoracic Surgery Volume 110, Issue 6, December 2020, Pages 1975-1981
van Diepen S, Katz JN, Albert NM, Henry TD, Jacobs AK, Kapur NK, Kilic A, Menon V, Ohman EM, Sweitzer NK, Thiele H, Washam JB, Cohen MG; on behalf of the American Heart Association Council on Clinical Cardiology; Council on Cardiovascular and Stroke Nursing; Council on Quality of Care and Outcomes Research; and Mission: Lifeline. Contemporary management of cardiogenic shock: a scientific statement from the American Heart Association. Circulation. 2017;136:e232–e268. doi: 10.1161/CIR.0000000000000525
Zoghbi, W. A., Adams, D., Bonow, R. O., Enriquez-Sarano, M., Foster, E., Grayburn, P. A., Hahn, R. T., Han, Y., Hung, J., Lang, R. M., Little, S. H., Shah, D. J., Shernan, S., Thavendiranathan, P., Thomas, J. D., & Weissman, N. J. (2017). Recommendations for noninvasive evaluation of native valvular regurgitation. Journal of the American Society of Echocardiography, 30(4), 303–371. https://doi.org/10.1016/j.echo.2017.01.007
48 min
July 09, 2024379. SGLT Inhibitors: The Biology of SGLT Inhibition with Dr. Katherine Tuttle
CardioNerds (Drs. Gurleen Kaur and Richard Ferraro) and episode FIT Lead Dr. Saahil Jumkhawala (Cardiology Fellow at the University of Miami) discuss SGLT inhibitors, focusing on the biology of SGLT and its inhibition, with Dr. Katherine Tuttle (Executive Director for Research at Providence Healthcare, Co-Principal Investigator of the Institute of Translational Health Sciences, and Professor of Medicine at the University of Washington). Show notes were drafted by Dr. Saahil Jumkhawala. The episode audio was engineered by CardioNerds intern Christiana Dangas.
This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Lexicon Pharmaceuticals.
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.
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Pearls – The Biology of SGLT Inhibition with Dr. Katherine Tuttle
SGLT inhibitors, while initially developed as antidiabetic medications, have been shown to be beneficial for cardiovascular and renal outcomes. These benefits result from their on-target glucosuric effects and additional off-target effects.
The side effect profiles of SGLTis are primarily mediated by glucose reabsorption in their target tissues. The side effect profile of SGLTis must be considered when prescribing these medications and is generally favorable for SGLT2is versus SGLT1is.
Once SGLTis are prescribed, patients should be given specific attention to their eGFR, serum potassium, and clinical evaluations of volume status and blood pressure.
Strategies to increase implementation of and reduce clinical inertia for these important class of medication remain an area of active investigation
Show notes – The Biology of SGLT Inhibition with Dr. Katherine Tuttle
What should prompt consideration of starting an SGLT inhibitor?
Considerations for SGLT inhibitor initiation are based on a history of heart failure, kidney disease, and diabetes status.
In the EMPA-KIDNEY trial, empagliflozin improved cardiovascular and kidney outcomes in those with low GFR (regardless of level of albuminuria).
What is the mechanism of action of SGLT2 inhibitors?
SGLT2 inhibitors improve glycemic control by blocking SGLT2 receptor-mediated reabsorption of glucose in the proximal convoluted tubule, where 80-90% of this reuptake occurs, and increased downstream excretion of glucose and sodium chloride. SGLT2 inhibitors provide only a modest glucose-lowering effect, particularly for patients with GFR <45.
How do SGLT2 inhibitors improve cardiac function?
Through corrected glomerular hyperfiltration, there is a reduction in blood pressure, a reduction in sympathetic neural activity, and increased glucosuria, improving diuresis. Systemically, there is an increase in erythropoietin, which raises red blood cell mass and oxygen-carrying capacity.
Beyond inhibition of the SGLT2 receptor, which is isolated to the proximal convoluted tubule, there are additional off-target effects. Through non-receptor-mediated mechanisms, glucose transport is blocked into cells by blocking GLUT1 and GLUT4 receptors. They also reduce the mTORC signal transduction pathway, thereby reducing inflammation and glycolysis, leading to a cardioprotective effect in myocytes.
In the DAPA-CKD and CREDENCE trials, GFR decreases of up to 30% were correlated with improved renal and cardiovascular outcomes.
The cardiovascular benefit of SGLT2 inhibitors is not dose-dependent.
Where are SGLT1 receptors located?
SGLT1 receptors are found primarily in small and large bowel enterocytes, as well as the kidney proximal tubule, beyond the convoluted segment.
Around 10% of glucose re-uptake is mediated by SGLT1 receptors in the proximal tubule.
What are some common side effects of SGLT inhibitors?
Given SGLT1 receptors’ presence in the gastrointestinal tract, the side effects of SGLT1 inhibition are primarily gastrointestinal upset through decreased glucose reabsorption in the gut.
SGLT2 inhibitors’ side effects are primarily sequelae of glucosuria, particularly those of genitourinary infections, volume depletion, and euglycemic ketoacidosis (most commonly in patients with diabetes who are longstanding insulin users).
Additionally, a GFR decline of >30% should be suggestive of other issues for patients taking these medications, most commonly volume depletion or hypotension.
References – The Biology of SGLT Inhibition with Dr. Katherine Tuttle
Cowie M.R., Fisher M. SGLT2 inhibitors: mechanisms of cardiovascular benefit beyond glycaemic control. Nat Rev Cardiol. 2020 Dec; 17(12):761-722.
Kuboto Y, Shimizu W. Clinical Benefits of Sodium-Glucose Cotransporter 2 Inhibitors and the Mechanisms Underlying their Cardiovascular Effects. JACC: Asia. 2022 Jun; 2:287-293.
Lopaschuk G.D., Verma S. Mechanisms of Cardiovascular Benefits of Sodium Glucose Co-Transporter 2 (SGLT2) Inhibitors. JACC Basic Trans Sci. 2020 Jun; 5(6):632-644.
Harrington J., Udell J.A., Jones W.S., Anker S.D., Bhatt D.L., Petrie M.C., & Butler J. Empagliflozin in patients post myocardial infarction: rationale and design of the EMPACT-MI trial. American Heart Journal. 2022; 253:86-98.
Talha K.M., Anker S.D., & Butler J. SGLT-2 inhibitors in heart failure: a review of current evidence. International Journal of Heart Failure. 2023; 5(2):82.
Tuttle K.R. Digging deep into cells to find mechanisms of kidney protection by SGLT2 inhibitors. J Clin Invest. 2023; 133(5).
34 min
June 26, 2024 378. Case Report: Severe Mitral Paravalvular Regurgitation Complicated by Hemolytic Anemia – Duke University
CardioNerds cofounder, Amit Goyal joins Dr. Belal Suleiman, Dr. Nkiru Osude, and Dr. David Elliott from Duke University. They discuss a case of severe mitral paravalvular regurgitation complicated by hemolytic anemia. Expert commentary is provided by Dr. Andrew Wang. Audio editing by CardioNerds Academy Intern, student doctor Adriana Mares.
“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 – Severe Mitral Paravalvular Regurgitation Complicated by Hemolytic Anemia – Duke University
20 min

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