Beyond the Boards Archives - Cardionerds

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Beyond the Boards Archives - Cardionerds episodes

August 17463. Multimodality Imaging in Chronic Coronary Artery Disease with Dr. Panithaya Chareonthaitawee
CardioNerds (Drs. Dr. Natalie Marrero, Dr. Ritika Tuli, and Dr. Rafael Toro Manotas) discuss multimodality imaging for risk stratification, evaluation, and management of chronic coronary artery disease with Dr. Panithaya Chareonthaitawee. Audio editing by CardioNerds intern Iman Razeghian.
This episode was produced as part of the CardioNerds Academy curriculum by House Taussig under the guidance of House Chief, Dr. Natalie Marrero and Academy Program Director, Dr. Gurleen Kaur. A matching review article will be published in US Cardiology Review, the official journal of CardioNerds. This discussion was planned in collaboration with the Mayo Clinic Cardiovascular Board Review Course.
In this episode, we discuss the pathophysiology and risk stratification of chronic coronary artery disease (CAD), as well as the current landscape of non-invasive evaluation of this condition. CAD remains a leading cause of morbidity and mortality despite advances in pharmacological and non-pharmacological strategies for the prevention and treatment of atherosclerotic disease. The concept of chronic CAD has shifted from the traditional model of stable, obstructive, flow-limiting disease, toward the current understanding of a dynamic process that extends beyond obstructive epicardial lesions to include non-obstructive plaque, diffuse atherosclerosis, and microvascular disease. Similarly, the imaging modalities used to evaluate CAD have evolved, and clinicians now have an extensive menu of options, each with distinct advantages and limitations, that must be selected carefully to maximize diagnostic accuracy and optimize treatment guidance, while also considering resource availability, local expertise, and high-value care. By the end of the episode, listeners will understand the pathophysiology of chronic CAD, risk-stratify patients with suspected CAD, recognize the advantages and pitfalls of each non-invasive diagnostic modality, and select the most appropriate diagnostic tool for a given clinical scenario.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Pearls:
Chronic CAD is a complex process that extends beyond obstructive epicardial stenosis to include non-obstructive disease, dynamic plaque burden and ischemia, diffuse atherosclerosis, microvascular dysfunction, vasospasm, among others.
When evaluating patients with suspected CAD, the diagnostic process should be guided by a specific and appropriate clinical question before ordering any tests.
The current diagnostic tool arsenal is broadly divided into anatomic and functional imaging modalities. These are complementary, each with distinct properties and limitations, addressing different clinical questions and assessing different aspects of disease.
Local availability and expertise, along with patient-specific considerations and contraindications, determine the choice of diagnostic modality. No single test is best for every patient.
INOCA and coronary microvascular dysfunction represent a common and increasingly recognized entity that is diagnosable and treatable; initial evaluation includes non-invasive testing such as stress PET and stress CMR.
References
Gulati M, Levy PD, Mukherjee D, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2021;144(22):e368-e454. doi:10.1161/CIR.0000000000001029 https://pubmed.ncbi.nlm.nih.gov/34709879/
Vrints C, Andreotti F, Koskinas KC, et al. 2024 ESC Guidelines for the management of chronic coronary syndromes. Eur Heart J. 2024;45(36):3415-3537. doi:10.1093/eurheartj/ehae177 https://pubmed.ncbi.nlm.nih.gov/39210710/
Virani SS, Newby LK, Arnold SV, et al. 2023 AHA/ACC/ACCP/ASPC/NLA/PCNA Guideline for the Management of Patients With Chronic Coronary Disease: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines. Circulation. 2023;148(9):e9-e119. doi:10.1161/CIR.0000000000001168 https://pubmed.ncbi.nlm.nih.gov/37471501/
Edvardsen T, Asch FM, Davidson B, et al. Non-Invasive Imaging in Coronary Syndromes: Recommendations of The European Association of Cardiovascular Imaging and the American Society of Echocardiography, in Collaboration with The American Society of Nuclear Cardiology, Society of Cardiovascular Computed Tomography, and Society for Cardiovascular Magnetic Resonance. J Am Soc Echocardiogr. 2022;35(4):329-354. doi:10.1016/j.echo.2021.12.012 https://pubmed.ncbi.nlm.nih.gov/35379446/
Douglas PS, Hoffmann U, Patel MR, et al. Outcomes of anatomical versus functional testing for coronary artery disease. N Engl J Med. 2015;372(14):1291-1300. doi:10.1056/NEJMoa1415516 https://pubmed.ncbi.nlm.nih.gov/39210710/
Sharma A, Coles A, Sekaran NK, et al. Stress Testing Versus CT Angiography in Patients With Diabetes and Suspected Coronary Artery Disease. J Am Coll Cardiol. 2019;73(8):893-902. doi:10.1016/j.jacc.2018.11.056 https://pubmed.ncbi.nlm.nih.gov/30819356/
SCOT-HEART Investigators, Newby DE, Adamson PD, et al. Coronary CT Angiography and 5-Year Risk of Myocardial Infarction. N Engl J Med. 2018;379(10):924-933. doi:10.1056/NEJMoa1805971 https://pubmed.ncbi.nlm.nih.gov/30145934/
Li Z, Xu T, Wang Z, et al. Prognostic Significance of Computed Tomography-Derived Fractional Flow Reserve for Long-Term Outcomes in Individuals With Coronary Artery Disease. J Am Heart Assoc. 2025;14(2):e037988. doi:10.1161/JAHA.124.037988 https://pubmed.ncbi.nlm.nih.gov/39791423/
Bateman TM, Al-Mallah MH, et al. Clinical indications for positron emission tomography myocardial perfusion imaging and myocardial blood flow quantification: An American Society of Nuclear Cardiology position statement. J Nucl Cardiol. 2026;57:102619. doi:10.1016/j.nuclcard.2025.102619 https://pubmed.ncbi.nlm.nih.gov/41482140/
Taqueti VR, Di Carli MF. Coronary Microvascular Disease Pathogenic Mechanisms and Therapeutic Options: JACC State-of-the-Art Review. J Am Coll Cardiol. 2018;72(21):2625-2641. doi:10.1016/j.jacc.2018.09.042 https://pubmed.ncbi.nlm.nih.gov/30466521/
Taqueti VR, Hachamovitch R, Murthy VL, et al. Global coronary flow reserve is associated with adverse cardiovascular events independently of luminal angiographic severity and modifies the effect of early revascularization. Circulation. 2015;131(1):19-27. doi:10.1161/CIRCULATIONAHA.114.011939 https://pubmed.ncbi.nlm.nih.gov/25400060/
Mehta PK, Huang J, Levit RD, Malas W, Waheed N, Bairey Merz CN. Ischemia and no obstructive coronary arteries (INOCA): A narrative review. Atherosclerosis. 2022;363:8-21. doi:10.1016/j.atherosclerosis.2022.11.009 https://pubmed.ncbi.nlm.nih.gov/36423427/
Kunadian V, Chieffo A, Camici PG, et al. An EAPCI Expert Consensus Document on Ischaemia with Non-Obstructive Coronary Arteries in Collaboration with European Society of Cardiology Working Group on Coronary Pathophysiology & Microcirculation Endorsed by Coronary Vasomotor Disorders International Study Group. EuroIntervention. 2021;16(13):1049-1069. doi:10.4244/EIJY20M07_01 https://pubmed.ncbi.nlm.nih.gov/32624456/
40 min
August 13462. Tricuspid Regurgitation with Dr. Sunil Mankad
CardioNerds (Dr. Apoorva Gangavelli, Dr. Cory Sejo, and Dr. Joseph Kassab), discuss tricuspid regurgitation evaluation and management with Dr. Sunil Mankad.
This episode was produced as part of the CardioNerds Academy curriculum by House Einthoven under the guidance of House Chief, Dr. Apoorva Gangavelli and Academy Program Director, Dr. Gurleen Kaur. A matching review article will be published in US Cardiology Review, the official journal of CardioNerds. This discussion was planned in collaboration with the Mayo Clinic Cardiovascular Board Review Course.
Audio editing by CardioNerds intern Emma Winakur.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Key Points:
Tricuspid regurgitation is common and associated with increased mortality at every stage, regardless of etiology. Outcomes are worse with worsening severity, so accurate grading is critical.
Etiology is critical to guide treatment decisions. Etiology includes primary vs secondary (atrial or ventricular) vs CIED-related TR. 3D echocardiography can be very helpful in determining TR etiology, especially in CIED-related TR.
Diuresis with the goal of euvolemia is step one. Additionally, underlying contributory conditions (eg. pulmonary HTN, HFrEF, atrial fibrillation) should be addressed, if appropriate, and then TR severity reassessed.
The choice between T-TEER and TTVR hinges on anatomy, RV function, pulmonary hypertension, and the ability to tolerate anticoagulation. T-TEER is generally first line in atrial functional TR with appropriate anatomy, in patients with poor RV function who cannot tolerate a sudden increase in RV afterload, or in patients who cannot tolerate the necessary anticoagulation with TTVR. TTVR is preferred with wide coaptation gaps and CIED-related TR.
This is a team sport. Multidisciplinary discussions utilizing imaging (TTE/TEE, CT), risk scores (TRI-SCORE or TRIO), patient preference, and prior institutional experience are essential for the effective treatment of severe TR.
Notes:
What is the clinical importance of tricuspid regurgitation?
TR is very common with approximately 4% of people over 75 having moderate or greater severity.
TR (even mild) is associated with increased mortality. Those outcomes worsen as the TR severity worsens, and this phenomenon is independent of the mechanism of regurgitation.
What is unique about the tricuspid valve compared to the other cardiac valves?
It is at an anterior location which allows it to be imaged well with transthoracic echocardiography
It is the largest valve and composed generally of 3 leaflets (but very often can have 4+ leaflets).
Importantly, the RV is compliant and changes size and shape readily based on loading conditions. The TV annulus similarly changes size and shape based on hemodynamic conditions such as preload.
What is a good framework for approaching the causes of tricuspid regurgitation?
Determine the presence and define the severity of TR.
Using TTE, we want to measure the right atrial size, the RV size, and any other concomitant valvular lesions.
Use TTE (2D and 3D) to characterize leaflet anatomy and characteristics.
Subtypes of TR mechanisms (many times etiology is mixed).
Primary: primary leaflet abnormality, occurs in ~10% of cases. Look for prolapse, flail, endocarditis, etc.
Secondary/functional: leaflets normal but surrounding structures are abnormal.
Atrial: RA and tricuspid annular dilation but normal RV size/shape, and can be related to arrhythmias like atrial fibrillation.
Ventricular: RV dilated and/or dysfunctional with leaflet tethering. Can be related to pulmonary hypertension or primary RV disease.
Cardiac implantable electronic device (CIED): Related to device (usually pacemakers or ICD) interaction with TV leaflets.
Includes perforation, entanglement in subvalvular apparatus, impingement, etc.
3D TTE particularly helpful to evaluate
How do we grade TR severity?
It is very important to grade the severity of TR, and this is generally done with echocardiography.
There are both quantitative and qualitative methods which use Doppler and various equations to estimate TR severity.
Current recommendations have expanded TR severity beyond mild/moderate/severe to include “massive” and “torrential” categories.
The most important parameters measured/calculated are vena contracta width, regurgitant volume, regurgitant fraction, and effective regurgitant orifice area. Helpful qualitative metrics include hepatic venous flow reversal.
When should additional studies beyond transthoracic echocardiography, such as transesophageal echocardiography (TEE), cardiac computed tomography (CT), and cardiac magnetic resonance imaging (MRI) be pursued?
TEE is particularly helpful if TTE views are poor. Since TEE is used during transcatheter intervention, a pre-procedure TEE to define anatomy, determine procedure candidacy, and plan for the procedure is critical.
CT is also helpful for procedure planning and has particular strengths in defining annulus size and geometry. A CT is required prior to transcatheter tricuspid valve replacement (TTVR).
MRI is helpful for measuring RV volumes and function, but is not generally used to assess TR severity.
What is the approach to the treatment for severe tricuspid regurgitation?
The first step is to try to determine the etiology. For secondary TR, treating the underlying condition is indicated. For example, pulmonary vasodilators for pulmonary HTN or guideline therapy for heart failure with reduced ejection fraction.
Diuretics are the mainstay for treatment, with the goal to obtain euvolemia. This may require inpatient admission to optimize volume status and medication regimen.
Once reversible etiologies are addressed, if the patient is still symptomatic from TR, additional therapies can be considered.
What is the role of right heart catheterizations (RHC) in patients with severe TR?
RHC is very helpful for many reasons. We use it in TR to help determine volume status, cardiac output, and RV function. Additionally, identifying and characterizing pulmonary hypertension (with pulmonary artery pressures and calculating pulmonary vascular resistance) is an important factor when choosing future therapies.
With severe tricuspid regurgitation, when should we refer for intervention (either with surgery or transcatheter repair or replacement)?
Once reversible etiologies are addressed and euvolemia has been achieved, if the patient is still symptomatic from TR despite aggressive medical optimization, additional therapies can be considered.
Once euvolemic, a repeat TTE should be ordered to reassess the severity of the TR.
Use calculators (for example, either the TRI-SCORE or TRIO score) to predict operative mortality for isolated TR surgery.
What are our transcatheter treatment options in severe tricuspid regurgitation, and how do we choose between them?
The primary approved transcatheter treatment options for severe TR include transcatheter tricuspid edge-to-edge repair (T-TEER) and transcatheter tricuspid valve replacement (TTVR), of which the Edwards EVOQUE valve is the only one currently approved by the FDA. There are other TTVR device under investigation.
These decisions should be made with a multi-disciplinary team including representation from cardiac imaging, interventional cardiology, and cardiothoracic surgery.
Factors that go into the decision between T-TEER and TTVR include anatomy (annulus width, coaptation gap, leaflet length), RV reserve, pulmonary hypertension presence, ability to tolerate anticoagulation, patient preference, and institutional experience.
T-TEER is generally the first line with atrial functional and suitable anatomy. It is successful at reducing TR but does not generally eliminate it.
TTVR with EVOQUE is preferred in certain anatomic considerations like a large coaptation gap or when there is CIED-related TR (as this was excluded in T-TEER trials).
Patients must be suitable for anticoagulation to receive TTVR as there is risk of leaflet thrombosis without it.
If moderate/severe pulmonary hypertension is present, or there is poor RV function, TTVR may be avoided as the sudden elimination of TR causes a sudden increase in RV afterload which may not be tolerated.
What is the role in advanced metrics for evaluating RV function?
Advanced metrics like RV/PA coupling are under investigation but have not made it into the guidelines. The clinical utility is not yet known.
Assessing the RV function is important as stated above. Dr. Mankad prefers using 3D TTE to calculate an RVEF, or tracking RV longitudinal free wall strain.
If you do encounter CIED-related TR, how do you treat it?
Evaluate with TTE or TEE. 3D is very helpful to identify relative anatomy and leaflet-device interactions.
There is no clear consensus about treatment if CIED-related TR is the primary mechanism of severe TR. If recently implanted, repositioning may be a valid option, but requires discussions with multiple teams including electrophysiology, advanced cardiac imaging, CT surgery, and interventional cardiology.
References
O’Gara PT, Lindenfeld J, Hahn RT, et al. 10 Issues for the Clinician in Tricuspid Regurgitation Evaluation and Management: 2025 ACC Expert Consensus Decision Pathway. J Am Coll Cardiol. 2025;S0735-1097(25)07047-0.
O’Gara PT, Little SH, Badhwar V, et al. Operator and Institutional Recommendations and Requirements for Tricuspid Interventions: 2026 ACC/AHA/ASE/HRS/STS Expert Consensus Systems of Care Document. J Am Coll Cardiol. 2026;S0735-1097(26)05481-1.
Hahn RT. Tricuspid Regurgitation. N Engl J Med. 2023;388(20):1876-1891.
Davidson LJ, Tang GHL, Ho EC, et al. The Tricuspid Valve: A Review of Pathology, Imaging, and Current Treatment Options: A Scientific Statement From the American Heart Association. Circulation. 2024;149(22):e1223-e1238.
19 min
August 11461. Pre-Pregnancy Risk Stratification and Counseling with Dr. Katie Young
CardioNerds (Dr. Apoorva Gangavelli, Dr. Rebecca Garber, and Dr. Tina Reddy), discuss pre-pregnancy risk stratification and counseling with Dr. Katie Young across a range of risks.
This episode was produced as part of the CardioNerds Academy curriculum by House Einthoven under the guidance of House Chief, Dr. Apoorva Gangavelli and Academy Program Director, Dr. Gurleen Kaur. A matching review article will be published in US Cardiology Review, the official journal of CardioNerds. This discussion was planned in collaboration with the Mayo Clinic Cardiovascular Board Review Course.
Audio editing by CardioNerds intern, Dr. Patrick Pekyi-Boateng.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Notes:
Why is pregnancy considered a “physiologic stress test,” and why does risk extend beyond delivery?
Blood volume, heart rate, and cardiac output rise while systemic vascular resistance falls, peaking in the late second/early third trimester; underlying (even undiagnosed) heart disease can be unmasked or worsened.
Postpartum (“fourth trimester”) is a high-risk period, not a safe zone – fluid shifts, rising SVR, and bleeding risk can precipitate decompensation in patients with heart failure, pulmonary hypertension, valvular disease, or aortopathy.
Adverse pregnancy outcomes (hypertensive disorders, gestational diabetes, preterm birth, fetal growth restriction, peripartum cardiomyopathy) are markers of future cardiovascular risk and warrant long-term preventive follow-up.
What is the practical framework for approaching pre-pregnancy cardiovascular risk?
Four broad categories: (1) patients who may need cardiac screening before pregnancy, (2) patients needing risk-factor/medication optimization, (3) known cardiovascular disease where pregnancy is reasonable with structured risk stratification, and (4) high-risk disease where pregnancy may need to be delayed, modified by intervention, or discouraged.
Testing should be targeted, not blanket – reserved for symptoms, abnormal exam, concerning family history, or reduced functional capacity.
How is risk stratified in patients with known cardiovascular disease?
Use a combination of tools per 2025 ESC guidelines: mWHO 2.0 (broad maternal risk category), CARPREG II (additional predictors of maternal cardiac events), and ZAHARA (useful in congenital heart disease).
Key lesion-specific factors: aortic size/growth, valve severity, ventricular function, symptoms, blood pressure, and family history of dissection.
Translate risk into practical terms for patients rather than leading with a numerical score.
Which cardiovascular medications require review before conception?
ACE inhibitors, ARBs, and ARNIs should be transitioned off before pregnancy; statins, MRAs, and SGLT2 inhibitors also need review.
DOACs are contraindicated in pregnancy and lactation; mechanical valve anticoagulation requires individualized shared decision-making, as no strategy is risk-free for mother and fetus.
Medication changes are best made proactively, before conception, rather than reactively.
This is not an exhaustive list! The medication list needs to be reviewed carefully.
Which conditions carry high or prohibitive risk in pregnancy?
Pulmonary arterial hypertension, Eisenmenger syndrome, severe ventricular dysfunction, prior peripartum cardiomyopathy with residual LV dysfunction, severe left-sided obstructive valve disease (e.g., severe mitral stenosis), mechanical valves, significant aortopathy, cyanotic congenital heart disease, and Fontan physiology.
Common theme: limited cardiovascular reserve and high risk of decompensation, thrombosis, arrhythmia, heart failure, aortic dissection, or death. These patients need expert multidisciplinary evaluation before pregnancy.
Severe mitral stenosis is poorly tolerated because tachycardia shortens diastolic filling time and raises left atrial pressure, risking pulmonary edema and decompensation.
When should genetic testing or counseling be offered?
Consider when a diagnosis may be inherited or affect the patient, pregnancy, or family members: inherited cardiomyopathies, aortopathies, channelopathies, select congenital heart disease, and some pulmonary hypertension syndromes.
Recurrence risk of congenital heart disease in offspring is roughly 6-10% when the mother has CHD; fetal echocardiography should be offered.
How should contraception be approached in high-risk cardiac patients?
Frame contraception as part of the cardiac care and reproductive safety plan to prevent unplanned high-risk pregnancy.
Long-acting reversible contraception is often preferred; progestin-only methods are generally safer than estrogen-containing options with thrombosis risk, pulmonary hypertension, or mechanical valves.
What are key delivery-planning considerations for cardiac patients?
Vaginal delivery is preferred unless there is an obstetric indication for cesarean or a specific cardiac reason (e.g., unstable maternal status, therapeutic INR) to avoid labor.
Planning should address delivery location, anesthesia involvement, telemetry needs, fluid management, and postpartum monitoring, clearly communicated across the multidisciplinary team in advance.
How should clinicians counsel patients when pregnancy is discouraged but strongly desired?
Acknowledge the patient’s goals and the emotional weight of the conversation; separate the goal (family building) from the timeline (safety now vs. after optimization).
If pregnancy remains prohibitively risky, discuss alternatives for family building and ensure adequate patient support.
What are the key gaps and future directions in cardio-obstetric risk stratification?
Current risk tools (mWHO, CARPREG II, ZAHARA) provide common language but do not fully capture functional status, prior pregnancy history, or how risk evolves over time.
Future direction: individualized, dynamic risk prediction incorporating imaging, biomarkers, exercise capacity, and social drivers of health, with better long-term links between pregnancy complications and cardiovascular prevention.
References
1. European Society of Cardiology. 2025 ESC Guidelines for the management of cardiovascular disease and pregnancy.
2. Mehta LS, et al. Cardiovascular Considerations in Caring for Pregnant Patients: A Scientific Statement From the American Heart Association. Circulation. 2020;141:e884-e903. PMID: 32362133. doi:https://doi.org/10.1161/CIR.0000000000000772
3. ACOG Practice Bulletin No. 212. Pregnancy and Heart Disease. Obstet Gynecol. 2019;133(5):e320-e356. PMID: 31022123. doi:https://doi.org/10.1097/AOG.0000000000003243
53 min
October 10, 2024395. Beyond the Boards: Channelopathies with Dr. Michael Ackerman
Dr. Amit Goyal, along with episode chair Dr. Dinu Balanescu (Mayo Clinic, Rochester), and FIT leads Dr. Sonu Abraham (University of Kentucky) and Dr. Natasha Vedage (MGH), dive into the fascinating topic of channelopathies with Dr. Michael Ackerman, a genetic cardiologist and professor of medicine, pediatrics, and pharmacology at Mayo Clinic, Rochester, Minnesota. Using a case-based approach, they review the nuances of diagnosis and treatment of channelopathies, including Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia (CPVT), and long QT syndrome. Dr. Sonu Abraham drafted show notes. Audio engineering for this episode was expertly handled by CardioNerds intern, Christiana Dangas.
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.
We Were Thrilled to Join the American Heart Association’s Scientific Sessions 2025!
AHA Scientific Sessions 2025 took place November 7–10 in New Orleans, LA — one of the premier annual gatherings in cardiovascular science and education.
It was an incredible opportunity to connect with colleagues, hear cutting-edge research, and contribute to the ongoing conversations shaping the future of cardiovascular care.
We’re grateful to everyone who joined us in New Orleans and made this year’s meeting so impactful.
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 Beyond the Boards Series
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Become a CardioNerds Patron!
Pearls and Quotes – Channelopathies
One cannot equate the presence of type 1 Brugada ECG pattern to the diagnosis of Brugada syndrome. Clinical history, family history, and/or genetic testing results are required to make a definitive diagnosis.
The loss-of-function variants in the SCN5A gene, which encodes for the α-subunit of the NaV1.5 sodium channel, is the only Brugada susceptibility gene with sufficient evidence supporting pathogenicity.
Exertional syncope is an “alarm” symptom that demands a comprehensive evaluation with 4 diagnostic tests: ECG, echocardiography, exercise treadmill test, and Holter monitor. Think of catecholaminergic polymorphic ventricular tachycardia (CPVT) in a patient with exertional syncope and normal EKG!
ICD therapy is never prescribed as monotherapy in patients with CPVT. Medical therapy with a combination of nadolol plus flecainide is the current standard of care.
Long QT syndrome is one of the few clinical scenarios where genetic testing clearly guides management, particularly with respect to variability in beta-blocker responsiveness.
Notes – Channelopathies
1. What are the diagnostic criteria for Brugada syndrome (BrS)?
Three repolarization patterns are associated with Brugada syndrome in the right precordial leads (V1-V2):
Type 1: Prominent coved ST-segment elevation displaying J-point amplitude or ST-segment elevation ≥2 mm, followed by a negative T wave.
Type 2/3: Saddleback ST-segment configuration with variable levels of ST-segment elevation.
It is important to note that only a type 1 pattern is diagnostic for Brugada syndrome, whereas patients with type 2/3 patterns may benefit from further testing.
The Shanghai score acknowledges that relying solely on induced type 1 ECG changes has limitations. Therefore, one cannot equate the presence of a type 1 Brugada ECG pattern alone to the diagnosis of Brugada syndrome. The score suggests incorporating additional information—such as clinical history, family history, and/or genetic testing results—to achieve a definitive diagnosis.
2. What is the significance of genetic testing in Brugada syndrome?
There are 23 alleged Brugada syndrome susceptibility genes published with varying levels of evidence. However, only one gene mutation, the loss-of-function variants in the SCN5A gene encoding for the α-subunit of the NaV1.5 sodium channel, is considered to have sufficient evidence.
The overall yield of BrS genetic testing is 20%. The presence of PR prolongation (>200 ms) along with type I EKG pattern increases the yield to 40%. On the contrary, in the presence of a normal PR interval, the likelihood of SCN5A positivity drops to <10%.
3. How would you risk-stratify a patient with Brugada syndrome?
Serious arrhythmic events (SAE), including resuscitated cardiac arrest and sudden cardiac death, rarely represent the initial symptoms of Brugada syndrome. Thus, risk stratification is important.
Factors that increase risk include:
Resuscitated cardiac arrest or history of cardiogenic syncope and the presence of a spontaneous type 1 ECG.
Positive genetic test – certain SCN5A variants were independent predictors for SAE.
Inducibility during programmed ventricular stimulation (EP study) using a double stimulation protocol (annualized risk is 1.5% per year for a positive study and 0.5% per year for a negative study).
4. What are the treatment options for Brugada syndrome?
The only drug with therapeutic potential in BrS is quinidine. The antiarrhythmic effect is achieved by prolonging the effective refractory period via inhibition of Ito potassium channel.
BrS plus a history of cardiac arrest, sustained VT, or syncope judged to be caused by ventricular arrhythmia would warrant an ICD.
In those refractory to first-line therapies, RVOT epicardial ablation is now an additional therapeutic option.
5. What are the four diagnostic tests to be done in a patient who presents with an episode of exertional syncope?
Exertional syncope is a high-risk presentation that demands a comprehensive evaluation! This includes:
EKG
Echocardiogram
Exercise treadmill test
Holter monitor
Do not stop at an EKG and echo alone!
Think of catecholaminergic polymorphic ventricular tachycardia (CPVT) in a patient with exertional syncope and a normal EKG!
6. What are the features on the exercise treadmill test that increase the suspicion for CPVT?
Bidirectional VT is considered a hallmark of CPVT, with digoxin toxicity being the only real imitator. This finding is specific in the absence of digoxin but not sensitive.
During exercise testing in CPVT, as the patient’s heart rate rises with increasing workload, PVCs begin to appear, progressing to bigeminy, couplets, and, in some instances, bidirectional couplets. The ectopy typically vanishes within 30 seconds of the recovery phase. This pattern increases suspicion of CPVT and warrants a detailed family history and genetic testing.
7. What are the genetic underpinnings of CPVT?
Mutations in the ryanodine receptor (RyR2 gene) render calcium release channels leaky, leading to diastolic calcium overload. This ultimately triggers arrhythmias in CPVT.
8. What are therapeutic interventions for a patient with CPVT?
Medical therapy is the mainstay of treatment in CPVT. Drugs include non-selective beta-blockers like nadolol or propranolol. Standard of care currently includes a combination of nadolol plus flecainide. An ICD is indicated only in the case of an aborted cardiac arrest. ICD therapy is never prescribed as monotherapy in these patients.
9. How do we correctly measure the QTc?
The QT interval is measured from the beginning of the QRS complex to the end of the T wave. The end of the T wave is determined using the maximum slope intercept method, in which a tangent line is drawn through the maximum down slope of the T wave. The point at which this tangent line crosses the isoelectric line is the end of the T wave. The U wave is excluded.
Best measured in leads II or V5.
Quick eyeball test: if the QT interval is more than ½ the RR interval, the QTc will be >460 ms.
10. What are the three primary mutations implicated in Long QT syndrome?
LQT1 (30-40% of cases)
Mutation: loss of function in potassium channel gene KCNQ1
ECG: broad-based T wave
Trigger: activity, adrenaline, exercise
BB responsiveness: +++ (nadolol or propranolol)
LQT2 (second most common)
Mutation: loss of function in potassium channel gene KCNH2
ECG: notched T wave
Trigger: auditory (alarm clock), post-partum
BB responsiveness: ++
LQT3
Mutation: gain of function or leakiness of sodium channel SCN5A (note: BrS is due to loss of function in the same gene)
ECG: normal T wave after prolonged isoelectric ST segment
Trigger: none, but typically happens during rest
BB responsiveness: + (propranolol); may consider combination therapy with mexiletine or mexiletine monotherapy.
References – Channelopathies
Charles Antzelevitch, Gan-Xin Yan, Michael J. Ackerman, Arthur A.M. Wilde et al. J-Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge, EP Europace, Volume 19, Issue 4, April 2017, Pages 665–694
Krahn AD, Behr ER, Hamilton R, Probst V, Laksman Z, Han HC. Brugada Syndrome. JACC Clin Electrophysiol. 2022 Mar;8(3):386-405. PMID: 35331438.
Chockalingam, P, Crotti, L, Girardengo, G. et al. Not All Beta-Blockers Are Equal in the Management of Long QT Syndrome Types 1 and 2: Higher Recurrence of Events Under Metoprolol. JACC. 2012 Nov, 60 (20) 2092–2099
Priori SG, Wilde AA, Tracy C et al. HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes: document endorsed by HRS, EHRA, and APHRS in May 2013 and by ACCF, AHA, PACES, and AEPC in June 2013. Heart Rhythm. 2013 Dec;10(12):1932-63. PMID: 24011539.
Viskin S, Rosovski U, Zeltser D et al. Inaccurate electrocardiographic interpretation of long QT: the majority of physicians cannot recognize a long QT when they see one. Heart Rhythm. 2005 Jun;2(6):569-74. PMID: 15922261.
Horner JM, Ackerman MJ. Ventricular ectopy during treadmill exercise stress testing in the evaluation of long QT syndrome. Heart Rhythm. 2008 Dec;5(12):1690. PMID: 19084807; PMCID: PMC3281579.
1 hr 6 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.
CardioNerds Beyond the Boards Series
CardioNerds Episode Page
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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
June 06, 2024375. Beyond the Boards: Foundations of Cardiovascular Prevention with Dr. Stephen Kopecky
CardioNerds (Amit Goyal and Dan Ambinder), Dr. Jaya Kanduri, and Dr. Jason Feinman discuss foundations of cardiovascular prevention with Dr. Stephen Kopecky. In this episode, the CardioNerds and topic expert Dr. Stephen Kopecky tackle cardiovascular prevention. They focus on how to identify patients at risk for cardiovascular disease by using the pooled cohort equation and discuss how to incorporate additional risk-enhancing factors in risk estimation. Later, they discuss the role of non-invasive imaging and testing for further patient risk stratification. Last, they discuss the appropriate pharmacologic interventions for patient care, how to determine what LDL-c to target for each patient, and how to modify your treatment modalities in response to side effects or the need for further lipid-lowering therapies.
Notes were drafted by Dr. Jason Feinman. Audio was engineered by CardioNerds Intern Christiana Dangas.
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.
CardioNerds Beyond the Boards Series
CardioNerds Episode Page
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Cardionerds Healy Honor Roll
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Pearls and Quotes – Foundations of Cardiovascular Prevention
The 2018 cardiovascular prevention guidelines indicate that a single equation, like the pooled risk equation, does not fit everyone. There are additional risk enhancers that are not factored into the pooled risk equation that can impact an individual’s risk
These factors are often conditions that increase inflammation but can also include family history, ethnicity, chronic kidney disease, metabolic syndrome, premature menopause or gestational diabetes, and rheumatologic conditions
Data from Get With The Guidelines demonstrates that the average LDL at the time of the first myocardial infarction is 105 mg/dL.
Coronary artery calcium scores or a carotid ultrasound can be used to further risk stratify patients. However, CAC is likely to be negative in young women. A CAC of zero can be used to “de-risk” some patients but should not be used to guide therapy in the setting of tobacco usage, diabetes mellitus, or familial hypercholesterolemia.
Strategies to mitigate risk include healthy lifestyle habits and selectively targeting key risk factors including LDL, hypertriglyceridemia, inflammation, and the GLP1-pathway. Upcoming medications may address elevated Lp(a).
Notes – Foundations of Cardiovascular Prevention
Notes: Notes drafted by Dr. Jason Feinman.
How do you assess an individual’s risk for cardiovascular disease?
The paramount role of primary prevention is the assessment and mitigation of an individual’s risk for ASCVD event.1
The 10-year ASCVD risk calculator is a commonly used tool to assess an individual’s risk and to guide shared decision-making conversations and recommendations.2
Individuals can be characterized as having low (less than 5%), borderline (5%-7.5%), intermediate (7.5%-20%), or high (greater than 20%) risk.2
The 10-year ASCVD risk calculator has varying validation in ethnic minorities, and other risk calculators, such as the Framingham CVD risk score, may be considered in those groups.3-5
Additional risk enhancers may be used to guide recommendations for individuals at borderline or intermediate risk.1
What additional imaging testing may be beneficial in the assessment of an individual’s risk?
Individuals with intermediate or borderline risk may benefit from further non-invasive imaging to help guide therapeutic recommendations.2
Coronary artery calcification is a marker of underlying atherosclerosis, which can help to reclassify patients to be at higher risk for ASCVD events and support interventions to help lower this risk.6
Conversely, a score of zero can help to reclassify individuals into lower-risk groups
A score of zero should be used with caution in young women who are more likely to have non-calcified plaque and should not be used as a marker of low risk in individuals with other risk factors, including diabetes mellitus and tobacco usage.1
What non-pharmacological interventions may be considered to lower an individual’s ASCVD risk?
The 2019 guidelines give a class I recommendation for a diet of vegetables, fruits, nuts, whole grains, and fish to lower ASCVD risk factors.1
Increased intake of sugar has been demonstrated to correlate with increased rates of type 2 diabetes mellitus and subsequent increased risk for cardiovascular events.7
At least 150 minutes per week of moderate-intensity or 75 minutes of vigorous intensive is recommended to reduce the risk of ASCVD events.1
What pharmacological interventions can be considered for individuals with prior ASCVD events or at high risk for ASCVD?
A moderate-intensity statin is recommended for individuals at intermediate risk of ASCVD events with risk enhancers with a goal reduction in LDL-c of 30% or more.1
For individuals at a high 10-year risk for ASCVD events, a 50% reduction in LDL-C is recommended.1
A doubling of a statin dose can be predicted to lead to a 6% further reduction in LDL-C
Ezetimibe can be considered as adjunct therapy for individuals receiving statin therapy who do not reach their target LDL-C.2
How do you determine the goal LDL-c?
LDL goal is based on a history of prior ASCVD events and the risk of future ASCVD events.
For secondary prevention, especially for individuals at high risk for ASCVD events, an LDL goal of at least less than 70 mg/dL is recommended2
References – Foundations of Cardiovascular Prevention
Arnett DK, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [published correction appears in Circulation. 2019 Sep 10;140(11):e649-e650] [published correction appears in Circulation. 2020 Jan 28;141(4):e60] [published correction appears in Circulation. 2020 Apr 21;141(16):e774]. Circulation. 2019;140(11):e596-e646. doi:10.1161/CIR.0000000000000678
Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [published correction appears in Circulation. 2019 Jun 18;139(25):e1182-e1186] [published correction appears in Circulation. 2023 Aug 15;148(7):e5]. Circulation. 2019;139(25):e1082-e1143. doi:10.1161/CIR.0000000000000625
Yang X, Li J, Hu D, et al. Predicting the 10-Year Risks of Atherosclerotic Cardiovascular Disease in Chinese Population: The China-PAR Project (Prediction for ASCVD Risk in China). Circulation. 2016;134(19):1430-1440. doi:10.1161/CIRCULATIONAHA.116.022367
Jung KJ, Jang Y, Oh DJ, et al. The ACC/AHA 2013 pooled cohort equations compared to a Korean Risk Prediction Model for atherosclerotic cardiovascular disease. Atherosclerosis. 2015;242(1):367-375. doi:10.1016/j.atherosclerosis.2015.07.033
D’Agostino RB Sr, Vasan RS, Pencina MJ, et al. General cardiovascular risk profile for use in primary care: the Framingham Heart Study. Circulation. 2008;117(6):743-753. doi:10.1161/CIRCULATIONAHA.107.699579
DeFilippis AP, Young R, Carrubba CJ, et al. An analysis of calibration and discrimination among multiple cardiovascular risk scores in a modern multiethnic cohort. Ann Intern Med. 2015;162(4):266-275. doi:10.7326/M14-1281
Löfvenborg JE, Andersson T, Carlsson PO, et al. Sweetened beverage intake and risk of latent autoimmune diabetes in adults (LADA) and type 2 diabetes. Eur J Endocrinol. 2016;175(6):605-614. doi:10.1530/EJE-16-0376
16 min
November 17, 2023344. Beyond the Boards: Disease of the Peripheral Arteries with Dr. Amy Pollak
CardioNerds (Drs. Amit Goyal, Jason Feinman, and Tiffany Dong) discuss Beyond the Boards: Diseases of the Peripheral Arteries with Dr. Amy Pollak. We review common presentations of peripheral vascular disease, ranging from aortic disease to the more distal vessels in an engaging case-based discussion. Dr. Pollack talks us through these cases, including the diagnosis and management of peripheral vascular diseases. Show notes were drafted by Dr. Matt Delfiner and episode audio was edited by student doctor Tina Reddy.
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.
CardioNerds Beyond the Boards Series
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll
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Subscribe to The Heartbeat Newsletter!
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Pearls and Quotes – Disease of the Peripheral Arteries
Risk factors for abdominal aortic aneurysm include traditional atherosclerotic risk factors such as age, hypertension, hyperlipidemia, and tobacco use.
Screening for AAA should be for men over the age of 65 years with a history of tobacco use. If present, medical management includes blood pressure and lipid lowering therapies to decrease the risk of expansion. Decision for surgical intervention relies on size and rate of growth of AAA, with clear indications if it grows> 10 mm in a year or diameter of 5.5 cm in men and 5.0 cm in women.
When diagnosis of PAD is not straightforward (presence of symptoms but ABI is normal), an exercise ankle-brachial index (ABI) test can be useful. An exercise-induced decrease in ABI by 20% or in ankle pressure by 30 mmHg is consistent with PAD.
For PAD, treatment with low dose rivaroxaban and aspirin yields lower event rates than with antiplatelet therapy alone. This in combination with lifestyle therapies (diet + exercise) and risk factor management (hypertension and hyperlipidemia) are the cornerstones of therapy. Revascularization is indicated for continued PAD symptoms despite conservative therapy.
Acute limb ischemia is an “acute leg attack” and is a life-threatening emergency. Common symptoms include pain, pallor, pulselesess, parasthesias, cold temperature (poikilothermia), and paralysis. Restoration of blood flow is paramount, and emergent or urgent revascularization is the first line therapy for those with symptoms < 2 weeks.
Notes – Disease of the Peripheral Arteries
Learning Objectives:
Describe screening and therapeutic strategy for AAA management.
Understand the risk factors and diagnosis of peripheral arterial disease.
Compare different management approaches for PAD.
Be able to recognize acute limb ischemia.
Describe the overall treatment strategy for acute limb ischemia.
Abdominal Aortic Aneurysms
Abdominal aortic aneurysms are a source of high morbidity and mortality. The US Preventative Services Task Force recommends one time screening ultrasound for AAA in men older than 65 years of age with a tobacco use history. Risk factors include age, hypertension, hyperlipidemia, and tobacco use. Patients with AAA between 3-3.9 mm should be monitored every 2-3 years. Sizes 4-5 cm should be re-imaged every 6-12 months. Additional screening can be done for individuals < 65 years who have a first degree relative with AAA.
Women are more likely to have aortic dissection at smaller diameters than men, which is why intervention (open vs endovascular repair) is recommended at 5 cm diameter for women versus at 5.5 cm for men. Additionally, repair is also warranted if a AAA grows more than 5 mm in 6 months or 10 mm in one year.
Risk factor management is key with AAA, including blood pressure, glucose, and lipid targeting. The presence of an AAA should be treated as secondary ASCVD prevention like coronary arterial disease, since AAA is an atherosclerotic disease equivalent. Tobacco cessation is of the utmost importance here.
Regarding strategy for repair: if the patient is not a surgical candidate, then endovascular repair is a reasonable option. If they are a surgical candidate, then the location of the aneurysm comes into play. Infrarenal or juxtarenal disease are more likely to require open repair.
Peripheral Arterial Disease
When a patient presents with claudication, in addition to thorough history and physical exam, checking for ABIs is important. Risk factors include known coronary disease, hypertension, hyperlipidemia, and diabetes. Women often report cramping in their calves/legs rather than outright pain.
ABI < 0.9 are consistent with PAD, with > 1.3 consistent with calcified and non-compressible vessels. Toe brachial index (TBI) cutoff is 0.7. If there is strong clinical suspicion but normal ABI, then performing the test after a period of exercise (calf raises, treadmill) can be clinically useful. An exercise induced decrease in ankle pressure by 30 mm or change in ABI by 20% is consistent with PAD.
Therapy for PAD includes supervised exercise training, lifestyle changes (e.g., tobacco cessation) and risk factor modification (blood pressure/lipids/glucose). Additionally, low dose rivaroxaban (2.5 mg twice daily) plus aspirin has been shown to decrease events compared to aspirin alone.
If there are continued symptoms despite the above therapy, then invasive management can be considered. This includes percutaneous or surgical revascularization. This would be proceeded with CTA imaging for further guidance. Invasive angiography is reasonable for someone with a higher likelihood of a single lesion amenable to percutaneous repair. Discrete and singular lesions are usually repaired percutaneously while more diffuse or multivessel disease, then surgical management may be indicated.
Acute Limb Ischemia
ALI can present with the 6 Ps: pain, pallor, pulselessness, parasthesias, poikilothermia, and paralysis. Limbs may (rarely) remain viable, with signs being a clear Doppler-able pulse without sensory or muscle loss. Otherwise, a limb is salvageable if there is a faint arterial Doppler signal. If there is muscle weakness, then the limb is considered threatened. If an arterial Doppler signal is completely lost, then the limb is considered non-viable.
ALI is an “acute leg attack.” The initial therapy is systemic anticoagulation with unfractionated heparin. If symptoms have been present for less than two weeks, then endovascular therapy with either thrombectomy or catheter-directed lysis are indicated. Major contraindications to lytic therapy include recent surgery, any history of intracranial bleeding or neoplasm, or if they are otherwise at a high bleeding risk. Non-viable limbs may better be served with amputation rather than revascularization.
References – Disease of the Peripheral Arteries
1. Eikelboom JW, Connolly SJ, Bosch J, et al. Rivaroxaban with or without Aspirin in Stable Cardiovascular Disease. N Engl J Med. 2017;377(14):1319-1330. doi:10.1056/NEJMoa1709118
https://www.nejm.org/doi/full/10.1056/NEJMoa1709118
2. Criqui MH, Matsushita K, Aboyans V, et al. Lower Extremity Peripheral Artery Disease: Contemporary Epidemiology, Management Gaps, and Future Directions: A Scientific Statement From the American Heart Association Circulation. 2021;144(9):e171-e191. doi:10.1161/CIR.0000000000001005
https://www.ahajournals.org/doi/full/10.1161/CIR.0000000000001005?rfr_dat=cr_pub++0pubmed&url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org
3. Lanzi S, Belch J, Brodmann M, et al. Supervised exercise training in patients with lower extremity peripheral artery disease. Vasa. 2022;51(5):267-274. doi:10.1024/0301-1526/a001024
https://econtent.hogrefe.com/doi/full/10.1024/0301-1526/a001024
4. Sabouret P, Cacoub P, Dallongeville J, et al. REACH: international prospective observational registry in patients at risk of atherothrombotic events. Results for the French arm at baseline and one year. Arch Cardiovasc Dis. 2008;101(2):81-88. doi:10.1016/s1875-2136(08)70263-8
https://www.sciencedirect.com/science/article/pii/S1875213608702638?via%3Dihub
5. Zucker EJ, Misono AS, Prabhakar AM. Abdominal Aortic Aneurysm Screening Practices: Impact of the 2014 U.S. Preventive Services Task Force Recommendations. J Am Coll Radiol. 2017;14(7):868-874. doi:10.1016/j.jacr.2017.02.020
https://www.jacr.org/article/S1546-1440(17)30200-4/fulltext
5. Hensley SE, Upchurch GR Jr. Repair of Abdominal Aortic Aneurysms: JACC Focus Seminar, Part 1. J Am Coll Cardiol. 2022;80(8):821-831. doi:10.1016/j.jacc.2022.04.066
https://www.jacc.org/doi/abs/10.1016/j.jacc.2022.04.066
6. Shishehbor MH, White CJ, Gray BH, et al. Critical Limb Ischemia: An Expert Statement. J Am Coll Cardiol. 2016;68(18):2002-2015. doi:10.1016/j.jacc.2016.04.071
https://www.jacc.org/doi/full/10.1016/j.jacc.2016.04.071
7. Kinlay S. Management of Critical Limb Ischemia. Circ Cardiovasc Interv. 2016;9(2):e001946. doi:10.1161/CIRCINTERVENTIONS.115.001946
https://www.ahajournals.org/doi/full/10.1161/CIRCINTERVENTIONS.115.001946
8. Gerhard-Herman MD, Gornik HL, Barrett C, et al. 2016 AHA/ACC Guideline on the Management of Patients With Lower Extremity Peripheral Artery Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [published correction appears in Circulation. 2017 Mar 21;135(12 ):e791-e792]. Circulation. 2017;135(12):e726-e779. doi:10.1161/CIR.0000000000000471
https://www.ahajournals.org/doi/10.1161/CIR.0000000000000471?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed
43 min
October 17, 2023337. Beyond the Boards: The Diagnosis and Management of Infective Endocarditis with Dr. Michael Cullen
CardioNerds (Drs. Amit Goyal, Matthew Delfiner, and Tiffany Dong) discuss infective endocarditis with distinguished clinician-educator Dr. Michael Cullen. We dive into the nuances of infective endocarditis, including native valve endocarditis, prosthetic valve endocarditis, and right-sided endocarditis.
Notes were drafted by Dr. Tiffany Dong, and audio editing was performed by student Dr. Adriana Mares.
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.
CardioNerds Beyond the Boards Series
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll
CardioNerds Journal Club
Subscribe to The Heartbeat Newsletter!
Check out CardioNerds SWAG!
Become a CardioNerds Patron!
Pearls and Quotes
The physical exam is crucial in the evaluation of infective endocarditis and includes cardiac auscultation and a search for sequelae of endocarditis, such as immunologic and embolic phenomena.
The modified Duke Criteria categorizes the diagnosis of infective endocarditis into four different buckets: definite endocarditis by pathology, definite endocarditis by clinical criteria, possible endocarditis, and rejected.
The diagnosis of endocarditis may involve several different imaging modalities, including transthoracic echocardiogram, transesophageal echocardiogram, 4D CT, and nuclear imaging.
For left-sided endocarditis, indications to operate include endocarditis due to S. aureus or fungi, heart failure, evidence of perivalvular complications, persistent bacteremia, and large vegetations.
The management of endocarditis often involves multiple teams, including cardiology, infectious disease, addiction medicine, neurology, anesthesiology, and cardiothoracic surgery.
Notes
What signs/complications of endocarditis are apparent on physical exam and labs?
A new or worsening cardiac murmur with possible signs of volume overload.
Vascular phenomena encompass splinter hemorrhages, conjunctival hemorrhages, Janeway lesions, mycotic aneurysms, and TIA/strokes.
Immunologic phenomena include glomerulonephritis, Roth spots, and Osler nodes.
Positive blood cultures with 2-3 samples collected.
Elevated inflammatory markers.
How does the modified Duke criteria assist in the diagnosis of infective endocarditis?
The modified Duke criteria separate the diagnosis of endocarditis into four categories: definite endocarditis by pathology, definite endocarditis by clinical criteria, possible endocarditis, and rejected endocarditis.
Definitive endocarditis by pathology requires pathologic confirmation of “bugs under the microscope.”
Definitive endocarditis by clinical criteria requires two major criteria, one major and two minor criteria, or all five minor criteria.
Possible endocarditis requires one major and one minor or three minor criteria.
Major criteria:
Positive blood culture for typical organism
Evidence of endocardial involvement (e.g., vegetation on echo)
Minor Criteria
Predisposing clinical factors (e.g., intravenous drug use, known valvulopathy)
Fever
Immunologic phenomena
Vascular phenomena
Blood culture for atypical organism
What is the role of TTE compared to TEE in endocarditis?
TTE and TEE both have their roles in the workup for endocarditis.
TTE can provide a baseline screen and yield a better understanding of ventricular size and function than transesophageal.
The strength of TEE is the ability to visualize smaller vegetations along with perivalvular complications that may be missed on TTE.
If clinical suspicion is high for endocarditis, repeat echocardiography is warranted.
What are other tools to evaluate for endocarditis in prosthetic valves?
TTE and TEE remain important and should be commonly utilized for the diagnosis of endocarditis.
FDG-PET can detect inflammation that could be suggestive of endocarditis. Patients should be at least six weeks after valve implantation; otherwise, FDG PET may detect normal postsurgical inflammation.
Gated 4D CT can also screen for perivalvular involvement and aid with surgical planning, especially in these patients who may undergo redo surgery.
What are the indications for surgery in infective endocarditis?
It is important to separate left-sided and right-sided endocarditis because the indications are different.
For left-sided endocarditis, indications for surgery include persistent bacteremia/fevers despite appropriate antibiotic therapy, S. aureus or fungal endocarditis, heart failure symptoms, perivalvular complications, and vegetations >20mm.
For right-sided endocarditis, indications for surgery include infection with a fungal organism, heart failure due to severe tricuspid regurgitation, vegetations >10mm with embolic phenomenon, persistent bacteremia despite appropriate therapy, and perivalvular involvement.
Often, medical therapy alone for right-sided endocarditis will be sufficient.
What is the role of multidisciplinary teams for endocarditis?
Endocarditis teams can involve cardiology, infectious disease, cardiothoracic surgery, neurology, anesthesiology, and addiction medicine.
Addiction medicine is a very important group, particularly in cases where endocarditis is related to IVDU. It is a class 1 indication to consult addiction medicine to give the patient the best long-term outcome.
Even if surgery is not warranted at initial hospitalization, it may be appropriate to have cardiac surgery weigh in and follow up with the patient in case there arises an indication for surgery.
References
Habib G, Lancellotti P, Antunes MJ, et al. 2015 ESC Guidelines for the management of infective endocarditis: The Task Force for the Management of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by: European Association for Cardio-Thoracic Surgery (EACTS), the European Association of Nuclear Medicine (EANM). European heart journal. Nov 21 2015;36(44):3075-3128. doi:10.1093/eurheartj/ehv319 https://academic.oup.com/eurheartj/article/36/44/3075/2293384
Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. Feb 2 2021;143(5):e35-e71. doi:10.1161/cir.0000000000000932
https://www.ahajournals.org/doi/10.1161/CIR.0000000000000923#d1e11386
Baddour LM, Wilson WR, Bayer AS, et al. Infective Endocarditis in Adults: Diagnosis, Antimicrobial Therapy, and Management of Complications: A Scientific Statement for Healthcare Professionals From the American Heart Association. Circulation. Oct 13 2015;132(15):1435-86. doi:10.1161/cir.0000000000000296
https://www.ahajournals.org/doi/pdf/10.1161/CIR.0000000000000296
35 min
August 08, 2023323. Beyond the Boards: Complications of Acute Myocardial Infarction with Dr. Jeffrey Geske
CardioNerds co-founder Dr. Amit Goyal and episode leads Dr. Jaya Kanduri (FIT Ambassador from Cornell University) and Dr. Jenna Skowronski (FIT Ambassador from UPMC) discuss Complications of acute myocardial infarction with expert faculty Dr. Jeffrey Geske. They discuss various complications of acute MI such as cardiogenic shock, bradyarrythmias, left ventricular outflow tract obstruction, ruptures (papillary muscle rupture, VSD, free wall rupture), and more. Show notes were drafted by Dr. Jaya Kanduri. Audio editing by CardioNerds Academy Intern, student doctor Tina Reddy.
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.
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Pearls and Quotes – Complications of Acute Myocardial Infarction
Sinus tachycardia is a “harbinger of doom”!
The triad for RV infarction includes hypotension, elevated JVP, and clear lungs. These patients are preload dependent and may need fluid resuscitation despite having an elevated JVP.
Bradyarrythmias in inferior MIs are frequently vagally mediated. The focus should be on medical management before committing to a temporary transvenous pacemaker, such as reperfusion, maintaining RV preload and inotropy, avoiding hypoxia, and considering RV-specific mechanical circulator support (MCS).
Worsening hypotension with inotropic agents (e.g., dobutamine, epinephrine, dopamine, norepinephrine) after a large anterior-apical MI should raise suspicion for dynamic left ventricular outflow tract obstruction due to compensatory hyperdynamic basal segments.
The myocardium after a late presentation MI is as “mushy as mashed potatoes”! Need to look out for papillary muscle rupture, VSD, and free wall rupture as potential complications. Papillary muscle rupture can occur with non-transmural infarcts, and often presents with flash pulmonary edema. VSDs will have a harsh systolic murmur and are less likely to present with pulmonary congestion. Free wall rupture can present as a PEA arrest. All of these complications require urgent confirmation on imaging and early involvement of surgical teams.
Notes – Complications of Acute Myocardial Infarction
How should we approach cardiogenic shock (CS) in acute myocardial infarction (AMI)?
Only 10% of AMI patients present with CS, but CS accounts for up to 70-80% of mortality associated with AMI, usually due to extensive LV infarction with ensuing pump failure.
Physical exam
Sinus tachycardia is considered a “harbinger of doom”, when the body compensates for low cardiac output by ramping up the heart rate
The presence of sinus tachycardia and low pulse and/or blood pressure in a patient with a large anterior MI should raise suspicion for cardiogenic shock
Be wary of giving IV beta blockers in this situation as negative inotropes can precipitate cardiogenic shock (Commit Trial)
When interpreting a patient’s blood pressure in the acute setting, it is helpful to know their baseline blood pressure and if they have a significant history of hypertension.
Patients <75 years of age with CS have improved survival at 6 months and at 1 year with early revascularization (SHOCK trial)
Mechanical circulatory support
Intra-aortic balloon pump (IABP)
No mortality benefit with IABP use in CS at 30 days and at 1 year (IABP-SHOCK II trial)
ACC/AHA guidelines give IABP a class IIa recommendation for medically refractory AMI-CS in the USA, whereas the ESC guidelines give it a class III recommendation.
Percutaneous left ventricular assist device (Impella)
No difference in mortality between IABP or Impella use after 30 days or 6 months (IMPRESS trial)
However, observational data like the Detroit & VAD registries show improvement in survival with Impella use in AMI-CS with the cost of excess complications (vascular injury, bleeding, etc)
Upcoming trials (DanGer Shock and Recover IV) will hopefully have more promising data supporting the use of Impella in AMI-CS
In the setting of discrepant guidelines, the decision for MCS should be multidisciplinary and based on clinical expertise.
For more on AMI-CS, enjoy CardioNerds #223. CCC: Approach to Acute Myocardial Infarction Cardiogenic Shock with Dr. Venu Menon
How does RV infarction present?
Physical exam
RV infarct triad: hypotension, elevated JVP, clear lungs
Hypotension precipitated by nitroglycerin administration highlights the preload dependent state of an infarcted RV
GI symptoms (nausea and emesis) are common
Patients may actually need fluids despite an elevated JVP because of an underfilled left ventricle
EKG
Consider a right sided leads (ST elevation in V1 and V4R are the most sensitive EKG markers of RV injury), but this should not delay emergent coronary angiography +/- PCI if suspicion for AMI is high
Rhythm
AV synchrony plays an important role in RV infarct given the dependence on preload
If a patient loses AV synchrony due to heart block or atrial fibrillation, they can become more unstable due to a further drop in RV preload and overall cardiac output
However, bradyarrythmias in inferior MIs are frequently vagally mediated, and therefore temporary
Strategy for management of an inferior MI with RV infarct should be to optimize all other aspects hemodynamically before placing a temporary transvenous pacemaker (risk of RV perforation)
Prompt reperfusion
Maintain RV preload
Inotropes
Avoid hypoxia (potent pulmonary vasoconstriction, can increase RV afterload)
MCS providing RV support (Protek-Duo, RP Impella, VA-ECMO)
For more on RV-predominant cardiogenic shock, enjoy CardioNerds #239. CCC: Approach to RV Predominant Cardiogenic Shock with Dr. Ryan Tedford
How does LVOT obstruction in a large anterior MI present?
Hypotension with dobutamine or norepinephrine in a patient with an anterior MI and apical infarct, should raise suspicion for dynamic left ventricular outflow tract obstruction due to compensatory hyperdynamic basal walls
Echocardiography is invaluable for diagnosis!
Management
Prompt reperfusion
IV fluids (preload dependent)
Beta blockers (eg: esmolol quick on, quick off)
Phenylephrine (can improve BP by increasing afterload)
Avoid positive inotropes (e.g., norepinephrine, epinephrine, dopamine, dobutamine, milrinone)
Avoid IABP
What are the different types of ruptures which may complicate a late-presentating MI?
Papillary muscle rupture
Posteromedial papillary more likely to be affected due to single coronary blood supply
Papillary muscles are subendocardial so rupture can occur with non-transmural infarcts
Presents with acute dyspnea from flash pulmonary edema and hypotension from drop in cardiac output
Exam with new systolic murmur which may not be audible due to rapid equalization of pressures. For the same reason, Doppler may also underestimate the degree of MR.
V wave from mitral regurgitation
Ventricular septal rupture
Risk factors: advanced age, female sex, first MI with lack of coronary collaterals
Presents with hypotension, chest discomfort, dyspnea
Exam with harsh systolic murmur with palpable thrill; pulmonary congestion is unusual unusual
V wave from increased flow through the pulmonary circuit (but not high enough to cause flash pulmonary edema)
Step up in RV saturation during right heart catheterization
Inferobasal VSD with RCA infarcts (near the valves and conduction tissue and with more serpentine lesions, leading to worse outcomes)
Apical VSD with LAD infarcts (can miss on TTE)
Free wall rupture
Risk factors: advanced age, female sex, first MI with lack of coronary collaterals
Partial rupture may present as a vagal event that heralds the initial tear; TTE with new pericardial effusion should raise suspicion of an incomplete rupture
Full rupture can present as PEA arrest with abysmally low survival
May partially heal as a pseudo-aneurysm
How do we manage rupture complications?
For any of the three rupture scenarios (VSR, papillary muscle rupture, or free wall rupture), time is of the essence to confirm the site of rupture and to get the surgical team involved
Can have abrupt, unexpected, unpredictable progression so need to bring in surgical expertise early
Papillary muscle rupture will need mitral valve replacement
For VSR closure, can pursue surgical versus percutaneous options depending on anatomical features of the lesion and patient characteristics
Intervention is more challenging in inferobasal VSRs with higher operative mortality, but also less amenable to percutaneous closure (less likely to have appropriate rims for closure)
If poor operative candidacy, more likely to opt for percutaneous options
If size of defect large, would more likely lean towards surgery
Can consider bridging with MCS if patient in CS (eg: IABP, Impella) as long as this will not delay the surgical intervention
References
Early intravenous then oral metoprolol in 45 852 patients with acute myocardial infarction: Randomised placebo-controlled trial. The Lancet. 2005;366(9497):1622-1632. doi:10.1016/s0140-6736(05)67661-1. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(05)67661-1/fulltext
Dzavik V. Early revascularization is associated with improved survival in elderly patients with acute myocardial infarction complicated by cardiogenic shock: A report from the Shock Trial Registry. European Heart Journal. 2003;24(9):828-837. doi:10.1016/s0195-668x(02)00844-8. https://www.nejm.org/doi/full/10.1056/nejm199908263410901
Thiele H, Zeymer U, Neumann F-J, et al. Intraaortic balloon support for myocardial infarction with Cardiogenic shock. New England Journal of Medicine. 2012;367(14):1287-1296. doi:10.1056/nejmoa1208410. https://www.nejm.org/doi/full/10.1056/nejmoa1208410
Ouweneel DM, Eriksen E, Sjauw KD, et al. Percutaneous mechanical circulatory support versus intra-aortic balloon pump in cardiogenic shock after acute myocardial infarction. Journal of the American College of Cardiology. 2017;69(3):278-287. doi:10.1016/j.jacc.2016.10.022. https://www.jacc.org/doi/epdf/10.1016/j.jacc.2016.10.022
O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013;127:e362-425. https://www.ahajournals.org/doi/10.1161/CIR.0b013e3182742cf6
Authors/Task Force members, Windecker S, Kolh P, et al. 2014 ESC/EACTS Guidelines on myocardial revascularization: The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS)Developed with the special contribution of the European Association of Percutaneous Cardiovascular Interventions (EAPCI). Eur Heart J 2014;35:2541-619. https://pubmed.ncbi.nlm.nih.gov/25173339/
Damluji AA, van Diepen S, Katz JN, et al. Mechanical complications of acute myocardial infarction: A scientific statement from the American Heart Association. Circulation. 2021;144(2). doi:10.1161/cir.0000000000000985. https://www.ahajournals.org/doi/full/10.1161/CIR.0000000000000985
31 min

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