Episodes Archives - Cardionerds

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Episodes Archives - Cardionerds episodes

July 14, 2023 317. Guidelines: 2021 ESC Cardiovascular Prevention – Question #30 with Dr. Eugenia Gianos

The following question refers to Section 6.1 of the 2021 ESC CV Prevention Guidelines. The question is asked by MGH internal medicine resident Dr. Christian Faaborg-Andersen, answered first by UCSD early career preventive cardiologist Dr. Harpreet Bhatia, and then by expert faculty Dr. Eugenia Gianos.
Dr. Gianos specializes in preventive cardiology, lipidology, cardiovascular imaging, and women’s heart disease; she is the Director of Women’s Heart Health at Lenox Hill Hospital and Director of Cardiovascular Prevention for Northwell Health.
The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #30

A 65-year-old woman with a history of hypertension, type 2 diabetes mellitus, and coronary artery disease with remote PCI to the RCA presents for follow-up. She has stable angina symptoms that are well controlled with metoprolol tartrate 25 mg BID and are not lifestyle limiting. She takes aspirin 81 mg daily and atorvastatin 40 mg daily. Her LDL-C is 70 mg/dL, hemoglobin A1c is 7.0%, and eGFR is >60. In clinic, her BP is 118/80 mmHg. What is the next step in management?
A
Increase atorvastatin for goal LDL-C < 55 mg/dL
B
No change in management
C
Add isosorbide mononitrate 30 mg daily
D
Stop aspirin
E
Start a sulfonylurea
Answer #30

Explanation

The correct answer is A – increase atorvastatin for goal LDL-C < 55 mg/dL.
In patients with established ASCVD, the ESC guidelines advocate for an LDL goal of < 55 mg/dL with at least a 50% reduction from baseline levels (Class I, LOE A). This patient has stable angina which is not lifestyle limiting; as such, further anti-anginal therapy is not necessary. She has known CAD with prior PCI, so aspirin therapy is appropriate for secondary prevention (Class I, LOE A). There is no indication for a sulfonylurea as her diabetes is well controlled. Notably, in persons with type 2 DM and ASCVD, the use of a GLP-1RA or SGLT2 inhibitor with proven outcome benefits is recommended to reduce CV and/or cardiorenal outcomes (Class I, LOE A).
Main Takeaway
For people with established ASCVD, the ESC-recommended LDL-C goal is < 55 mg/dL with a goal reduction of at least 50%.
Guideline Loc.
Section 6.1

CardioNerds Decipher the Guidelines – 2021 ESC Prevention Series
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9 min
July 13, 2023 316. Guidelines: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure – Question #24 with Dr. Ileana Pina

The following question refers to Sections 10.2 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.
The question is asked by Western Michigan University medical student and CardioNerds Intern Shivani Reddy, answered first by Mayo Clinic Cardiology Fellow and CardioNerds Academy House Faculty Leader Dr. Dinu Balanescu, and then by expert faculty Dr. Ileana Pina.
Dr. Pina is Professor of Medicine and Quality Officer for the Cardiovascular Line at Thomas Jefferson University, Clinical Professor at Central Michigan University, and Adjunct Professor of Biostats and Epidemiology at Case Western University. She serves as Senior Fellow and Medical Officer at the Food and Drug Administration’s Center for Devices and Radiological Health.
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 #24
Mr. E. Regular is a 61-year-old man with a history of HFrEF due to non-ischemic cardiomyopathy (latest LVEF 40% after >3 months of optimized GDMT) and persistent atrial fibrillation. He has no other medical history. He has been on metoprolol and apixaban and has also undergone multiple electrical cardioversions and catheter ablations for atrial fibrillation but remains symptomatic with poorly controlled rates. His blood pressure is 105/65 mm Hg. HbA1c is 5.4%. Which of the following is a reasonable next step in the management of his atrial fibrillation?
A
Anti-arrhythmic drug therapy with amiodarone. Stop apixaban.
B
Repeat catheter ablation for atrial fibrillation. Stop apixaban.
C
AV nodal ablation and RV pacing. Shared decision-making regarding anticoagulation.
D
AV nodal ablation and CRT device. Shared decision-making regarding anticoagulation.
Answer #24
Explanation
The correct answer is D – AV nodal ablation and CRT device along with shared decision-making regarding anticoagulation.”
Maintaining sinus rhythm and atrial-ventricular synchrony is helpful in patients with heart failure given the hemodynamic benefits of atrial systole for diastolic filling and having a regularized rhythm.
Recent randomized controlled trials suggest that catheter-based rhythm control strategies are superior to rate control and chemical rhythm control strategies with regards to outcomes in atrial fibrillation. For patients with heart failure and symptoms caused by atrial fibrillation, ablation is reasonable to improve symptoms and quality of life (Class 2a, LOE B-R). However, Mr. Regular has already had multiple failed attempts at ablations (option B).
For patients with AF and LVEF ≤50%, if a rhythm control strategy fails or is not desired,
and ventricular rates remain rapid despite medical therapy, atrioventricular nodal ablation with implantation of a CRT device is reasonable (Class 2a, LOE B-R). The PAVE and BLOCK-HF trials suggested improved outcomes with CRT devices in these patients.
RV pacing following AV nodal ablation has also been shown to improve outcomes in patients with atrial fibrillation refractory to other rhythm control strategies. In patients with EF >50%, there is no evidence to suggest that CRT is more beneficial compared to RV-only pacing. However, RV pacing may produce ventricular dyssynchrony and when compared to CRT in those with reduced EF (≤ 50%), CRT produced more benefit (Option C).
Although adjustments in antiarrhythmic medications and repeat ablation may be considered, these are unlikely to provide long-term benefit to Mr. E. Regular, who already failed antiarrhythmic regimens and multiple attempts at cardioversion and ablation (Options A, B).
In patients with chronic heart failure and atrial fibrillation, the decision to use anticoagulation for the prevention of cerebrovascular events is generally based on the CHA2DS2-VASc score. Mr. Regular’s CHA2DS2-VASc score is 1 (+1 for HF, no points for: hypertension, age 65-74 or ≥75, diabetes, stroke/TIA/TE, vascular disease, female gender). Chronic anticoagulation therapy is recommended for patients with CHA2DS2-VASc scores ≥2 for men and ≥3 for women (Class 1, LOE A). Therefore, based on the CHA2DS2-VASc score alone, Mr. Regular would not necessarily warrant anticoagulation. However, HF is a hypercoagulable state and serves as an independent risk factor for stroke, systemic embolism, and mortality in the setting of AF. In patients
with HF and a CHA2DS2-VASc score of 1, those with AF had a 3-fold higher risk compared with individuals without concomitant AF. Because HF is a risk factor, additional risk factors may not be required to support the use of anticoagulation in patients with HF, and the decision to anticoagulate can be individualized according to risk versus benefit. The guidelines give a Class 2a recommendation for chronic anticoagulation in men and women with chronic HF and permanent-persistent-paroxysmal AF who have no additional risk factors (LOE B-NR). Therefore, decisions regarding anticoagulation in this context should incorporate patient values, comorbidities, and informed shared decision making.
Main Takeaway
In summary, the “ablate and pace” strategy of AV nodal ablation and CRT device implantation improve outcomes in patients with heart failure with reduced LVEF and atrial fibrillation refractory to chemical and catheter-based rhythm control strategies and failure of rate control options.
Guideline Loc.
Section 10.2

Decipher the Guidelines: 2022 Heart Failure Guidelines Page
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11 min
July 12, 2023315. Case Report: A Mystery Mass in the Heart – University of Chicago – Northshore University
In this episode, CardioNerds co-founder Amit Goyal joins Dr. Iva Minga, Dr. Kevin Lee, and Dr. Juan Pablo Salazar Adum from the University of Chicago – Northshore in Evanston, IL to discuss a case of primary cardiac diffuse large B-cell lymphoma. The ECPR for this episode is provided by Dr. Amit Pursnani (Advanced Cardiac Imaging, Fellowship program director, NorthShore University HealthSystem). Audio editing by CardioNerds Academy Intern, Dr. Akiva Rosenzveig.
Case synopsis: A 77-year-old man with no significant medical history presents to the emergency department with progressive shortness of breath for 1 week. He reports an unintentional 15-pound weight loss in the prior month as well as constipation and abdominal/flank pain. On examination he was found to be tachycardic with a regular rhythm and further evaluation with a chest X-ray and chest CT scan demonstrated a large pericardial effusion. This was further investigated with an urgent echocardiogram that revealed a large pericardial effusion with a large mass attached to the pericardial side of the RV free wall, as well as signs of early cardiac tamponade. A pericardiocentesis was performed and 550mL of bloody fluid was withdrawn. The fluid was sent for laboratory analysis and cytology. A cardiac MRI demonstrated a large invasive mass in the pericardium and RV wall consistent with cardiac lymphoma. Cytology confirmed diffuse large B-cell lymphoma. Subsequent CT and PET scans did not find any other site of malignancy, giving the patient a diagnosis of primary cardiac diffuse large B-cell lymphoma. The patient underwent R-CHOP chemotherapy and was followed closely with repeat cardiac MRI and PET scans which demonstrated resolution of the cardiac mass at his one-year surveillance follow-up.
This case was published in US Cardiology Review, the official journal of CardioNerds. To learn more, access the case report article here.
“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.
CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases’, with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ).
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Pearls – A Mystery Mass in the Heart – Cardiac Lymphoma
The most common cause of malignant cardiac masses is metastasis.
Primary cardiac tumors are rare.
Cardiac tumors are separated into 2 categories: benign and malignant. They are often differentiated based on their location and their degree of tissue invasion.
Multimodality imaging is essential in the diagnosis, management, and surveillance of cardiac masses.
A multidisciplinary team approach is invaluable for management of patients with cardiac tumors.
Show Notes – A Mystery Mass in the Heart – Cardiac Lymphoma
1. What is the clinical presentation of cardiac masses?
Cardiac masses can have a variable presentation. They can present with arrhythmias, angina, heart failure symptoms, or pericardial effusion. Patients can also be asymptomatic; the masses can be found incidentally on cardiac or chest imagining.
2. What is the differential diagnosis for cardiac masses?
Cardiac masses are separated into benign and malignant. The most common malignant cardiac masses are metastases from a distant source. The location of the mass is important in narrowing the differential.
3. What imaging modalities are used to diagnose cardiac masses?
Multimodality imaging is needed to describe the mass in detail and guide diagnosis. An echocardiogram is usually the first imaging modality. Cardiac MRI is a great modality that allows for the detailed visualization as well as tissue characterization of the mass. Cardiac CT, chest CT, and PET scans are also imagining modalities that can be used in the management of the mass.
4. How do you manage cardiac masses?
Management of cardiac masses depends on etiology (benign or malignant) and the associated hemodynamic changes associated with it. For example, if a benign cardiac mass is associated with significant valvular regurgitation, cardiac surgery needs to be considered for management. A multidisciplinary team including cardiology, heart failure, critical care cardiology, cardio-oncology, oncology, cardiac surgery, and other specialties may be involved in the management of cardiac masses and their manifestations.
References – A Mystery Mass in the Heart – Cardiac Lymphoma
1. Alerhand, S., & Carter, J. (2019). What echocardiographic findings suggest a pericardial effusion is causing tamponade? American Journal of Emergency Medicine, 37(2), 321-326.
2. McAllister, H. A., & Fenoglio, J. J. (1978). Tumors of the Cardiovascular System. Atlas of Tumor Pathology, Series 2. Armed Forces Institute of Pathology, Washington DC, 2, 20.
3. Tyebally, S., Chen, D., Bhattacharyya, S., Mughrabi, A., Hussain, Z., Manisty, C., Westwood, M., Ghosh, A. K., & Guha, A. (2020). Cardiac Tumors: JACC CardioOncology State-of-the-Art Review. JACC. CardioOncology, 2(2), 293-311.
4. Motwani, M., Kidambi, A., Herzog, B. A., Uddin, A., Greenwood, J. P., & Plein, S. (2013). MR imaging of cardiac tumors and masses: a review of methods and clinical applications. Radiology, 268(1), 26-43.
5. Spodick, D. H. (2003). Acute cardiac tamponade. New England Journal of Medicine, 349(7), 684-690.
45 min
July 11, 2023 314. Mastering the Art of Patient Care with Dr. Michelle Kittleson and the CardioNerds Interns
In this episode, Dr. Gurleen Kaur (medicine resident at Brigham and Women’s Hospital and Director of CardioNerds Internship) and CardioNerds Academy interns Dr. Akiva Rosenzveig (medicine intern at Cleveland Clinic), Dr. Chelsea Tweneboah (medicine intern at Stonybrook University), student doctor Shivani Reddy (medical student at Western Michigan University), student doctor Diane Masket (medical student at Rowan School of Osteopathic Medicine), and student doctor Tina Reddy (medical student at Tulane University School of Medicine) discuss with Dr. Michelle Kittleson (Director of Education in Heart Failure and Transplantation, Director of HF Research, and Professor of Medicine at Cedars Sinai) about Mastering the Art of Patient Care. Dr. Kittleson shares pearls of wisdom from her book on topics including career transitions, mentorship, dealing with uncertainty, learning from mistakes, delivering difficult news, and being a woman and parent in medicine.
This episode was planned by Dr. Gurleen Kaur and episode audio was edited by student doctor Tina Reddy.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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46 min
July 09, 2023313. Stimulant-Associated Cardiomyopathy with Dr. Soraya Azari and Dr. Jonathan Davis
Dr. Amit Goyal (CardioNerds co-founder), Dr. Jessie Holtzman (House Faculty in CardioNerds Academy and cardiology fellow at UCSF), and Dr. Megan McLaughlin (CardioNerds Scholar and cardiology fellow at UCSF) discuss stimulant-associated cardiomyopathy with Dr. Jonathan Davis (Associate Professor at UCSF the Director of the Heart Failure Program at Zuckerberg San Francisco General Hospital) and Dr. Soraya Azari (Associate Clinical professor at UCSF, with specialty in hospital medicine, primary care, HIV medicine, and addiction medicine).
Methamphetamine-associated heart failure admissions have steadily increased in the United States over the past decade. Substance use disorders more broadly are thought to complicate at least 15% of all heart failure hospitalizations and amphetamine use has been shown to be an independent predictor of heart failure readmission across the country. At safety net and public hospitals, these numbers may rise even higher. This episode reviews the pathophysiology of stimulant associated cardiomyopathy, highlights treatment options for stimulant use disorder, and discusses novel models of co-management of heart failure and substance use disorder.
Notes were drafted by Dr. Jessie Holtzman. Audio editing by CardioNerds academy intern, Pace Wetstein.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Pearls – Stimulant-Associated Cardiomyopathy
Though there are no pathognomonic traits of stimulant-associated cardiomyopathy, common echocardiographic features include biventricular dilated cardiomyopathy and/or pulmonary hypertension with a dilated, hypokinetic right ventricle and underfilled left ventricle. Enjoy CardioNerds Episode 312. Case Report: Life in the Fast Lane Leads to a Cardiac Conundrum to learn from a case of stimulant associated pulmonary arterial hypertension.
Not all cardiomyopathy in patients who use stimulants is due to stimulant use. Do your due diligence. Patients who use stimulants should undergo a broad work-up to diagnose the etiology of cardiomyopathy.
Tips for taking a substance use history:
Ask permission to discuss the topic.
Normalize the behavior.
Use specific drug names (also, learn the local drug nicknames!).
Ask about any history of prior treatment and periods of abstinence.
Screen for risk of harm or overdose
Try using a phrase like “I’m asking you this because I want to know if the way you are using drugs can impact your health and keep you safe.”
There are no FDA-approved medications to treat stimulant use disorder. Common off-label therapies include mirtazapine and bupropion/naltrexone.
Contingency management programs work off the principle of operant conditioning; they reward patients for maintaining abstinence from substance use.
For clinicians to seek assistance in providing treatment for stimulant use disorder, important resources include:
SAMSA (national help line 1-800-662-HELP or online resource locator)
HarmReduction.Org
Never Use Alone hotline (800-484-3731)
Show notes – Stimulant-Associated Cardiomyopathy
1. What are common clinical presentations of stimulant-associated cardiomyopathy?
Stimulants have multifactorial physiologic impacts, due both to pharmacologic properties (adrenergic stimulation and vasoconstriction) and direct toxic effects. Clinical manifestations may include hypertension, tachyarrhythmias, acute myocardial infarction, cardiomyopathy, pulmonary hypertension, aortic dissection, and sudden cardiac death.
On echocardiogram, stimulant-associated cardiomyopathy may manifest as biventricular dilated cardiomyopathy, compensatory tachycardia, LV thrombus, and/or pulmonary hypertension (WHO Group I)
2. What is the pathophysiology of stimulant associated cardiomyopathy?
Though the exact mechanisms driving stimulant-associated cardiomyopathy are unknown, myocardial injury is thought to be related to excess catecholamines and the generation of reactive oxygen species, mitochondrial dysfunction, and the downstream effects of microvascular dysfunction and vasospasm.
Some authors have proposed a two-hit phenomenon whereby stimulant use and vulnerable genetics result in more severe clinical presentations.
3. What are common treatment options for stimulant-associated cardiomyopathy and stimulant use disorder in the presence of cardiovascular disease?
As with heart failure in general, start by ensuring that patients receive appropriate goal-directed medical therapy (GDMT) with an ACEI/ARB/ARNI, beta-blocker, MRA, and SGLTi.
If patients struggle with medication adherence, be sure to address the social determinants of health to allow for improved adherence. For instance, consider using bubble packs to help mitigate polypharmacy.
4. What is the Heart Plus Clinic and how can cardiologists work in an interdisciplinary fashion to address both cardiovascular disease and substance use disorders?
The Heart Plus clinic is a multidisciplinary team that links addiction medicine providers and the cardiovascular teams together. The clinic uses contingency management to incentivize abstinence from substance use and works to address barriers to getting medications, taking medications, and navigating polypharmacy. Results are promising so far, with a pilot study demonstrating less stimulant use, more GDMT use, less urgent care use, and more primary care use, along with greater engagement, continuity, and rapport.
5. How do you take a substance use history?
Ask permission: “Is it ok if I ask you about ***”
Normalize the behavior: “Substance use is common” or “I have a lot of patients struggling with ***”
Use specific names when obtaining a drug use history (not just alcohol, tobacco, “drugs”). Learn the names of drugs in your region.
Try using phrases like “I’m asking you this because I want to know if the way you are using drugs can impact your health and keep you safe.”
Ask about their history of past treatment and periods of abstinence.
Screen for patients at risk of harm and/or overdose due to patterns of use and be sure to prescribe naloxone.
6. What are some useful resources for treating patients with active substance use disorders?
Though there currently no FDA-approved medications to treat stimulant use disorder, common off-label therapies include mirtazapine and bupropion/naltrexone.
Contingency management programs work off the principle of operant conditioning and reward patients for maintaining abstinence from substance use. In contingency management programs, a behavior is chosen that you want to see more frequently, and a reward is given. The reward must be given close to the time of behavior and be of sufficient magnitude to demonstrate the desired effect.
There are many resources to help both clinicians and patients treat substance sue disorders. Resources include the SAMSA national help line (1-800-662-HELP) or online resource locator for clinicians. Patients may also access HarmReduction.Org and the NeverUseAlone hotline (800-484-3731) for harm reduction resources.
References – Stimulant-Associated Cardiomyopathy
1. DesJardin J, Leyde S, Davis J. Weathering the perfect storm: management of heart failure in patients with substance use disorders. Heart. 2021;107(16):1353-4. doi: 10.1136/heartjnl-2021-319103.
2. Kevil CG, Goeders NE, Woolard MD, Bhuiyan MS, Dominic P, Kolluru GK, et al. Methamphetamine Use and Cardiovascular Disease. Arterioscler Thromb Vasc Biol. 2019;39(9):1739-46. doi: 10.1161/ATVBAHA.119.312461.
3. Kolaitis NA, Saggar R, De Marco T. Methamphetamine-associated pulmonary arterial hypertension. Curr Opin Pulm Med. 2022;28(5):352-60.
4. Leyde S, Abbs E, Suen LW, Martin M, Mitchell A, Davis J, et al. A Mixed-methods Evaluation of an Addiction/Cardiology Pilot Clinic With Contingency Management for Patients With Stimulant-associated Cardiomyopathy. J Addict Med. 2023;17(3):312-8. doi: 10.1097/ADM.0000000000001110.
5. Manja V, Nrusimha A, Gao Y, Sheikh A, McGovern M, Heidenreich PA, et al. Methamphetamine-associated heart failure: a systematic review of observational studies. Heart. 2023;109(3):168-77. doi: 10.1136/heartjnl-2022-321610.
6. Reddy PKV, Ng TMH, Oh EE, Moady G, Elkayam U. Clinical Characteristics and Management of Methamphetamine-Associated Cardiomyopathy: State-of-the-Art Review. J Am Heart Assoc. 2020;9(11):e016704. doi: 10.1161/JAHA.120.016704. https://www.ahajournals.org/doi/epub/10.1161/JAHA.120.016704
40 min
June 23, 2023312. Case Report: Life in the Fast Lane Leads to a Cardiac Conundrum – Los Angeles County + University of Southern California
CardioNerds (Drs. Amit Goyal and Dan Ambinder) join Dr. Emily Lee (LAC+USC Internal medicine resident) and Dr. Charlie Lin (LAC+USC Cardiology fellow) as the discuss an important case of stimulant-related (methamphetamine) cardiovascular toxicity that manifested in right ventricular dysfunction due to severe pulmonary hypertension. Dr. Jonathan Davis (Director, Heart Failure Program at Zuckerberg San Francisco General Hospital and Trauma Center) provides the ECPR for this episide. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig.
With the ongoing methamphetamine epidemic, the incidence of stimulant-related cardiovascular toxicity continues to grow. We discuss the following case: A 36-year-old man was hospitalized for evaluation of dyspnea and volume overload in the setting of previously untreated, provoked deep venous thrombosis. Transthoracic echocardiogram revealed severe right ventricular dysfunction as well as signs of pressure and volume overload. Computed tomography demonstrated a prominent main pulmonary artery and ruled out pulmonary embolism. Right heart catheterization confirmed the presence of pre-capillary pulmonary arterial hypertension without demonstrable vasoreactivity. He was prescribed sildenafil to begin management of methamphetamine-associated cardiomyopathy and right ventricular dysfunction manifesting as severe pre-capillary pulmonary hypertension.
“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.
CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases’, with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ).
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
CardioNerds Case Reports Page
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll
CardioNerds Journal Club
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Check out CardioNerds SWAG!
Become a CardioNerds Patron!
Case Media – stimulant-related (methamphetamine) cardiovascular toxicity
Pearls – stimulant-related (methamphetamine) cardiovascular toxicity
1. Methamphetamine, and stimulants in general, can have a multitude of effects on the cardiovascular and pulmonary systems. Effects of methamphetamine are thought to be due to catecholamine toxicity with direct effects on cardiac and vascular tissues. Acutely, methamphetamine can cause vascular constriction and vasospasm, while chronic exposure is associated with endothelial damage. Over time, methamphetamine can cause pulmonary hypertension, atherosclerosis, cardiac arrhythmias, and dilated cardiomyopathy.
2. Methamphetamines are the second most commonly misused substances worldwide after opiates. Patients with methamphetamine-associated pulmonary arterial hypertension (PAH) have more severe pulmonary vascular disease, more dilated and dysfunctional right ventricles, and worse prognoses when compared to patients with idiopathic PAH. Additionally, patients with methamphetamine-associated cardiomyopathy and PAH have significantly worse outcomes and prognoses when compared to those with structurally normal hearts without evidence of PAH. Management includes multidisciplinary support, complete cessation of methamphetamine use, and guideline-directed treatment of PAH.
3. The diagnosis of pulmonary hypertension (PH) begins with the history and physical, followed by confirmatory testing using echocardiography and invasive hemodynamics (right heart catheterization). Initial serological evaluation may include routine biochemical, hematologic, endocrine, hepatic, and infectious testing. Though PH is traditionally diagnosed and confirmed in a two-step, echocardiogram-followed-by-catheterization model, other diagnostics often include electrocardiography, blood gas analysis, spirometry, ventilation/perfusion assessment, CT scans, MRIs, and/or genetic testing to evaluate for the myriad of etiologies that may contribute to the development of PH.
4. PH is characterized by remodeling of the pulmonary vasculature and a progressive increase of pulmonary vascular load, often resulting in right ventricular hypertrophy, remodeling, and dysfunction. PH is defined hemodynamically by a mean pulmonary arterial pressure ≥ 20 mmHg at rest when measured by right heart catheterization (RHC). Pre-capillary pulmonary hypertension due to pulmonary vascular disease is further defined by an elevation in pulmonary vascular resistance (PVR) of at least 3 wood units (WU).
5. Medications used to treat pulmonary arterial hypertension fall into four general mechanistic classes: calcium channel blockers, endothelin receptor antagonists, phosphodiesterase-5 inhibitors, and prostacyclin receptor agonists.
Show Notes – stimulant-related (methamphetamine) cardiovascular toxicity
How is pulmonary hypertension diagnosed with right heart catheterization (RHC)?
Pulmonary hypertension is defined by mean pulmonary arterial pressure (mPAP) ≥ 20 mmHg at rest. Pulmonary hypertension has three hemodynamic phenotypes – pre-capillary PH, post-capillary PH, and combined pre-/post-capillary PH. Isolated pre-capillary PH is defined by pulmonary vascular resistance (PVR) ≥ 3 woods units and pulmonary artery wedge pressure (PAWP) ≤ 15 mmHg. Isolated post-capillary PH is defined by PVR < 3 woods units and PAWP > 15 mmHg. PVR is calculated by dividing the mean trans-pulmonary gradient (= PAWP – mPAP) by the cardiac output.
CharacteristicsClinical groupsIsolated pre-capillary PHmPAP >20 mmHg
PAWP ≤ 15 mmHg
PVR ≥ 3 WUWHO 1,3,4, and 5Isolated post-capillary PHmPAP >20 mmHg
PAWP > 15 mmHg
PVR < 3 WUWHO 2 and 5Combined pre- & post-capillary PHmPAP >20 mmHg
PAWP > 15 mmHg
PVR ≥ 3 WUWHO 2 and 5
Classification of PAH by WHO Groups:
WHO Group 1
Pulmonary Arterial HypertensionWHO Group 2
Pulmonary hypertension due to left sided heart diseaseWHO Group 3
Pulmonary hypertension due to lung disease or hypoxiaWHO Group 4
Chronic thromboembolic pulmonary hypertension and other pulmonary artery obstructionsWHO Group 5
Pulmonary hypertension with multifactorial mechanismsIdiopathicLeft ventricular systolic and/or diastolic dysfunctionChronic obstructive pulmonary diseaseChronic thromboembolic pulmonary hypertensionHematological Disease (Sickle cell disease)HereditaryLeft-sided valvular heart diseaseInterstitial lung diseaseObstruction of the pulmonary circulation by tumor or inflammationSystemic disorders (Sarcoidosis, Langerhans cell granulomatosis)Drug and toxin inducedOther mixed restrictive or obstructive lung diseaseMetabolic disorders (Gaucher’s disease)Associated with connective tissue diseaseSleep-disordered breathingAssociated with HIV infectionAlveolar hypoventilation disordersAssociated with portal hypertensionChronic exposure to high altitudeCongenital heart diseaseSchistosomiasis
What is vasoreactivity testing?
Pulmonary vasoreactivity testing is used to identify patients who may respond favorably to calcium channel blocker (CCB) treatment. Typically, this includes patients with idiopathic pulmonary arterial hypertension, heritable pulmonary arterial hypertension, or substance-related pulmonary arterial hypertension. It is usually performed at the time of RHC. Inhaled nitric oxide (NO) at 10–20 parts per million (ppm) is the standard of care for vasoreactivity testing with alternatives including intravenous adenosine and epoprostenol. A significant response to vasodilator therapy is defined by a reduction of the mean PAP by at least 10 mmHg and concurrent decrement of the absolute value to less than 40 mmHg, without a decrease in cardiac output. Vasoreactive PH should be treated with CCB therapies such as nifedipine, diltiazem, and amlodipine. Vasoreactivity is relatively rare, occurring in 10% or fewer individuals with PH who undergo testing. PH without vasoreactivity of significant response to CCB therapy should be managed with alternative class of medications (see below).
What is the medical treatment for PAH?
Medication treatment of pulmonary arterial hypertension comes in 4 general categories with the general mechanism is listed:
Calcium channel blockers (nifedipine, diltiazem and amlodipine used in high doses) – used in patients with positive vasoreactivity testing.
Endothelin receptor antagonists (ambrisentan, bosentan, macitentan) – inhibit binding of endothelin, a vasoconstrictive peptide, to its receptors on smooth muscle cells, which is enriched in pulmonary vasculature, resulting in vasodilation and subsequent decrease in pulmonary arterial pressure.
Phosphodiesterase 5 inhibitors and guanylate cyclase stimulators (sildenafil, tadalafil, riociguat) – ihibition of the cyclic guanosine monophosphate (cGMP) degrading enzyme phosphodiesterase type 5 results in vasodilation through the NO/cGMP pathway in the pulmonary vasculature, which contains substantial amounts of this enzyme.
Prostacyclin analogues and prostacyclin receptor agonists (epoprostenol, iloprost, treprostinil, beraprost) – prostacyclin is produced predominantly by endothelial cells and induces potent vasodilation of all vascular beds and patients with PAH have been shown to have a reduction of prostacyclin synthase expression in the pulmonary arteries.
References –
Ben-Yehuda O, Siecke N. Crystal Methamphetamine: A Drug and Cardiovascular Epidemic. JACC Heart Fail. Mar 2018;6(3):219-221. doi:10.1016/j.jchf.2018.01.004
Benza RL, Gomberg-Maitland M, Miller DP, et al. The REVEAL Registry risk score calculator in patients newly diagnosed with pulmonary arterial hypertension. Chest. Feb 2012;141(2):354-362. doi:10.1378/chest.11-0676
Benza RL, Gomberg-Maitland M, Elliott CG, et al. Predicting Survival in Patients With Pulmonary Arterial Hypertension: The REVEAL Risk Score Calculator 2.0 and Comparison With ESC/ERS-Based Risk Assessment Strategies. Chest. Aug 2019;156(2):323-337. doi:10.1016/j.chest.2019.02.004
Chin KM, Channick RN, Rubin LJ. Is methamphetamine use associated with idiopathic pulmonary arterial hypertension? Chest. Dec 2006;130(6):1657-63. doi:10.1378/chest.130.6.1657
Galiè N, Humbert M, Vachiery JL, et al. 2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension: The Joint Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS): Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC), International Society for Heart and Lung Transplantation (ISHLT). Eur Heart J. Jan 1 2016;37(1):67-119. doi:10.1093/eurheartj/ehv317
Hassoun PM. Pulmonary Arterial Hypertension. N Engl J Med. Dec 16 2021;385(25):2361-2376. doi:10.1056/NEJMra2000348
Hoeper MM, Humbert M, Souza R, et al. A global view of pulmonary hypertension. Lancet Respir Med. Apr 2016;4(4):306-22. doi:10.1016/s2213-2600(15)00543-3
Kevil CG, Goeders NE, Woolard MD, et al. Methamphetamine Use and Cardiovascular Disease. Arterioscler Thromb Vasc Biol. Sep 2019;39(9):1739-1746. doi:10.1161/atvbaha.119.312461
Reddy PKV, Ng TMH, Oh EE, Moady G, Elkayam U. Clinical Characteristics and Management of Methamphetamine-Associated Cardiomyopathy: State-of-the-Art Review. J Am Heart Assoc. Jun 2 2020;9(11):e016704. doi:10.1161/jaha.120.016704
Zhao SX, Kwong C, Swaminathan A, Gohil A, Crawford MH. Clinical Characteristics and Outcome of Methamphetamine-Associated Pulmonary Arterial Hypertension and Dilated Cardiomyopathy. JACC Heart Fail. Mar 2018;6(3):209-218. doi:10.1016/j.jchf.2017.10.006
1 min
June 22, 2023 311. Guidelines: 2021 ESC Cardiovascular Prevention – Question #29 with Dr. Laurence Sperling

The following question refers to Section 5.2 of the 2021 ESC CV Prevention Guidelines. The question is asked by MGH medicine resident Dr. Christian Faaborg-Andersen, answered first by Dr. Jessie Holtzman, and then by expert faculty Dr. Laurence Sperling.
Dr. Laurence Sperling is the Katz Professor in Preventive Cardiology at the Emory University School of Medicine and Founder of Preventive Cardiology at the Emory Clinic. Dr. Sperling was a member of the writing group for the 2018 Cholesterol Guidelines, serves as Co-Chair for the ACC’s Cardiometabolic and Diabetes working group, and is Co-Chair of the WHF Roadmap for Cardiovascular Prevention in Diabetes.
The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #29

What percentage of the European population currently meets the recommended physical activity guidelines (150 minutes moderate-intensity activity weekly or 75 minutes vigorous-intensity activity weekly)?
A
<10%
B
10-25%
C
25-50%
D
50-75%
E
>75%
Answer #29

Explanation
The correct answer is A: <10% of the European population currently meets the recommended physical activity guidelines.
The American Heart Association, European Society of Cardiology, and World Health Organization all share the recommendation that adults should engage in 150 minutes per week of moderate-intensity physical activity or 75 minutes per week of vigorous-intensity activity. They recognize that additional health benefits may be garnered from incremental increases to 300 minutes per week of moderate intensity activity or 150 minutes per week of vigorous intensity activity, with a recommendation to include both aerobic and muscular strength training activities.

According to the WHO, physical inactivity is the 4th leading cause of death in the world. The statistics regarding physical inactivity are staggering. Recent studies have shown that <10% of the European population meets the minimum recommended levels of physical activity. Similarly, ¼ adults and ¾ adolescents (aged 11-17) do not currently meet the global recommendations for physical activity. The World Health Organization has created a Global Action Plan on Physical Activity 2018-2030 with the goal to achieve a 15% relative reduction in the global prevalence of physical inactivity by 2030.
Society level interventions to increase physical activity have been proposed including school-based activity programs, improved accessibility of exercise facilities across the socioeconomic spectrum, and governmental consideration of physical activity when designing cities (i.e. including pedestrian and cycling lanes). Other policy suggestions with varying levels of evidence include focused media campaigns, economic incentives, targeting labeling of physical activity opportunities, and work-place wellness programs.
Main Takeaway
Despite growing awareness of the health consequences of sedentary behavior, fewer than 10% of adults currently meet the minimum recommended quantity of physical activity. Public health leaders may continue to consider novel legislative initiatives to augment physical activity on a societal level with architectural design and financial incentives.
Guideline Loc.
Section 5.2

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June 19, 2023 310. Guidelines: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure – Question #23 with Dr. Anu Lala

The following question refers to Section 9.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.
The question is asked by Keck School of Medicine USC medical student & CardioNerds Intern Hirsh Elhence, answered first by Cedars Sinai medicine resident, soon to be Vanderbilt Cardiology Fellow, and CardioNerds Academy Faculty Dr. Breanna Hansen, and then by expert faculty Dr. Anu Lala.
Dr. Lala is an advanced heart failure and transplant cardiologist, associate professor of medicine and population health science and policy, Director of Heart Failure Research, and Program Director for the Advanced Heart Failure and Transplant fellowship training program at Mount Sinai. Dr. Lala is Deputy Editor for the Journal of Cardiac Failure. Dr. Lala has been a champion and role model for CardioNerds. She has been a PI mentor for the CardioNerds Clinical Trials Network and continues to serve in the program’s leadership. She is also a faculty mentor for this very 2022 heart failure decipher the guidelines series.
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 #23
Mrs. Hart is a 63-year-old woman with a history of non-ischemic cardiomyopathy and heart failure with reduced ejection fraction (LVEF 20-25%) presenting with 5 days of worsening dyspnea and orthopnea.

At home, she takes carvedilol 12.5mg BID, sacubitril-valsartan 24-46mg BID, empagliflozin 10mg daily, and furosemide 40mg daily.

On admission, her exam revealed a blood pressure of 111/79 mmHg, HR 80 bpm, and SpO2 94%. Her cardiovascular exam was significant for a regular rate and rhythm with an audible S3, JVD to 13 cm H2O, bilateral lower extremity pitting edema with warm extremities and 2+ pulses throughout. What initial dose of diuretics would you give her?
A
Continue home Furosemide 40 mg PO
B
Start Metolazone 5 mg PO
C
Start Lasix 100 mg IV
D
Start Spironolactone
Answer #23
Explanation
The correct answer is C – start Furosemide 100 mg IV.
This is the most appropriate choice because patients with HF admitted with evidence of significant fluid overload should be promptly treated with intravenous loop diuretics to improve symptoms and reduce morbidity (Class 1, LOE B-NR). Intravenous loop diuretic therapy provides the most rapid and effective treatment for signs and symptoms of congestion. Titration of diuretics has been described in multiple recent trials of patients hospitalized with HF,
often initiated with at least 2 times the daily home diuretic dose (mg to mg) administered intravenously. Titration to achieve effective diuresis may require doubling of initial doses, adding a thiazide diuretic, or adding an MRA that has diuretic effects in addition to its cardiovascular benefits.
Choice A is incorrect as continuing oral loop diuretics is not recommended for acute decongestion. Moreover, Ms. Hart has become congested despite her home, oral diuretic regimen.
Choice B and D are incorrect as starting a thiazide diuretic or a mineralocorticoid receptor antagonist are not first-line therapy for acute HF. Rather, in patients hospitalized with HF when diuresis is inadequate to relieve symptoms and signs of congestion, it is reasonable to intensify the diuretic regimen using either: a. higher doses of intravenous loop diuretics; or b. addition of a second diuretic (Class 2a, LOE B-NR).
After instituting intravenous loop diuretic therapy, escalating attempts to achieve net diuresis include serial doubling of intravenous loop diuretic doses, which can be done by bolus or infusion, and sequential nephron blockade with addition of a thiazide diuretic, as detailed specifically in the protocol for the diuretic arms of the CARRESS and ROSE trials.
MRAs have mild diuretics properties and the addition of MRAs can help with diuresis in addition to significant cardiovascular benefits in patients with HF.
For patients hospitalized with HF, therapy with diuretics and other guideline-directed medications should be titrated with a goal to resolve clinical evidence of congestion to reduce symptoms and rehospitalizations (Class 1, LOE B-NR).
For patients requiring diuretic treatment during hospitalization for HF, the discharge regimen should include a plan for adjustment of diuretics to decrease rehospitalizations (Class 1, LOE B-NR).
Main Takeaway
Patients admitted with acute HF should be promptly treated with intravenous loop diuretics. If current level of diuresis becomes inadequate to relieve symptoms and signs of congestion, it is reasonable to intensify the diuretic regimen using either: higher doses of intravenous loop diuretics or addition of a second diuretic (e.g., thiazide or MRA). All patients should have their diuretic regimen updated on discharge.
Guideline Loc.
Section 9.3

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19 min
June 18, 2023309. Atrial Fibrillation: Situational Assessment of Stroke and Bleeding Risk with Dr. Hafiza Khan
Dr. Daniel Ambinder (CardioNerds Co-Founder), Dr. Kelly Arps (Series Co-Chair and EP fellow at Duke University), Dr. Stephanie Fuentes Rojas (FIT Lead and EP fellow at Houston Methodist), and Dr. Ingrid Hsiung (Cardiology Fellow at Baylor Scott & White Health) discuss situational assessment of stroke and bleeding risk with expert faculty Dr. Hafiza Khan (Electrophysiologist at Baylor Scott & White Health). In this episode, we discuss stroke and bleeding risk in specific situations such as prior to cardioversion, triggered episodes, and perioperatively. These are scenarios that are commonly encountered and pose specific challenges. Episode notes were drafted by Dr. Stephanie Fuentes. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian.
This CardioNerds Atrial Fibrillation series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Kelly Arps and Dr. Colin Blumenthal.
This series is supported by an educational grant from the Bristol Myers Squibb and Pfizer Alliance. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds.
We have collaborated with VCU Health to provide CME. Claim free CME here!
Disclosures: Dr. Ellis discloses grant or research support from Boston Scientific, Abbott-St Jude, advisor for Atricure and Medtronic.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Pearls and Quotes – Atrial Fibrillation: Situational Assessment of Stroke and Bleeding Risk
In patients with persistent atrial fibrillation with tachycardia induced cardiomyopathy, timely restoration of normal rhythm is important. In patients not on established oral anticoagulation one option is to wait 3 weeks on oral anticoagulation prior to considering cardioversion. Another option is to pursue TEE prior to cardioversion as TEE is currently the gold standard imaging modality to exclude a LAA thrombus.
Following cardioversion (chemical or electrical), anticoagulation must not be interrupted for 4 weeks due to atrial stunning. This is especially true for patients who have been in atrial fibrillation for an extended period of time.
Individualizing assessment of stroke and bleeding risk is imperative when determining perioperative anticoagulation (AC) management. ACC has a helpful app (ManageAnticoag App) to make this easier.
When considering AC in triggered atrial fibrillation (e.g., pneumonia, sepsis), it is important to consider the substrate that made the patient susceptible to developing atrial fibrillation. AC is favored in patients with high CHA2DS2-VAsC score and many traditional risk factors for atrial fibrillation as they are at high risk for future development of atrial fibrillation.
Atrial fibrillation is a marker of poor outcomes in patients who have undergone coronary artery bypass graft (CABG) surgery. It is unclear if patients should be started on long-term AC for new onset atrial fibrillation after CABG regardless of risk factors. This is currently being investigated in the PACES trial.
Notes – Atrial Fibrillation: Situational Assessment of Stroke and Bleeding Risk
How do we choose an imaging modality for excluding LAA thrombus exclusion prior to cardioversion?
TEE is the gold standard. It also provides other information that is important for management of atrial fibrillation (e.g. LA size/volume, presence/degree of mitral regurgitation/stenosis, ejection fraction).
Gated cardiac CTA may have a growing role for evaluation of LAA thrombus.
What is the data behind the recommendation for uninterrupted AC following cardioversion and what is atrial stunning?
All patients should be anticoagulated for four weeks after cardioversion, regardless of the mechanism of cardioversion or CHA2DS2-VAsC score. As discussed in prior episodes, those who meet long term criteria for AC should be anticoagulated indefinitely.
The term “atrial stunning” refers to the electro-mechanical dissociation of the LAA following cardioversion. The longer one is in atrial fibrillation, the longer it takes for the LAA contraction/LAA flow velocities to recover after restoration of normal rhythm. During the period of atrial stunning, there is increased risk of LAA thrombus formation, hence AC should not be interrupted. The first 72 hours post cardioversion are the highest risk for LAA thrombus formation followed by the subsequent 4 weeks.
What is the approach of perioperative AC management in patients with atrial fibrillation?
ACC has a helpful app (ManageAnticoag App), to individualize the decision of when/how to stop and resume AC peri-procedurally.
One needs to ascertain three factors: 1) surgical bleeding risk, 2) stroke risk, and 3) the patient’s individual bleeding risk (e.g., medications, supplements, renal function, etc.).
The BRDIGE trial investigated the need to bridge patients on and off anticoagulation perioperatively. The trial was small and patient characteristics of the study (mostly male, low percentage of patients with high CHADS score) do not allow for generalizability of study findings to all patients.
Many patients do not require perioperative bridging, but individual patient factors should be used to make this decision. High risk features that warrant heparin bridging include recent stroke, mechanical valve, or mitral stenosis. Should consider bridging in patients with high CHA2DS2-VAsC score as these patients only made up a small portion of the BRIDGE trial.
What is the approach to AC in patients with triggered atrial fibrillation?
Similar to a fire, atrial fibrillation requires a substrate (i.e., combustible material) and a trigger (i.e., a match) to initiate. Though you can treat and therefore remove the trigger (e.g., pneumonia), patients with a substrate conducive to atrial fibrillation remain at high risk of atrial fibrillation in the future. If they were to convert to atrial fibrillation without clear symptoms in the future, they would be at risk for stroke and might not be started on AC. As such, long-term AC should be evaluated in a similar manner to those with paroxysmal or persistent atrial fibrillation without a clear trigger.
The patient population with true “triggered” atrial fibrillation may be limited to those with thyrotoxicosis as hyperthyroidism can trigger atrial fibrillation even in patients with structurally normal hearts and background risk for future atrial fibrillation.
Atrial fibrillation after cardiac surgery (e.g., CABG, mitral valve repair/replacement) should be managed with a coordinated heart team approach. Anticoagulation should likely be favored if bleeding risk is acceptable and patient has known risk factors, especially in valve surgeries where patients often have had longstanding LA pressure or volume overload. Atrial fibrillation following CABG has been associated with poor outcomes, though it is currently unclear if patients without traditional risk factors require long-term AC. This is currently being studied in the PACES trial.
References
January, C.T, Wann, L.S, Alpert, J.S., Calkins, H, Cigarroa, J.E., Cleveland, J.C., Conti, J.B., Ellinor P.T et al 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American college of Cardiology/American heart Asocciation Task Force on Practice Guidelines and the Heart Rhythm Society. Journal of the American College of Cardiology, 6421, e1-76.
Dagres N, Kornej J, Hindricks G, et al. Prevention of Thromboembolism After Cardioversion of Recent-Onset Atrial Fibrillation. J Am Coll Cardiol. 2013 Sep, 62 (13) 1193–1194.https://doi.org/10.1016/j.jacc.2013.06.019
32 min
June 12, 2023 308. Guidelines: 2021 ESC Cardiovascular Prevention – Question #28 with Dr. Roger Blumenthal

The following question refers to Section 4.7 and Table 18 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern Student Dr. Shivani Reddy, answered first by Fellow at Johns Hopkins Dr. Rick Ferraro, and then by expert faculty Dr. Roger Blumenthal.
Dr. Roger Blumenthal is professor of medicine at Johns Hopkins where he is Director of the Ciccarone Center for the Prevention of Cardiovascular Disease. He was instrumental in developing the 2018 ACC/AHA CV Prevention Guidelines. Dr. Blumenthal has also been an incredible mentor to CardioNerds from our earliest days.
The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Question #28

Mr. A. C. is a 78-year-old gentleman with a long-standing history of HTN receiving antihypertensive medications & dietary management for blood pressure control. What is the target diastolic blood pressure recommendation for all treated patients such as Mr. A.C.?
A
< 80 mmHg
B
< 90 mmHg
C
< 70 mmHg
D
< 95 mmHg
E
< 100 mmHg
Answer #28
Explanation
The correct answer is A: DBP < 80 mmHg
Blood pressure treatment targets: when drug treatment is used, the aim is to control BP to target within 3 months. Blood pressure treatment targets in the 2021 ESC Prevention guidelines are more aggressive than previously recommended, as evidence now suggests the previously recommended targets were too conservative, especially for older patients.
The magnitude of BP lowering is the most important driver of benefit.
·       It is recommended that the first objective of treatment is to lower BP to <140/90 mmHg in all patients, and that subsequent BP targets are tailored to age and specific comorbidities (Class 1).
·       In treated patients aged 18-69 years, it is recommended that SBP should ultimately be lowered to a target range of 120 – 130 mmHg in most patients (Class 1).
·       In treated patients aged ≥70 years, it is recommended that SBP should generally be targeted to <140 and down to 130 mmHg if tolerated (Class 1).
·       In all treated patients, DBP is recommended to be lowered to <80 mmHg (Class I).
This change in the BP target range for older people compared with the 2016 ESC prevention guidelines is supported by evidence that these treatment targets are safely achieved in many older patients and are associated with significant reductions in the risk of major stroke, HF, and CV death. It also takes into account that the even lower SBP in the intensively treated group in SPRINT (Systolic Blood Pressure Intervention Trial) (mean 124 mmHg) probably reflects a conventional office SBP range of 130-139 mmHg. It is recognized, however, that the evidence supporting more strict targets is less strong for very old people (>80 years) and those who are frail. Also, in these older and especially frail patients, it may be difficult to achieve the recommended target BP range due to poor tolerability or adverse effects, and high-quality measurement and monitoring for tolerability and adverse effects is especially important in these groups.
Main Takeaway
The first step in HTN management in all groups is a reduction to SBP < 140 mmHg and DBP < 80 mmHg, with further targets depending on age and comorbidities as specified by Table 18 of the 2021 ESC Prevention Guidelines.
Guideline Loc.
1.     4.7.5.3 page 3285
2.     Table 18 page 3287

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