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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.
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What signs/complications of endocarditis are apparent on physical exam and labs?
How does the modified Duke criteria assist in the diagnosis of infective endocarditis?
What is the role of TTE compared to TEE in endocarditis?
What are other tools to evaluate for endocarditis in prosthetic valves?
What are the indications for surgery in infective endocarditis?
What is the role of multidisciplinary teams for endocarditis?
The following question refers to Section 4.7 of the 2021 ESC CV Prevention Guidelines. The question is asked by student Dr. Shivani Reddy, answered first by NP Carol Patrick, and then by expert faculty Dr. Eileen Handberg.
Dr. Handberg is an Adult Nurse Practitioner, Professor of Medicine, and Director of the Cardiovascular Clinical Trials Program in the Division of Cardiovascular Medicine at the University of Florida. She has served as Chair of the Cardiovascular Team Section and the Board of Trustees with the ACC and is the President Elect for the PCNA.
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.
Ms. BW presents after her best friend was diagnosed with hypertension and is interested in measuring her own blood pressure.
According to the ESC Guidelines, what BP screening approach is recommended for making a diagnosis of hypertension?
A
Repeated measurements in one visit
B
A single measurement in a single visit
C
Repeated measurements in more than one visit
D
Reported patient history
Explanation
The correct answer is C – Repeated measurements in more than one visit.
It is recommended to base the diagnosis of hypertension on repeated office BP measurements on more than one visit except when hypertension is severe (e.g., Grade 3—defined as SBP > 180 and/ or DBP >110mmHg—and especially in high-risk patients) (Class I, LOE C). In addition to recommending repeat measurements across visits, the guidelines provide a number of considerations for appropriately measuring blood pressure, such as taking measurements when seated in a quiet environment for 5 minutes and measuring in both arms at the first visit and using the higher-level value arm for visits thereafter (see Table 14 on page 3283).
Additionally, home blood pressure monitoring is recommended as an alternative to repeated office measurements. Blood pressure measurements are taken with a semiautomated, validated cuff for 3 consecutive days – and 6-7 days being preferred – in the morning and at night, averaged over that period. Notably, home blood pressure thresholds for the diagnosis of hypertension are lower than for that of in-office measurements, with a daytime systolic of 135mmHg or diastolic of 85mmHg given as the level at which hypertension is diagnosed, as opposed to 140mmHg and 90mmHg for systolic and diastolic levels, respectively, given for in-office diagnosis.
Main Takeaway
With the exception of those with severely elevated blood pressures, the diagnosis of hypertension requires repeated measurements across multiple office visits.
Guideline Loc.
Sections 4.7.1 and 4.7.2, Table 13 and 14, Figure 14
CardioNerds Decipher the Guidelines – 2021 ESC Prevention Series
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The following question refers to Section 7.8 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.
The question is asked by Stony Brook University Hospital medicine resident and CardioNerds Intern Dr. Chelsea Tweneboah, answered first by Mayo Clinic Cardiology Fellow and CardioNerds Academy Chief Dr. Teodora Donisan, and then by expert faculty Dr. Michelle Kittleson.
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.
A 69-year-old man was referred to the cardiology clinic after being found to have a reduced left ventricular ejection fraction and left ventricular hypertrophy. For the last several months he has been experiencing progressively worsening fatigue and shortness of breath while getting to the 2nd floor in his house. He has a history of bilateral carpal tunnel syndrome and chronic low back pain. He takes no medications. On exam, his heart rate is 82 bpm, blood pressure is 86/60 mmHg, O2 saturation is 97% breathing ambient air, and BMI is 29 kg/m2. He has a regular rate and rhythm with normal S1 and S2, bibasilar pulmonary rales, and 1+ pitting edema in both legs. EKG shows normal sinus rhythm with a first-degree AV delay and low voltages. Transthoracic echocardiogram shows a moderately depressed LVEF of 35-39%, severe concentric hypertrophy with a left ventricular posterior wall thickness of 1.5 cm and strain imaging showing globally reduced longitudinal strain with apical sparring. There is also biatrial enlargement and a small pericardial effusion. A pharmacologic nuclear stress test did not reveal any perfusion defects. A gammopathy panel including SPEP, UPEP, serum and urine immunofixation studies, and serum free light chains are unrevealing. A 99mTc-Pyrophosphate scan was positive with grade 3 uptake. In addition to starting diuretics, what is the next most appropriate step for managing for this patient?
A
Start metoprolol succinate
B
Start sacubitril/valsartan
C
Perform genetic sequencing of the TTR gene
D
Perform endomyocardial biopsy
Explanation
The correct answer is C – perform genetic sequencing of the TTR gene.
This patient has findings which raise suspicion for cardiac amyloidosis. There are both cardiac (low voltages on EKG and echocardiogram showing marked LVH with biatrial enlargement and small pericardial effusion as well as a characteristic strain pattern) and extra-cardiac (bilateral carpal tunnel syndrome and low back pain) features to suggest amyloidosis. The diagnosis of cardiac amyloidosis requires a high index of suspicion and most commonly occurs due to a deposition of monoclonal immunoglobulin light chains (AL-CM) or transthyretin (ATTR-CM). ATTR may cause cardiac amyloidosis as either a pathogenic variant (ATTRv) or as a wild-type protein (ATTRwt).
Patients for whom there is a clinical suspicion for cardiac amyloidosis should have screening for serum and urine monoclonal light chains with serum and urine immunofixation electrophoresis and serum free light chains (Class 1, LOE B-NR). Immunofixation electrophoresis (IFE) is preferred because serum or urine plasma electrophoresis (SPEP or UPEP) are less sensitive. Together, measurement of serum IFE, urine IFE, and serum FLC is >99% sensitive for AL amyloidosis. Negative studies as in our patient essentially exclude AL amyloidosis from consideration.
In patients with high clinical suspicion for cardiac amyloidosis, without evidence of serum or urine monoclonal light chains, bone scintigraphy should be performed to confirm the presence of transthyretin cardiac amyloidosis (Class 1, LOE B-NR). As in this patient’s case, the 99mTc-Pyrophosphate scan with a grade 2/3 cardiac uptake in the absence of a serum or urinary monoclonal protein has a very high specificity and positive predictive value for ATTR-CM. This allows for a noninvasive diagnosis of ATTR-CM, obviating the need for an endomyocardial biopsy and so option D is inaccurate.
In patients for whom a diagnosis of transthyretin cardiac amyloidosis is made, genetic testing with TTR gene sequencing is recommended to differentiate hereditary variant from wild-type transthyretin cardiac amyloidosis (Class 1, LOE B-NR). Differentiating ATTRv from ATTRwt is important because confirmation of ATTRv would trigger genetic counseling and potential cascade screening of family members and TTR silencer therapies, such as inotersen and patisiran (currently only approved for the treatment of polyneuropathy caused by ATTRv amyloidosis).
Routine guideline-directed medical treatment (GDMT) for neurohormonal blockade may be poorly tolerated in patients with ATTR-CM and EF ≤40%. Due to restrictive physiology, they may be predisposed to more hypotension with ARNi, ACEi, and ARB. Similarly, patients with ATTR-CM rely on their heart rate response to preserve the cardiac output, thus BB may worsen HF symptoms. In this case, our patient already has a borderline blood pressure without these medications. Both options A and B are false.
Main Takeaway
In patients for whom a diagnosis of transthyretin cardiac amyloidosis is made, TTR gene sequencing is recommended to differentiate pathologic variant (ATTRv) from wild-type transthyretin cardiac amyloidosis (ATTRwt). This has implications in terms of screening for family members and management options for ATTRv.
For patients with ATTR-CM and EF ≤40%, GDMT may be poorly tolerated.
Guideline Loc.
Section 7.8, Figure 13
Decipher the Guidelines: 2022 Heart Failure Guidelines Page
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The following question refers to Section 7.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.
The question is asked by Palisades Medical Center medicine resident & CardioNerds Academy Fellow Dr. Maryam Barkhordarian, answered first by Hopkins Bayview medicine resident & CardioNerds Academy Faculty Dr. Ty Sweeny, and then by expert faculty Dr. Gregg Fonarow.
Dr. Fonarow is the Professor of Medicine and Interim Chief of UCLA’s Division of Cardiology, Director of the Ahmanson-UCLA Cardiomyopathy Center, and Co-director of UCLA’s Preventative Cardiology Program.
The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
Mr. Gene D’aMeTi, a 53-year-old African American man with ischemic cardiomyopathy and heart failure with reduced ejection fraction (LVEF 30-35%), is recently admitted with acutely decompensated heart failure and acute kidney injury on chronic kidney disease stage III. His outpatient regiment includes sacubitril-valsartan 97-103mg BID, carvedilol 25mg BID, and hydralazine 50mg TID.
Sacubitril-valsartan was held because of worsening renal function. Despite symptomatic improvement with diuresis, his renal function continues to decline. He is otherwise well perfused & with preservation of other end organ function.
Throughout this hospitalization, he has steadily become more hypertensive with blood pressures persisting in the 170s/90s mmHg. What would be an appropriate adjustment to his medication regimen at this time?
A
Resume Losartan only
B
Start Amlodipine
C
Increase current Hydralazine dose
D
Start Isosorbide dinitrate therapy
E
Both C & D
Explanation
The correct answer is E – both increasing the current hydralazine dose (C) and starting isosorbide dinitrate therapy (D).
Although ACEI/ARB therapy (choice A) has shown a mortality and morbidity benefit in HFrEF, caution should be used in patients with renal insufficiency. In this patient with ongoing decline in renal function, RAAS-inhibiting therapies (ACEi, ARB, ARNI, MRA) should be avoided. In this case, as his RAAS-I has been stopped, it would be reasonable to increase current therapies to target doses (or nearest dose tolerated), as these demonstrated both safety and efficacy in trials (Class 1, LOE A). Considering that his high dose ARNI was stopped, it is unlikely that either hydralazine or isosorbide dinitrate alone, even at maximal doses, would be sufficient to control his blood pressure (Options C and D, respectively). Interestingly, in the original study by Massie et. Al (1977), the decision was made to combine these therapies as the result was thought to be superior to either medication alone. ISDN would provide preload reduction, while Hydralazine would decrease afterload. Consequently, we do not have data looking at the individual benefit of either medication in isolation.
In self-identified African Americans with NYHA class III or IV HFrEF already on optimal GDMT, the addition of hydralazine & isosorbide dinitrate is recommended to improve symptoms and reduce mortality and morbidity (Class 1, LOE A). In this case, as the patient has evidence of progressive renal disfunction, we are limited in using traditional RAAS-I, such as ACEI, ARB, or ARNI. In patients with current or previously symptomatic HFrEF who cannot be given first-line agents (like ARNi, ACEi, ARB) due to intolerance or renal insufficiency, combination therapy of hydralazine & isosorbide dinitrate might be considered to reduce morbidity and mortality (Class 2b, LOE C-LD).
Dihydropyridine calcium channel blockers such as Amlodipine (choice B) are not recommended for treatment of HFrEF (COR 3, LOE A), though may be considered for treating elevated blood pressure despite optimization of GDMT.
Main Takeaway
In self-identified African Americans, the addition of hydralazine & isosorbide dinitrate to GDMT has additional mortality & morbidity benefits.
Should a patient have drug intolerances or renal dysfunction that precludes the use of ACEi/ARB/ARNi, hydralazine & isosorbide dinitrate is a reasonable alternative.
Guideline Loc.
· Section 7.3.5-8
· Table 14, Table 15
Decipher the Guidelines: 2022 Heart Failure Guidelines Page
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In this episode, CardioNerds Dr. Daniel Ambinder, Dr. Giselle Suero Abreu, and Dr. Saahil Jumkhawala discuss thromboembolic disease in cardio-oncology with faculty expert Dr. Joshua Levenson, the Associate Program Director of the cardiology fellowship and an Assistant Professor of Medicine at the University of Pittsburg School of Medicine. Venous (VTE) and arterial thromboembolic (ATE) events are precipitants of morbidity and mortality in patients with cancer. Here, we discuss the pathophysiology of thromboembolism, risk factors and epidemiology for ATE and VTE, the role of risk prediction and patient stratification, and the approach to treatment for and prophylaxis of thromboembolic events with anticoagulation. Show notes were drafted by Dr. Saahil Jumkhawala and episode audio was edited by CardioNerds Intern Dr. Tina Reddy.
This episode is supported by a grant from Pfizer Inc.
This CardioNerds Cardio-Oncology 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. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here.
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What are the incidence and main manifestations of thromboembolic events (venous and arterial) in patients with active malignancy?
Approximately 10% of outpatients with active cancer have venous thromboembolic events, many of which are asymptomatic. Clinically relevant VTEs are predominantly deep venous thrombosis (DVTs) with pain and/or swelling of the involved extremities or pulmonary emboli (PEs) resulting in chest pain and/or shortness of breath. VTE is the number one preventable cause of death for all hospitalized patients, and the ability to prevent and treat these events is crucial, particularly in high-risk populations such as patients with cancer.
Are there any high-risk associations with specific cancer subtypes?
Patients with metastatic disease and those receiving chemotherapy are more likely to develop arterial or venous thromboembolic events. Patients with acute myelogenous leukemia (AML) and thrombocytopenic patients are at the lowest risk for thromboembolic events. Multiple myeloma patients on medication such as proteasome inhibitors or lenalidomide appear at particular risk. Patients with localized, early-stage cancers such as breast, prostate, and melanoma are also at lower risk.
What are the main risk factors to identify patients at a higher risk of developing thrombotic complications?
Patients with a sedentary lifestyle, deconditioning, and undergoing active treatment with chemotherapy are at the highest risk of developing DVT or PE.
How should we approach choosing the optimal type and duration of anticoagulation for acute pulmonary embolism (PE) in the setting of malignancy?
This remains an area of active research. Historically, patients would receive systemic anticoagulation with heparin followed by warfarin. Low molecular weight heparin (LMWH) has been found to be superior to warfarin in this patient population. In the recent trials comparing LMWH to direct oral anticoagulants (DOACs), particularly apixaban, edoxaban, and rivaroxaban, a similar incidence of VTEs and relatively equivalent bleeding events have been found. This has transitioned the field towards the higher use of DOACs, except for gastric cancers, in which DOACs have been found to have higher bleeding risk. Dabigatran has been found to be associated with a higher incidence of bleeding and gastrointestinal side effects compared to other DOACs. Important considerations for the use of DOACs are the patient’s renal function and the ability to take oral medications or issues with gastrointestinal absorption.
For acute PE, three months of treatment is the minimum for the standard of care. For patients with ongoing treatment with systemic chemotherapy or radiation, treatment for at least six months may be considered, or even indefinitely, if risk factors for recurrence persist. Shared decision-making with patients regarding the relevant risks and benefits of ongoing anticoagulation remains critical.
What are some risk assessment models to help identify patients at high risk for developing recurrent thrombotic events?
The Khorana score, which includes prechemotherapy platelet count ≥350 x109/L, elevated WBC >11 x109/L, low hemoglobin <10g/dL, or BMI ≥35 kg/m2 may help risk-stratify higher-risk patients. Certain types of cancers place patients at different risks; for example, gastric and pancreatic cancers confers higher risk, while patients with lung cancers, lymphoma, or genitourinary cancers confer a mildly elevated risk.
Patients with no risk factors have less than <1% risk of PE or DVT in the following 2.5 months, those with 1 or 2 points have about 2% risk of PE or DVT in the following 2.5 months, and those with >3 points have about 7% risk of PE or DVT in the following 2.5 months.
How does one manage recurrent thrombotic events, particularly while patients are already on an oral anticoagulant?
One major consideration in patients with recurrent thrombotic events is ensuring adherence, as there may be concerns with patient education, access, or cost which need to be addressed. Once compliance is confirmed, a patient can be switched from one DOAC to another DOAC or from one DOAC to LWMH, with the twice-daily dose having the strongest evidence for efficacy.
Rarely, concurrent treatment with antiplatelet therapy and LWMH may be considered in patients at very high risk for recurrent thrombotic events, particularly in patients with widely disseminated cancers with vascular complications. Notably, workup for underlying hypercoagulability should be considered in patients with localized malignancies with recurrent thromboembolic events.
What are considerations for scenarios with high bleeding risk when there is a strong indication for anticoagulation?
For patients with chemotherapy-induced thrombocytopenia, thromboelastography (“TEG” scan) may be valuable in guiding whether patients are hyper- or hypo-coagulable. Patients with platelet count <20K should generally not be on anticoagulation. For patients anticipated to have thrombocytopenia sustained through treatment, discussion with the treating oncology team may guide towards withholding ongoing anticoagulation. Mobility and sequential compression devices (SCDs) should be advised for patients to avoid the development of DVTs while patients are in the hospital. As platelet counts rise, consideration of subtherapeutic doses of heparin may be considered.
Any lesion with metastasis to the brain is at risk for bleeding. Discussion with oncology, neuro-oncology, and neurosurgery is crucial in identifying the risk of hemorrhage of these lesions. Primary brain tumors, such as glioblastoma, are associated with an elevated risk of DVT, likely attributable in part to reduced mobility and VEGF-targeted treatment.
Management of malignant pericardial effusions varies by etiology. Patients with local malignant pericardial effusion may be managed with pericardiocentesis with catheter drainage versus pericardial window, depending on clinician availability and expertise.
What is the role of inferior vena cava (IVC) filters in the management of patients at high risk for developing thromboembolic events?
For patients with active DVT and PE burden with active or very high risk for bleeding, it may be considered to place a retrievable IVC filter with the goal of removal within 4-6 weeks, and anticoagulation restarted as soon as possible. Of note, IVC filters that remain in place for longer periods of time place the risk of the development of thrombi and distal embolization.
How does the management of arterial thrombotic events for patients with active malignancy differ from the treatment of venous thromboembolic disease?
Arterial thrombotic events may be sequelae of atherosclerotic cardiovascular disease, dysfunction of the coagulation cascade, or both. Patients with atherosclerotic cardiovascular disease are at higher risk for developing cardiovascular events when treated for cancer. Certain patients, such as men with prostate cancer, appear to be at higher risk related to hormonal derangements during treatment. Proactive management of atherosclerotic risk factors in these patients is imperative with modalities such as coronary computed tomography (CT) scans to identify the burden of atherosclerotic coronary disease with coronary calcium scoring. These patients may benefit from more aggressive treatment with statin therapy and antiplatelet therapy. Patients with preexisting coronary disease being treated with endocrine therapies or VEGF tyrosine kinase inhibitors (TKIs) may be at higher risk for atherosclerotic cardiovascular events during treatment and, therefore indicated for more aggressive lifestyle and risk factor modification.
International Cardio-Oncology Society ( IC-OS). IC-OS exits to advance cardiovascular care of cancer patients and survivors by promoting collaboration among researchers, educators and clinicians around the world. Learn more at https://ic-os.org/.
Join CardioNerds Co-Founder Dr. Dan Ambinder, Dr. Nino Isakadze (EP Fellow at Johns Hopkins Hospital), Dr. Karan Desai (Cardiology Faculty at Johns Hopkins Hospital and Johns Hopkins Bayview) join Digital Health Expert, Dr. La Princess Brewer (Associate Professor of Medicine Mayo Clinic Rochester) for another installment of the Digital Health Series. In this specific episode, we discuss how digital health can both reduce and amplify health disparities. This series is supported by an ACC Chapter Grant in collaboration with Corrie Health. Notes were drafted by Dr. Karan Desai. Audio editing was performed by student Dr. Shivani Reddy.
In this series, supported by an ACC Chapter Grant and in collaboration with Corrie Health, we hope to provide all CardioNerds out there a primer on the role of digital heath in cardiovascular medicine. Use of versatile hardware and software devices is skyrocketing in everyday life. This provides unique platforms to support healthcare management outside the walls of the hospital for patients with or at risk for cardiovascular disease. In addition, evolution of artificial intelligence, machine learning, and telemedicine is augmenting clinical decision making at a new level fueling a revolution in cardiovascular disease care delivery. Digital health has the potential to bridge the gap in healthcare access, lower costs of healthcare and promote equitable delivery of evidence-based care to patients.
This CardioNerds Digital Health series is made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Nino Isakadze and Dr. Karan Desai.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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CardioNerds co-founder Dr. Dan Ambinder joins CardioNerds join Dr. Pooja Prasad, Dr. Khoa Nguyen and expert Dr. Abigail Khan (Assistant Professor of Medicine, Division of Cardiovascular Medicine, School of Medicine) from Oregon Health & Science University and discuss a case of mechanical valve thrombosis. Audio editing by CardioNerds Academy Intern, student doctor Adriana Mares.
A 23-year-old pregnant woman with a mechanical aortic valve presented to the maternal cardiac clinic for a follow-up visit. On physical exam, a loud grade three crescendo-decrescendo murmur was audible and transthoracic echocardiography revealed severely elevated gradients across the aortic valve. Fluoroscopy confirmed an immobile leaflet disk. Thrombolysis was successfully performed using a low dose ultra-slow infusion of thrombolytic therapy, leading to normal valve function eight days later.
Treatment options for mechanical aortic valve thrombosis include slow-infusion, low-dose thrombolytic therapy or emergency surgery. In addition to discussing diagnosis and management of mechanical valve thrombosis, we highlight the importance of preventing valve thrombosis during the hypercoagulable state of pregnancy with careful pre-conception counseling and a detailed anticoagulation plan.
See this case published in European Heart Journal – Case Reports.
“To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all.” – Sir William Osler. CardioNerds thank the patients and their loved ones whose stories teach us the Art of Medicine and support our Mission to Democratize Cardiovascular Medicine.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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How can we counsel and inform women with heart disease who are contemplating pregnancy?
Adapted from the 2018 ESC Guidelines for the management of cardiovascular diseases during pregnancy
What is the differential diagnosis for a new murmur in a pregnant person who has undergone heart valve replacement?
What are diagnostic modalities for the evaluation of suspected prosthetic valve thrombosis?
What are the treatment options for prosthetic valve thrombosis in pregnant patients?
What are the anticoagulation and antiplatelet strategies for pregnant patients with mechanical heart valves?
The following question refers to Section 4.5 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Maryam Barkhordarian, answered first by pharmacy resident Dr. Anushka Tandon, and then by expert faculty Dr. Noreen Nazir.
Dr. Nazir is Assistant Professor of Clinical Medicine at the University of Illinois at Chicago, where she is the director of cardiac MRI and the preventive cardiology program.
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.
Mr. V is a 37-year-old man who presents to clinic after a recent admission for anterior STEMI and is status-post emergent percutaneous intervention to the proximal LAD. He has mixed hyperlipidemia and a 10 pack-year history of (current) tobacco smoking. Which of the following points related to tobacco use is LEAST appropriate for today’s visit?
A
Providing assessment and encouragement for smoking cessation, even if for only a 30-second “very brief advice” intervention.
B
Reviewing and offering pharmacotherapy support options for smoking cessation if Mr. V expresses readiness to quit today.
C
Recommending a switch from traditional cigarettes to e-cigarettes as a first step towards cessation, as e-cigarettes are safer for use.
D
Discussing that smoking cessation is strongly recommended for all patients, regardless of potential weight gain.
Explanation
Answer C is LEAST appropriate and therefore is the correct answer.
Answer C is not appropriate. Although e-cigarettes may be more effective than nicotine replacement therapy (NRT) for smoking cessation, the long-term effects of e-cigarettes on cardiovascular and pulmonary health are unknown. According to the 2019 ACC/AHA prevention guidelines, e-cigarettes may increase the risk of CV and pulmonary diseases; their use has been reportedly associated with arrhythmias and hypertension. Therefore, neither the ESC nor ACC/AHA suggest clinicians recommend e-cigarettes over traditional cigarettes to patients.
Answer A: Smoking cessation is one of the most effective CVD risk-lowering preventive measures, with significant reductions in (repeat) myocardial infarctions or death. ESC guidelines emphasize the importance of encouraging smoking cessation even in settings where time is limited. “Very brief advice” on smoking is a proven 30-second clinical intervention, developed in the UK, which identifies smokers, advises them on the best method of quitting, and supports subsequent quit attempts. While ESC does not explicitly suggest a frequency of assessment, the 2019 ACC/AHA guidelines specifically recommend that “all adults should be assessed at every healthcare visit for tobacco use and their tobacco use status recorded as a vital sign to facilitate tobacco cessation.”
Answer B: The ESC suggests (class 2) that offering follow-up support, nicotine replacement therapy, varenicline, and bupropion individually or in combination should be considered in smokers. A meta-analysis of RCTs in patients with ASCVD reflects that varenicline (RR 2.6), bupropion (RR 1.4), telephone therapy (RR 1.5), and individual counselling (RR 1.6) all increased quit rates versus placebo; NRT therapies were well-tolerated but had inconclusive effects on quit rates (RR 1.22 with 95% CI 0.72-2.06). The 2019 ACC/AHA recommendation to combine behavioral and pharmacotherapy interventions to maximize quit rates is a class 1 recommendation.
Answer D: The ESC gives a class 1 recommendation to recommending smoking cessation regardless of weight grain. Smokers who quit may expect an average weight gain of 5 kg, but the health benefits of tobacco cessation (both CVD and non-CVD related) consistently outweigh risks from weight gain. Weight gain does not lessen the ASCVD benefits of cessation. The 2019 ACC/AHA guidelines do not specifically comment on weight considerations with smoking cessation.
Main Takeaway
Stopping smoking is potentially the most effective of all preventive measures. All smoking of tobacco should be stopped, as tobacco use is strongly and independently causal of ASCVD (Class 1). Smoking cessation should be regularly assessed for and encouraged, and pharmacotherapy and follow-up support for cessation should be considered for patients who are ready for a quit attempt.
Guideline Loc.
Section 4.5, Table 9
CardioNerds Decipher the Guidelines – 2021 ESC Prevention Series
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The following question refers to Section 7.2 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.
The question is asked by Cleveland Clinic internal medicine resident and CardioNerds Intern Akiva Rosenzveig, answered first by UPMC Harrisburg cardiology fellow and CardioNerds Academy House Faculty Leader Dr. Ahmed Ghoneem, and then by expert faculty Dr. Randall Starling.
Dr. Starling is Professor of Medicine and an advanced heart failure and transplant cardiologist at the Cleveland Clinic where he was formerly the Section Head of Heart Failure, Vice Chairman of Cardiovascular Medicine, and member of the Cleveland Clinic Board of Governors. Dr. Starling is also Past President of the Heart Failure Society of America in 2018-2019. Dr. Staring was among the earliest CardioNerds faculty guests and has since been a valuable source of mentorship and inspiration. Dr. Starling’s sponsorship and support was instrumental in the origins of the CardioNerds Clinical Trials Program.
The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
Which of the following sentences regarding diuretics in the management of heart failure is correct?
A
In HF patients with minimal congestive symptoms, medical management with diuretics alone is sufficient to improve outcomes.
B
Prescribing a loop diuretic on discharge after a HF hospitalization may improve short term mortality and HF rehospitalization rates.
C
The combination of thiazide (or thiazide-like) diuretics with loop diuretics is preferred to higher doses of loop diuretics in patients with HF and congestive symptoms.
D
The maximum daily dose of furosemide is 300 mg.
Explanation
Choice B in correct. The guidelines give a Class 1 recommendation for diuretics in HF patients who have fluid retention to relieve congestion, improve symptoms, and prevent worsening heart failure. Recent data from the non-randomized OPTIMIZE-HF (Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure) registry revealed reduced 30-day all-cause mortality and hospitalizations for HF with diuretic use compared with no diuretic use after hospital discharge for HF.
Choice A is incorrect. With the exception of mineralocorticoid receptor antagonists (MRAs), the effects of diuretics on morbidity and mortality are uncertain. As such, diuretics should not be used in isolation, but always combined with other GDMT for HF that reduce hospitalizations and prolong survival.
Choice C is incorrect. The use of a thiazide or thiazide-like diuretic (e.g., metolazone) in combination with a loop diuretic inhibits compensatory distal tubular sodium reabsorption, leading to enhanced natriuresis. In a propensity-score matched analysis in patients with hospitalized HF, the addition of metolazone to loop diuretics was found to increase the risk for hypokalemia, hyponatremia, worsening renal function, and mortality, whereas use of higher doses of loop diuretics was not found to adversely affect survival. The guidelines recommend that the addition of a thiazide (e.g., metolazone) to treatment with a loop diuretic should be reserved for patients who do not respond to moderate- or high-dose loop diuretics to minimize electrolyte abnormalities (Class I, LOE B-NR).
Choice D is incorrect. The guidelines recommend a maximum total daily dose of 600mg of furosemide or 10mg of bumetanide or 200mg of torsemide.
Main Takeaway
In summary, diuretics are recommended in heart failure patients who have fluid retention to relieve congestion, improve symptoms, and prevent worsening heart failure. Maintenance diuretics on HF hospitalization discharge may help prevent recurrent HF hospitalizations. They should be used in combination with other GDMT to improve HF outcomes. Combining loop and thiazide diuretics may cause serious electrolyte abnormalities and should be reserved for patients who do not respond to moderate- or high-dose loop diuretics.
Guideline Loc.
Section 7.2, Table 12
Decipher the Guidelines: 2022 Heart Failure Guidelines Page
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Eisenmenger syndrome is an end-stage complication of congenital heart disease that occurs when a left to right shunt causes pulmonary over-circulation, leading to vascular remodeling, increased vascular resistance, and ultimately even shunt reversal. Aside from cardiac complications, this pathology has unique complications secondary to chronic cyanosis. In this episode of CardioNerds co-founder Dr. Amit Goyal, ACHD series co-chair Dr. Josh Saef, and Dr. Khaled Tuwairqi (ACHD cardiologist at King Faisal / Elite Hospitals) join Dr. Alexander (Sasha) Optowsky (Director of the Adult Congenital Heart Disease Program at Cincinnati Childrens) to discuss diagnosis and management of Eisenmenger syndrome. Show notes were drafted by Dr. Anna Scandinaro and episode audio was edited by CardioNerds Academy Intern Dr. Akiva Rosenzveig.
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.
The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark.
The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more
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1. How does Eisenmenger syndrome develop? Does everyone with a left-to-right shunt develop it? Can it develop as an iatrogenic complication?
The pulmonary vasculature is not used to seeing the increased flow it receives in the context of a left to right shunt. Over time this leads to an increase in pulmonary vascular resistance and pulmonary hypertension. When pulmonary pressures exceed systemic pressures, this causes shunt reversal with right to left shunting causing deoxygenated blood to cross from right side of the heart to the left side bypassing the lungs and causing cyanosis.
The process of developing Eisenmenger syndrome is chronically progressive and so adaptive changes have time to occur. Not all persons with unrepaired shunts will develop Eisenmenger syndrome and it is not completely understood why these differences exist.
Eisenmenger syndrome can be acquired by the creation of palliative aorto-pulmonary shunts which cause pulmonary over-circulation with elevated PVR. This is less commonly seen now, due to earlier corrective repairs occurring at younger ages instead of palliative repairs with plans to perform corrective repairs at older ages. This could be seen in a patient who had a palliative repair in 1960-1980s and was lost to follow up. Eisenmenger syndrome is uncommon in Blalock-Taussig-Thomas (BTT) shunts (especially classic BTT) due to their small size and relatively limited flow.
2. What must-not miss conditions may mimic Eisenmenger syndrome?
Large vessel obstruction, specifically bilateral pulmonary artery stenosis and double chamber right ventricle (gradient through the RVOT leading to R->L shunt causing cyanosis), may mimic Eisenmenger syndrome. Their management and natural history differ from Eisenmenger syndrome and can be reversed with treatment.
3. How should one initiate a workup for Eisenmenger syndrome?
History – ask about symptoms of dyspnea, decreased exercise tolerance, and cyanosis. It is important to establish a detailed surgical history.
Physical exam – specifically assess for the presence (or absence) of a murmur, loud P2 suggestive of pulmonary hypertension, and differential cyanosis (suggestive of PDA – hint see Episode 263 for more information on PDAs and Eisenmenger syndrome). Additional Pearl: take blood pressure on opposite side of a BTT shunt, as a BTT can affect the BP!
EKG – look for evidence of right ventricular hypertrophy: RAD, RVH.
CXR – may show prominent pulmonary trunk.
Laboratory evaluation – should include CBC, iron panel, uric acid, CMP, and BNP to evaluate for signs of secondary erythrocytosis.
Echocardiogram – define the anatomy, calculate right ventricular systolic pressure, pulmonary artery diastolic pressure from pulmonary regurgitation jet, and flow across RVOT and LVOT for estimate of Qp/Qs.
Cardiac cath – measure pressures and saturations, calculate Qp/Qs, assess response to vasodilator challenge, calculate CO by Fick (not thermodilution assumptions for thermodilution are not met with shunts), and rule out mimics.
Remember: You must have had a right heart cardiac catheterization to diagnose someone with Eisenmenger syndrome. When reviewing external data, it is always important to interpret the primary data yourself to ensure the right diagnosis and management.
4. What are some multi-organ complications that can be seen in Eisenmenger syndrome secondary to cyanosis and secondary erythrocytosis (kidney’s response to cyanosis)?
5. What is a life-threatening emergency that should be considered if a patient with Eisenmenger syndrome presents with neurologic symptoms? How about hemoptysis?
In a patient with Eisenmenger syndrome presenting with neurologic symptoms there should be a high index of suspicion for cerebral abscess. Chronic hypoxemia leads to secondary erythrocytosis leading to hyperviscosity in the central venous blood, this causes a favorable environment for bacterial growth.
Hemoptysis is not uncommon in this population and is a life threatening complication of Eisenmenger syndrome which requires a broad but direct differential to treat emergent cases quickly. The differential diagnosis includes pulmonary infections (Eisenmenger syndrome can cause decreased immune function), pulmonary vasoocclusive disease, aorto-pulmonary collaterals, as well as pulmonary artery in-situ thrombosis. Obtaining a Chest CTA is a high yield clinical tool to help establish this diagnosis. Interventional colleagues will be instrumental in treatment of many of these complications. Hemoptysis and iatrogenic surgical death used to be a high cause of mortality; this has decreased in recent years.
6. What steps can be taken to minimize operative risk in patients with Eisenmenger syndrome? Do we use routine phlebotomy in this population?
Surgery should be performed with an experienced cardiac anesthesiologist. Operative risk in Eisenmenger syndrome is lower than in pulmonary arterial hypertension as patients with Eisenmenger syndrome are able to increase their cardiac output by increasing right to left shunting at the expense of their oxygenation. Bubble filters should be used as available to minimize risk of air and paradoxical embolism. For non-urgent operations, exchange transfusions before surgery can improve clotting function. Coagulations labs are affected by high hematocrit (less plasma = fewer clotting factors); you will need to adjust citrate in the tube for an accurate PT/PTT.
Routine phlebotomy is no longer used in this population in the absence of moderate to severe hyperviscosity symptoms. Instead, the focus has shifted to iron deficiency. Repleting iron can improves symptoms of hyperviscosity, increases exercise capacity, and reduces stroke risk.
7. What is “Treat to Close” and should it be used in Eisenmenger syndrome?
The new area of “Treat to Close” is an evolving area without much data to support its practice. There is a need for randomized clinical trials and further investigation to clarify its use. Indications for shunt closure can be found in the 2018 AHA/ACC and the 2020 ESC Guidelines for the Management of Adults with Congenital Heart Disease. It is contraindicated to close a shunt when Eisenmenger syndrome has developed.
8. Is it safe for someone with Eisenmenger syndrome to become pregnant?
Among the few cardiac conditions where pregnancy is contraindicated are pulmonary arterial hypertension and Eisenmenger syndrome. In a pregnant woman with a resting oxygen saturation of less than 90%, babies are born small for gestational age, and most are born premature. In a pregnant woman with a resting oxygen saturation of less than 85%, less than 10% of babies are born alive. The maternal death rate is approximately 30% in these patients. Of note, some PAH medications are contraindicated in pregnancy.
9. Do patients with Eisenmenger syndrome receive heart transplants?
Transplantation in Eisenmenger syndrome requires both heart and lung transplant. The number of heart-lung transplant for congenital heart disease is a small proportion and even less so for Eisenmenger syndrome. Transplantation is complicated in patients with Eisenmenger syndrome due to the multi-organ system dysfunction that is often present.
Opotowsky, Alexander R., et al. “Pheochromocytoma and paraganglioma in cyanotic congenital heart disease.” The Journal of Clinical Endocrinology & Metabolism 100.4 (2015): 1325-1334.
Silversides, Candice K., et al. “Pulmonary thrombosis in adults with Eisenmenger syndrome.” Journal of the American College of Cardiology 42.11 (2003): 1982-1987.
Baumgartner, Helmut, et al. “2020 ESC Guidelines for the management of adult congenital heart disease: the Task Force for the management of adult congenital heart disease of the European Society of Cardiology (ESC). Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC), International Society for Adult Congenital Heart Disease (ISACHD).” European heart journal 42.6 (2021): 563-645.
Stout, Karen K., et al. “2018 AHA/ACC guideline for the management of adults with congenital heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines.” Journal of the American College of Cardiology 73.12 (2019): e81-e192.
Regitz-Zagrosek, Vera, et al. “2018 ESC guidelines for the management of cardiovascular diseases during pregnancy: the task force for the management of cardiovascular diseases during pregnancy of the European Society of Cardiology (ESC).” European heart journal 39.34 (2018): 3165-3241.
Adult Congenital Heart Association
Founded in 1998, the Adult Congenital Heart Association is an organization begun by and dedicated to supporting individuals and families living with congenital heart disease and advancing the care and treatment available to our community. Our mission is to empower the congenital heart disease community by advancing access to resources and specialized care that improve patient-centered outcomes. Visit their website (https://www.achaheart.org/) for information on their patient advocacy efforts, educational material, and membership for patients and providers
CHiP Network
The CHiP network is a non-profit organization aiming to connect congenital heart professionals around the world. Visit their website (thechipnetwork.org) and become a member to access free high-quality educational material, upcoming news and events, and the fantastic monthly Journal Watch, keeping you up to date with congenital scientific releases. Visit their website (https://thechipnetwork.org/) for more information.
Heart University
Heart University aims to be “the go-to online resource” for e-learning in CHD and paediatric-acquired heart disease. It is a carefully curated open access library of educational material for all providers of care to children and adults with CHD or children with acquired heart disease, whether a trainee or a practicing provider. The site provides free content to a global audience in two broad domains: 1. A comprehensive curriculum of training modules and associated testing for trainees. 2. A curated library of conference and grand rounds recordings for continuing medical education. Learn more at www.heartuniversity.org/
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