Episodes Archives - Cardionerds

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Episodes Archives - Cardionerds episodes

February 08, 2024357. CardioOncology: Cardiac Tumors with Dr. Juan Lopez-Mattei
CardioNerds co-founder Dr. Dan Ambinder, series chair Dr. Teodora Donisan, and Dr. Sukriti Banthiya discuss cardiac tumors with Dr. Juan Lopez-Mattei, a nationally recognized expert in the fields of cardio-oncology and the director of cardiac imaging at the Lee Health Heart Institute. Here, we explore the topic of cardiac tumors, with a focus on distinguishing between primary and secondary tumors. We delve into the symptoms, diagnostic methods, and treatment options. Show notes were drafted by Dr. Sukriti Banthiya and episode audio was edited by CardioNerds Intern and student Dr. Diane Masket.
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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Pearls and Quotes – Cardiac Tumors
Keep it simple when approaching an intracardiac mass; start with transthoracic echocardiography (TTE) and use transesophageal echocardiography (TEE) or cardiac magnetic resonance (CMR) based on the clinical context. Use TEE when suspecting valvular vegetations or thrombi & CMR for intracavitary cardiac masses.
Cardiac tumors can manifest with a variety of symptoms; however, they are more commonly diagnosed as an incidental finding!
When faced with the dilemma of selecting the most suitable imaging modality for evaluating a cardiac mass, consider the following hierarchy: begin with TTE as the first choice, followed by CMR. If the patient cannot undergo CMR, the next step is cardiac computed tomography (CT) or Fluorodeoxyglucose F18 positron emission tomography (FDG-PET).
TEE is especially useful for the evaluation of small, highly mobile cardiac masses!
Imaging cannot substitute a tissue diagnosis of cardiac masses. However, in cases of advanced malignancy, it may not always be necessary.
Show notes – Cardiac Tumors
Segment One: A big “picture” Approach to Cardiac Tumors
Let’s start with an overview of cardiac masses
Neoplastic vs non-neoplastic
Neoplastic lesions can be further classified into Primary Cardiac Tumors (PCT’s) & Secondary Cardiac Tumor (SCT’s)
A majority of PCTs are benign (up to 90%!); however, rarely, they may be malignant.
SCTs are more common than PCTs, and, by definition, they are malignant tumors.
Now, let’s look at the tools you can use to aid with the diagnosis of cardiac masses…
Step 1: Investigate the cardiac mass initially with TTE.
Step 2: Collect clues through history-taking & examination.
If suspecting valvular vegetations (as in infective endocarditis!) or left atrial appendage thrombus, characterize the mass further with TEE.
Consider the possibility of metastatic cardiac tumors in patients with a known malignancy, as they are more common than primary cardiac tumors.
In cases where it is uncertain if the mass is a cardiac tumor or thrombus, use CMR to differentiate the two entities.
Some findings on TTE that support the presence of a thrombus include left ventricular dysfunction with segmental wall motion abnormalities and/or apical aneurysm as these result in local pockets of stasis (think: Virchow’s triad)
Step 3: Put it all together!
Think about whether a tissue biopsy will be needed. If yes, determine whether a negative margin or open biopsy will be required.
Segment Two: Symptoms, Symptoms, Symptoms!
Cardiac tumors may be symptomatic and present in the 3 key ways as outlined below (Think COD 🐟). However, they are more commonly identified as incidental findings!
Constitutional symptoms (fever, arthralgias, weight loss, malaise/fatigue)
Obstruction – Interfering with blood outflow, arrhythmias, interference with valves causing regurgitation, pericardial effusion +/- tamponade (presyncope, syncope, dyspnea, chest discomfort)
Distal embolization (pulmonary or systemic thromboembolic phenomenon)
When a metastatic tumor is present, distinguishing symptoms originating from the heart becomes challenging due to potential overlap with symptoms caused by the primary malignancy. This stands in contrast to cases of primary cardiac tumors like myxomas, where symptom localization to the heart is more straightforward.
Segment Three: Multimodality Imaging
Imaging modalityBest used forAdvantagesDisadvantagesTTEInitial diagnostic modality Masses arising from valvesGood spatial resolution Understanding of hemodynamic significance of massLack of tissue characterization Poor acoustic window in select casesTEESmall highly mobile valvular lesions (<1cm) Visualization of structures with greater accuracy compared to TTE Use of enhancing agents can help differentiate vascular tumors from non-vascular & thrombusLack of tissue characterizationCMRDifferentiates tumor from thrombus. Identifies non-tumor masses or “pseudo-masses,” e.g. cysts, lipomasTissue characterization w/ T1, T2 weighted imaging and gadolinium enhancementLower temporal resolution Limited availability Interference from implanted electrical devicesCT & FDG-PETDifferentiates benign from malignant tumorsAlternative to CMR in pts. w/ claustrophobia & older generation cardiac devicesCT with limited soft tissue & temporal resolution compared to CMR Dietary preparation before FDG
Segment Four: The Issue With Tissue!
Tissue diagnosis is essential for the diagnosis of primary cardiac tumors; however, it may be less important for metastatic tumors to the heart in cases of known advanced-stage malignancies such as melanoma, breast, and lung.
An overview of a rare primary cardiac malignancy: Carney Complex!
A complex hereditary syndrome that affects multiple organs, including the heart, skin & endocrine organs.
Epidemiology:
Autosomal dominant
Young age groups in both sexes
Clinical presentation
Intra-cardiac/extra-cardiac myxomas; intra-cardiac myxomas are multiple, bilateral (atrial and ventricular) & multicentric.
Skin findings commonly include lentigines and blue nevi.
Endocrine abnormalities include Cushing syndrome, pituitary & adrenal adenomas, thyroid dysfunction.
Diagnosis
Clues on CMR
SSFP (dteady-state free precession) cine imaging, an association of punctiform areas of high & low signal intensity consistent with “Blackberry appearance”
Hypoperfused enhancement pattern at first-pass perfusion imaging
High signal T2-imaging, iso-intense on T1-weighted imaging
Treatment
Surgical resection
Annual surveillance for Carney complex as they frequently recur (compared with surveillance every 3-5 years for non-Carney myxomas)
Genetic testing for PRKAR1 mutations in 1st degree family members
Segment Five: “Secondary” to None
Secondary cardiac tumors (SCT’s)
Epidemiology:
Cardiac metastasis is 20-40 times more common than primary cardiac tumors.
Etiology:
Routes of spread: hematogenous, lymphatic, transvenous, direct invasion
Most common malignancies to metastasize to heart include melanomas, carcinomas of breast, lung and esophageal.
Clinical Presentation
Pericardial effusion, tamponade
Arrhythmias – “resistant” to antiarrhythmic drugs
Heart failure due to myocardial infiltration
Valvular dysfunction due to intracavitary masses that impede blood flow.
Diagnosis
Echocardiography is the initial test of choice.
MRI
Most malignancies exhibit low signal on T1-weighted imaging & high signal intensity on T2-weighted imaging.
Exception, metastaticmelanoma, which appears hyperintense on T1-weighted imaging due to paramagnetic T1 shortening effects of melanin.
FDG-PET/CT
In cardiac metastasis, the myocardium has high metabolic activity and can mimic FDG uptake seen in a tumor.
Ensure adequate dietary preparation to suppress glucose uptake of normal healthy myocardium.
Multi-disciplinary approach to management
Tissue diagnosis is necessary.
Referral to an interventional cardiologist for transvenous biopsy, or
Referral to a cardiac surgeon for minimally invasive surgery
Note – tissue diagnosis can come from another metastatic site.
Pathologist to confirm the malignant nature of the tumor.
Cardio-oncologist to facilitate multidisciplinary team discussion involving oncologist and cardiac surgeon on the best approach to treatment.
Neoadjuvant chemotherapy or radiotherapy vs. cardiac surgery
References – Cardiac Tumors
Tyebally, Sara, Daniel Chen, Sanjeev Bhattacharyya, Abdallah Mughrabi, Zeeshan Hussain, Charlotte Manisty, Mark Westwood, Arjun K. Ghosh, and Avirup Guha. “Cardiac Tumors: JACC CardioOncology State-of-the-Art Review.” JACC. CardioOncology 2, no. 2 (June 2020): 293–311. https://doi.org/10.1016/j.jaccao.2020.05.009.
Basson, Craig T., and H. Thomas Aretz. “Case 11-2002: A 27-Year-Old Woman with Two Intracardiac Masses and a History of Endocrinopathy.” Edited by Richard C. Cabot, Nancy Lee Harris, William F. McNeely, Jo-Anne O. Shepard, Sally H. Ebeling, Stacey M. Ellender, and Christine C. Peters. New England Journal of Medicine 346, no. 15 (April 11, 2002): 1152–58. https://doi.org/10.1056/NEJMcpc010057.
Colin, Geoffrey C., Bernhard L. Gerber, Mihaela Amzulescu, and Jan Bogaert. “Cardiac Myxoma: A Contemporary Multimodality Imaging Review.” The International Journal of Cardiovascular Imaging 34, no. 11 (November 2018): 1789–1808. https://doi.org/10.1007/s10554-018-1396-z.
Meet Our Collaborators
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/.
39 min
January 23, 2024 356. 2023 ACC/AHA/ACCP/HRS Atrial Fibrillation Guidelines – Key Takeaways with Dr. José Joglar and Dr. Mina Chung
CardioNerds Atrial Fibrillation Series Co-Chairs Dr. Colin Blumenthal (University of Pennsylvania Cardiology fellow) and Dr. Kelly Arps (Duke University Electrophysiology Fellow) join the 2023 atrial fibrillation guideline writing committee Chair Dr. José Joglar (UT Southwestern) and Vice Chair Dr. Mina Chung (Cleveland Clinic). They review the key takeaways from the 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation. Audio editing by CardioNerds academy intern, student doctor Pace Wetstein.
This podcast was developed in collaboration with the American Heart Association. For more on these guidelines, access the AHA Science News AF Guideline landing page.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
CardioNerds Atrial Fibrillation Page
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56 min
January 16, 2024355. Case Report: Hypertension With a Twist – Mount Sinai Medical Center
CardioNerds nerd out with Drs. Karishma Rahman (Mount Siani Vascular Medicine fellow), Shu Min Lao (Mount Sinai Rheumatology fellow), and Constantine Troupes (Mount Sinai Vascular Surgery fellow). They discuss the following case: A 20-year-old woman with a history of hypertension (HTN), initially thought to be secondary to a mid-aortic syndrome that resolved after aortic stenting, presents with a re-occurrence of HTN. The case will go through the differential diagnosis of early onset HTN focusing on structural etiologies of HTN, including mid-aortic syndrome and aortitis. We will also discuss the multi-modality imaging used for diagnosis and surveillance, indications and types of procedural intervention, and how to diagnose and treat an underlying inflammatory disorder leading to aortitis. The expert commentary was provided by Dr. Daniella Kadian-Dodov, Associate Professor of Medicine and Vascular Medicine specialist at the Icahn School of Medicine at Mount Sinai. Audo editing was performed by Dr. Chelsea Amo-Tweneboah, CardioNerds Academy Intern and medicine resident at Stony Brook University Hospital.
“To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all.” – Sir William Osler. CardioNerds thank the patients and their loved ones whose stories teach us the Art of Medicine and support our Mission to Democratize Cardiovascular Medicine.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here.
CardioNerds Case Reports Page
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll
CardioNerds Journal Club
Subscribe to The Heartbeat Newsletter!
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Case Media – Hypertension With a Twist
Pearls – Hypertension With a Twist
Early onset hypertension (HTN) and lower extremity claudication should raise suspicion for aortic stenosis (including mid-aortic syndrome). Initial evaluation should include arterial duplex ultrasound and cross-sectional imaging such as CT or MR angiogram of the chest, abdomen, and pelvis to assess for arterial stenosis involving the aorta and/or branching vessels.
Mid-aortic syndrome can have multiple underlying etiologies. Concentric aortic wall thickening should raise suspicion for an underlying inflammatory disorder. Initial evaluation should include inflammatory markers such as ESR, CRP, and IL-6, but normal values do not exclude underlying aortitis.
While Takayasu arteritis is the most common inflammatory disorder associated with mid-aortic syndrome, IgG4-RD should also be a part of the differential diagnosis. IgG subclass panel can detect IgG4-RD with elevated serum IgG4 levels, but some cases can require pathology for diagnosis.
Catheter based intervention is a safe and effective treatment of aortic stenosis for both primary aortic stenosis and post-procedural re-stenosis.
Multi-modality imaging, including cross-sectional imaging and duplex ultrasound, plays a central role for the diagnosis, management, and post-procedural surveillance of aortic disease.
A multi-disciplinary team (as exemplified by the participants of this podcast!) is essential for the management of complex aortopathy cases to optimize clinical outcomes.
Show Notes – Hypertension With a Twist
1. Early onset HTN can have multiple etiologies – aortic stenosis (including but not limited to secondary to congenital aortic coarctation and mid–aortic syndrome, as well as in stent re-stenosis if there is a history of aortic stenting), thrombosis, infection, inflammatory/autoimmune disorders, renovascular disease, polycystic kidney disease, and endocrine disorders.
2. Mid-aortic syndrome is characterized by segmental or diffuse narrowing of the abdominal and/or distal descending aorta with involvement of the branches of the proximal abdominal aorta (renal artery, celiac artery, superior mesenteric artery) and represents approximately 0.5 to 2% of all cases of aortic narrowing. Underlying etiologies include genetic syndromes, inflammatory, non-inflammatory, and idiopathic. It is important to have a high suspicion of underlying inflammatory disorders if cross-sectional imaging reveals concentric aortic wall thickening1,2.
3. The current treatment options for aortic stenosis (of the aorta here…not the aortic valve) include balloon angioplasty, aortic stenting, and surgical repair. While studies show the efficacy of balloon angioplasty and aortic stenting, data is limited as studies were mostly done in children3,4.
4. Aortitis5-16 can have multiple etiologies including infectious (such as TB, syphilis, HIV, bacterial, fungal), inflammatory disorders (such as large vessel vasculitis, IgG4-RD, Behcet syndrome, relapsing polychondritis, spondyloarthritis, SLE, and rheumatoid arthritis), and idiopathic. Sometimes, hereditary connective tissue disorders (such Marfan syndrome,, Ehlers-Danlos syndrome, and Loeys-Dietz syndrome) are included in the differential diagnosis, however, they would present as an aortic intramural hematoma (IMH) that typically would appears as eccentric wall thickening (rather than concentric wall thickening more consistent with aortitis).
5. While Takayasu arteritis is the most common inflammatory disorder associated with mid-aortic syndrome, IgG4-RD should also be a part of the differential diagnosis. IgG4-RD is characterized by lymphoplasmacytic infiltrates featuring IgG4 positive plasma cells. It presents in predominantly males between ages 40-70 years of age. The rate of vascular involvement is approximately 8% for aortitis and 20-36% periaortitis. It can be diagnosed with elevated serum IgG4 levels or from tissue biopsy where pathology would show dense lymphoplasmacytic infiltrates in a storiform fibrosis pattern with obliterative phlebitis and >40% plasma calls and >10 positive plasma cells/high power field. It is treated initially treated with high dose steroids with transition to steroid sparing agents such as Rituximab (RTX), azathioprine, mycophenolate, and methotrexate with RTX being the preferred agent10,14.
6. In cases of re-stenosis after initial balloon angioplasty and stenting, indications for re-intervention include hypertension in the setting of imaging evidence of re-stenosis (e.g. > 50% percent aortic narrowing relative to the aortic diameter at the diaphragm level) and
pressure gradient across the coarctation > 20 mmHg. The timing of re-intervention in cases of aortitis secondary to underlying inflammatory disorders will require a multi-disciplinary discussion to determine when underlying inflammatory disorder is sufficiently controlled for re-intervention.
References – Hypertension With a Twist
Bacha E, Hijazi ZM. Management of Coarctation of the Aorta. U: UpToDate, Fulton DR ed UpToDate [Internet] Waltham, MA: UpToDate. 2020.
Lazea C, Al-Khzouz C, Sufana C, et al. Diagnosis and management of genetic causes of middle aortic syndrome in children: a comprehensive literature review. Therapeutics and Clinical Risk Management. 2022:233-248.
Rodés-Cabau J, Miró J, Dancea A, et al. Comparison of surgical and transcatheter treatment for native coarctation of the aorta in patients≥ 1 year old. The Quebec Native Coarctation of the Aorta Study. American heart journal. 2007;154(1):186-192.
Meadows J, Minahan M, McElhinney DB, McEnaney K, Ringel R. Intermediate outcomes in the prospective, multicenter Coarctation of the Aorta Stent Trial (COAST). Circulation. 2015;131(19):1656-1664.
Nikiphorou E, Galloway J, Fragoulis GE. Overview of IgG4-related aortitis and periaortitis. A decade since their first description. Autoimmunity reviews. 2020;19(12):102694.
Kadian-Dodov D, Seo P, Robson PM, Fayad ZA, Olin JW. Inflammatory Diseases of the Aorta: JACC Focus Seminar, Part 2. Journal of the American College of Cardiology. 2022;80(8):832-844.
Sohrabi B, Jamshidi P, Yaghoubi A, et al. Comparison between covered and bare Cheatham-Platinum stents for endovascular treatment of patients with native post-ductal aortic coarctation: immediate and intermediate-term results. JACC: Cardiovascular Interventions. 2014;7(4):416-423.
Marvisi C, Buttini EA, Vaglio A. Aortitis and periaortitis: the puzzling spectrum of inflammatory aortic diseases. La Presse Médicale. 2020;49(1):104018.
Bossone E, Pluchinotta FR, Andreas M, et al. Aortitis. Vascular pharmacology. 2016;80:1-10.
Carruthers MN, Topazian MD, Khosroshahi A, et al. Rituximab for IgG4-related disease: a prospective, open-label trial. Annals of the rheumatic diseases. 2015;74(6):1171-1177.
Wallace ZS, Perugino C, Matza M, Deshpande V, Sharma A, Stone JH. Immunoglobulin G4–related disease. Clinics in chest medicine. 2019;40(3):583-597.
Wallace ZS, Naden RP, Chari S, et al. The 2019 American College of Rheumatology/European league against rheumatism classification criteria for IgG4‐related disease. Arthritis & Rheumatology. 2020;72(1):7-19.
Onen F, Akkoc N. Epidemiology of Takayasu arteritis. La Presse Médicale. 2017;46(7-8):e197-e203.
Ebbo M, Grados A, Samson M, et al. Long-term efficacy and safety of rituximab in IgG4-related disease: data from a French nationwide study of thirty-three patients. PLoS One. 2017;12(9):e0183844.
Maz M, Chung SA, Abril A, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of giant cell arteritis and Takayasu arteritis. Arthritis Care & Research. 2021;73(8):1071-1087.
Lupi-Herrera E, Sanchez-Torres G, Marcushamer J, Mispireta J, Horwitz S, Vela JE. Takayasu’s arteritis. Clinical study of 107 cases. American heart journal. 1977;93(1):94-103.
47 min
January 09, 2024354. Obesity: Obesity & Cardiovascular Disease Risk with Dr. Jaime Almandoz
CardioNerds Dr. Rick Ferraro (cardiology fellow at Johns Hopkins Hospital) and Dr. Eunice Dugan (cardiology fellow at the Cleveland Clinic) join episode lead Dr. Tiffany Brazile (cardiology fellow at the University of Texas Southwestern Medical Center and postdoctoral fellow at the Institute for Exercise and Environmental Medicine) to discuss the impact of obesity on cardiovascular disease risk, differential risk in specific populations, and effective strategies for counseling patients. They are joined by expert Dr. Jaime Almandoz, Medical Director of the Weight Wellness Program and an Associate Professor of Medicine at the University of Texas Southwestern Medical Center. Audio editing was performed by CardioNerds Academy Intern, student Dr. Tina Reddy.
This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Novo Nordisk. See below for continuing medical education credit.
Claim CME for this episode HERE.
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 Prevention Page
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Cardionerds Healy Honor Roll
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Pearls and Quotes – Obesity & Cardiovascular Disease Risk
The durability of metabolically healthy obesity (i.e., normal A1c, lipids, LFTs, BMP, normotensive) is limited. Within 5 years, a third of adults with “metabolically healthy” obesity will develop a cardiometabolic complication.
The biomechanical and psychosocial complications of obesity are just as important as the cardiometabolic complications. Biomechanical and psychosocial complications, including obstructive sleep apnea, joint pain, and mood disorders also influence cardiovascular disease risk.
Weight loss is not always the patient’s goal. Meet patients where they are and understand their challenges, concerns, and long-term goals with respect to their cardiovascular health and obesity. This information provides an opportunity to frame the conversation in a supportive and engaging way that allows for patient education.
Body mass index (BMI) is a screening tool for obesity, but is not sufficient for providing individualized care.
Obesity management methods that result in rapid weight loss may not be appropriate for all patients. These methods, such as bariatric surgery and GLP1-receptor agonists, require regular monitoring, follow-up, and multidisciplinary care (e.g., nutritionist, exercise physiologist, endocrinologist, cardiologist, psychologist, etc.).
Show notes – Obesity & Cardiovascular Disease Risk
Is it possible to be healthy at any size?
Whether an individual can be healthy at any size depends on the definition of health and its durability.
Approximately 10-15% of adults with obesity are metabolically healthy.
The risk for developing cardiometabolic disease is higher in obese versus non-obese adults. One in three adults with metabolically healthy obesity will develop cardiometabolic complications (i.e., insulin resistance/diabetes, hyperlipidemia, hypertension) within five years. Thus, metabolically healthy obesity may represent a transient phenotype with adverse long-term consequences.
Consider non-metabolic health consequences of obesity that also influence cardiovascular disease risk.
Obstructive sleep apnea, joint pain leading to decreased physical activity, and mood disorders are key considerations here and encompass the biomechanical and psychosocial consequences of obesity.
Does large, rapid weight loss result in poorer long-term weight loss than slower, gradual weight loss?
When approaches to weight loss are not sustainable, such as extremely low-calorie diets or extreme fitness regimens, the results and associated health benefits are less likely to be durable.
Rapid, large-magnitude weight loss is appropriate for some adults with obesity and can be achieved through bariatric surgery and/or anti-obesity medications. Safety and sustainability are supported by regular follow-up, monitoring, and multidisciplinary care to incorporate nutritional and physical activity recommendations.
Obesity management must be individualized to meet patient needs and goals while accounting for comorbid conditions (e.g., frailty, fall risk, disordered eating, etc.)
What are some best practices for incorporating the diagnosis of obesity into a patient’s assessment, including cardiovascular disease risk?
Seek to understand what the patient wants to achieve during the office visit.
Inquire about the patient’s health journey, goals, concerns, and challenges.
In addition to addressing the patient’s expressed goals, frame the conversation in terms of concerns you have about the patient’s health.
Incorporate objective measures, such as body composition, waist circumference, cardiorespiratory fitness, and biomarkers that can help support your concerns and management goals.
Does obesity impact men and women differently?
Prevalence: of adults with obesity, women are more likely than men to have severe obesity. Obesity is also more prevalent in women of certain racial/ethnic minorities as compared to men.
Fat distribution: men tend to have more visceral or central adiposity, which is associated with increased cardiometabolic risk. Earlier in adulthood, women tend to have more body fat in the gluteofemoral region. With advancing age and menopause, the distribution of excess adipose tissue in women often shifts to the visceral/central region and may enhance cardiometabolic risk.
What are the practical methods for evaluating and measuring obesity during a patient visit?
BMI is a screening tool for obesity. It is blind to body composition and fat distribution. Cut points for BMI and the association with cardiovascular disease risk vary by race/ethnicity. Consideration of different BMI cut points for patients of various racial/ethnic backgrounds is important when evaluating candidacy for bariatric surgery or anti-obesity medications.
Waist circumference is a useful measure to estimate visceral/central adiposity. Cut points for men and women have been established that are associated with increased cardiovascular disease risk across multiple studies.
Measures of body composition provide valuable information about fat and lean body masses. DEXA scans and MRIs also provide data on fat distribution; however, they are impractical and expensive for regular use in the clinical setting. Bioelectrical impedance can provide body composition data efficiently during a clinic visit.
What are alternative validated tools beyond the Pooled Cohort Equation that can be used to estimate ASCVD risk in various ethnic/racial groups?
The QRISK3 calculator is an alternative assessment tool for 10-year ASCVD risk that has been validated in 9 different ethnic groups. The calculator includes novel variables, such as chronic kidney disease, history of migraines, severe mental illness, erectile dysfunction, and family history of premature ASCVD. https://www.qrisk.org/
What are the mechanisms by which obesity impacts the development of cardiovascular disease?
Obesity and lipotoxicity can impact cardiovascular disease development through multiple mechanisms, including inflammation that can lead to a prothrombotic state, insulin resistance, and alterations in lipid metabolism that can promote atherosclerosis.
The distribution of body fat is highly heterogeneous and is partially driven by genetics. Brown adipose tissue has a high mitochondrial load and is involved in adaptive thermogenesis. White adipose tissue is considered more of a storage form of adipose tissue that also functions as an endocrine organ and provides insulation/protection for vital organs.
Ectopic fat depots, such as hepatic steatosis or epicardial adipose tissue, are metabolically active and can influence adjacent tissues through humoral and neurohormonal signals. These fat depots may also exert mechanical effects on the organs they surround. The ways in which individuals accrue fat in these different locations, the specific mechanisms by which they may increase cardiovascular disease development, and whether targeted therapies to reduce specific fat depots are incompletely understood.
References – Obesity & Cardiovascular Disease Risk
Wilding JPH, Batterham RL, Calanna S, et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity. N Engl J Med. 2021;384(11):989-1002. doi:10.1056/NEJMoa2032183 https://pubmed.ncbi.nlm.nih.gov/33567185/
Marso SP, Daniels GH, Brown-Frandsen K, et al. Liraglutide and Cardiovascular Outcomes in Type 2 Diabetes. N Engl J Med. 2016;375(4):311-322. doi:10.1056/NEJMoa1603827 https://pubmed.ncbi.nlm.nih.gov/27295427/
Marso SP, Bain SC, Consoli A, et al. Semaglutide and Cardiovascular Outcomes in Patients with Type 2 Diabetes. N Engl J Med. 2016;375(19):1834-1844. doi:10.1056/NEJMoa1607141 https://pubmed.ncbi.nlm.nih.gov/27633186/
Gerstein HC, Colhoun HM, Dagenais GR, et al. Dulaglutide and cardiovascular outcomes in type 2 diabetes (REWIND): a double-blind, randomised placebo-controlled trial. Lancet. 2019;394(10193):121-130. doi:10.1016/S0140-6736(19)31149-3 https://pubmed.ncbi.nlm.nih.gov/31189511/
31 min
December 29, 2023353. Atrial Fibrillation: Anticoagulation Pharmacology & Clinical Decision-Making with Dr. Ashley Lochman and Dr. Chris Domenico
CardioNerds co-founder Dr. Amit Goyal, series co-chair Dr. Colin Blumenthal, and episode lead Dr. Anushka Tandon to discuss pharmacologic anticoagulation options in atrial fibrillation with Drs. Ashley Lochman and Chris Domenico. The case-based review helps clarify some key concepts, such as when warfarin is preferred for anticoagulation, who may be a good DOAC (direct-acting oral anticoagulant) candidate, how to choose an appropriate DOAC agent, and how to manage anticoagulation therapy in patients already on antiplatelet therapies. Notes were drafted by Dr. Anushka Tandon. The episode audio was edited by student Dr. Shivani Reddy.
This CardioNerds Atrial Fibrillation series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Kelly Arps and Dr. Colin Blumenthal.
This episode was planned and recorded prior to the release of the 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation. Please refer to this guideline document for the most updated recommendations.
We have collaborated with VCU Health to provide CME. Claim free CME here!
This episode is made possible with support from Glass.Health – The first digital notebook designed for doctors. Follow @GlassHealthHQ for the latest product updates!
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
CardioNerds Atrial Fibrillation Page
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll
CardioNerds Journal Club
Subscribe to The Heartbeat Newsletter!
Check out CardioNerds SWAG!
Become a CardioNerds Patron!
Pearls and Quotes – Anticoagulation Pharmacology
Avoid potentially fatal errors with this terminology tip for correctly referencing non-warfarin oral anticoagulant agents: it’s DOAC (like, please DO use AntiCoagulation), not NOAC (imagine someone interpreting that as “NO AntiCoagulation for this patient” at discharge – yikes)!
Sometimes, an oldie really is a goodie – warfarin is recommended over DOACs for patients with mechanical heart valves, moderate-to-severe mitral stenosis, anti-phospholipid antibody syndrome (APLS), left ventricular (LV) thrombus, higher INR goals, or DOAC failure. Patient preference and medication costs should also be considered – at the end of the day, “the best drug is the drug that a patient is willing to take!”
Standard-dose rivaroxaban or apixaban may be considered for use in patients weighing >120kg or with BMI >40; use of other DOACs should be limited to pts weighing =/< 120kg or with BMI =/< 40.
The pharmacists involved in this podcast promise they don’t have stock in apixaban! It just often happens to be the preferred DOAC option in certain scenarios – think patients with severe renal impairment (including ESRD) or with an increased risk for bleeding events (including older adults, those with a history of GI bleed, etc).
In general, dual therapy (DOAC or warfarin + P2Y12 inhibitor) is non-inferior to triple therapy (oral anticoagulant + P2Y12 inhibitor + aspirin) at preventing thrombotic events but is associated with a lower risk of bleeding events. Most patients can be transitioned to dual therapy after 7-30 days on triple therapy post-percutaneous coronary intervention.
What’s that on the horizon? Factor XI inhibitors may become the breakout stars of anticoagulation – multiple investigational agents are being studied for their potential to reduce thrombotic risk without significantly increasing bleeding risk in patients with indications for anticoagulation therapy…at least that’s the theorize hope. Watch this space!
Notes – Anticoagulation Pharmacology
In which cases is warfarin preferred over DOACs in patients with atrial fibrillation?
Long-term anticoagulation with warfarin is indicated in patients with atrial fibrillation and either a mechanical valve or moderate-to-severe mitral stenosis (i.e., valvular atrial fibrillation as defined in the 2019 AHA/ACC/HRS guidelines on atrial fibrillation [1]). The REALIGN trial [2] showed increased rates of thromboembolic and bleeding complications with dabigatran vs. warfarin in patients with mechanical valves, and the PROACT Xa trial [3] found similarly higher rates of thromboembolic events with apixaban vs. warfarin in patients with On-X mechanical valves. However, DOACs are appropriate for use in patients with bioprosthetic valves.
Warfarin is preferred over DOACs in patients with APLS (antiphospholipid syndrome). In triple-positive patients, DOACs should absolutely be avoided (as supported by the TRAPS study [4], which was stopped early due to findings of increased thromboembolic events with rivaroxaban vs. warfarin). Warfarin should also be preferentially used in single- and double-positive patients as well (as suggested by findings from the ASTRO-APS study [5]).
There are some newer data to suggest apixaban may be non-inferior to warfarin in treating patients with LV thrombus; however, data overall is very mixed, and anticoagulating these patients with warfarin currently remains the preferred and more cautious approach.
Other situations in which warfarin may be preferred are when a higher INR goal or a customized anticoagulation approach is required, in instances of DOAC failure, or in cases where cost or patient preference are driving factors.
What patient-specific factors should be considered when deciding whether someone is a good candidate for DOAC therapy?
Weight/BMI: previous guidance suggested against the use of DOACs in pts weighing >120kg or with a BMI >40. However, ISTH updated their guidance in 2021 [6] to support using rivaroxaban and apixaban for VTE treatment or prevention “regardless of body weight and BMI”; these DOACs are often used in patients with obesity for non-VTE indications (e.g., thromboprophylaxis in atrial fibrillation). Data to support this include a post-hoc analysis of the ARISTOTLE trial (apixaban in atrial fibrillation), which showed that patients weighing >120kg (~5% of the study population) had similar results to the overall study population. It’s important to use adjusted body weight when calculating CrCl to estimate renal function and determine DOAC dosing in obese patients. Other DOACs should be avoided in pts >120kg/with BMI >40 due to limited or unconvincing data at this time.
Hepatic impairment: DOACs have varying hepatic metabolism (apixaban is the most hepatically cleared and dabigatran the least), but limited data exist for DOAC dose adjustments in patients with hepatic impairment. DOACs should NOT be used in Child-Pugh Class C/severe hepatic disease, while rivaroxaban (and betrixaban)[GU1] should also NOT be used in moderate/CP Class B patients. DOACs should be avoided in patients with decompensated/unstable cirrhosis. Aside from these caveats, DOACs may be considered for use in mild-moderate (Class A/B) hepatic impairment (with exceptions as above).
Renal impairment: DOACs may be used in stable CKD with appropriate renal dose adjustments; DOAC therapies should be held in the context of AKI. Dabigatran is the most renally cleared and generally avoided for this reason. Apixaban is the least renally cleared and is generally the preferred agent in patients with renal impairment, including ESRD (in the context of which apixaban use is supported by data, including that from a 2022 cohort study [7] vs. warfarin).
Drug Interactions: rivaroxaban, apixaban, edoxaban, and dabigatran are all P-gp substrates that will be affected by P-gp inducers or inhibitors (e.g., dronedarone, amiodarone, digoxin, diltiazem, verapamil, antiepileptics, antifungals, chemotherapy agents, and St. John’s Wort). Rivaroxaban and apixaban are substrates of CYP450 enzymes, prominently 3A4, 3A5, and 2J2. Apixaban is also metabolized by 1A2 and 2C 8/9/19 to a lesser degree. Some DOACs may interact with atorvastatin or ticagrelor, but these interactions are not typically a barrier to concurrent therapy if clinically indicated. Running a drug interaction report or consulting a pharmacist to help evaluate and safely navigate drug interactions is extremely helpful in these scenarios.
*In addition to DOAC package inserts, the AHA guide to DOAC use [8] is a great resource that summarizes renal/hepatic dosing considerations, drug interactions, and anticoagulant transition recommendations.
What safety profile and bleeding risk considerations exist for warfarin versus DOACs?
Warfarin has been studied versus individual DOACs; generally, DOACs are preferred from a safety standpoint due to lower risk of bleeding. The RE-LY trial [9] showed no difference in major bleeding but less intracranial hemorrhage (ICH) with dabigatran when compared to warfarin. The ROCKET-AF [10] trial showed a greater Hgb drop/need for transfusion with rivaroxaban but higher critical/fatal bleeding (including ICH) incidence with warfarin. In the ARISTOTLE [11] trial, apixaban was associated with significantly lower bleeding outcomes than warfarin, except for GI bleeding (for which there was no significant difference between groups). Edoxaban had a lower incidence of overall GI bleed (upper and lower GI bleeding combined), but not individual upper or lower GI bleeding, than warfarin in the ENGAGE [12] trial.
There are no direct head-to-head trials comparing DOACs, though some data suggest apixaban is associated with a lower bleeding risk than rivaroxaban (no difference in ICH), and that rivaroxaban may be associated with a higher risk of hemorrhagic stroke.
In older adults, DOACs can be used without safety concerns over warfarin, though avoiding dabigatran may be suggested due to a signal for increased bleeding outcomes in older adult patients. The ELDERCARE-AF [13] trial from Japan showed no difference in major bleeding, but higher rates of GI bleeding and all bleeding, with edoxaban vs. placebo in adults >/= 80 years. Overall, apixaban is generally considered safe to use/the preferred DOAC option in patients with a history of GI bleeding.
What is the recommended anti-thrombotic approach for patients with indications for both antiplatelet therapy and anticoagulation (for example, patients with atrial fibrillation undergoing PCI)?
Assessing the appropriateness of dual vs. triple therapy involves balancing the risk of stent thrombosis vs. stroke risk.
Among P2Y12 inhibitors, clopidogrel is typically recommended over ticagrelor or prasugrel due to its lower incidence of bleeding events and because clopidogrel was also the most commonly used P2Y12 inhibitor in dual versus triple therapy trials.
The WOEST trial [14] found no increased thrombosis risk but a reduced bleeding risk in patients given dual therapy post-PCI with clopidogrel and warfarin vs. those given triple therapy with warfarin, clopidogrel, and aspirin. The REDUAL-PCI trial [15] found a similarly reduced bleeding risk without statistically increased thrombotic risk in patients receiving dual therapy with dabigatran + P2Y12i vs. continuing triple therapy with P2Y12i + aspirin + warfarin. The PIONEER-AF [16] trial found lower bleeding risk with rivaroxaban + P2Y12 therapy than with warfarin-DAPT triple therapy without differences in thrombotic outcomes; the caveat here is that the 15mg daily rivaroxaban dose used is not approved for stroke prevention (that dose is 20mg daily). The AUGUSTUS trial [17] showed dual apixaban + P2Y12i therapy to have lower bleeding risk and unchanged efficacy than VKA dual therapy or triple therapy with apixaban or VKA. Importantly, these trials were not powered to differentiate ischemic outcomes.
As for when patients should be transitioned from triple (OAC + P2Y12 + ASA) to dual therapy (OAC + P2Y12), data from medication-specific trials can help guide the approach. For patients anticoagulated with warfarin or dabigatran, a triple therapy duration of 30 days may be appropriate based on WOEST (up to 1 year) and REDUAL-PCI trials (up to 3 months for patients with a DES). In PIONEER-AF, patients were randomized directly to rivaroxaban + P2Y12 therapy without first receiving triple therapy, but in clinical practice, triple therapy is often instituted for 7-30 days before transitioning to dual therapy with rivaroxaban and P2Y12 inhibitor. For apixaban, a shorter 7-day course of triple therapy appears appropriate.
*The 2022 ACC ECDP is a fantastic reference resource to help guide the management of anticoagulation and antiplatelet therapy in patients with atrial fibrillation or VTE undergoing PCI or with ASCVD [18].
What’s the scoop on factor XI, which appears to be clinically important for thrombosis but not hemostasis, as a potential drug target? Might this be the future of anticoagulation pharmacotherapy?
Factor XI is a part of the contact pathway of coagulation. It is activated by thrombin and factor XIIa and is thought to activate factor IX. Factor XI appears to contribute to thrombin generation and thereby amplify thrombus growth; it may also reduce fibrin degradation. Higher levels of factor XI appear correlated to increased clotting risk, while factor XI levels are poorly correlated with bleeding risk. The excitement around factor XI as a drug target stems from the thought that XI inhibition may decrease thrombotic risk without significantly changing bleeding risk.
Currently, there are several drugs in development and multiple ongoing clinical trials examining therapeutic viability. Oral, intravenous, and subcutaneous formulations of factor XI inhibitors are all being studied, in forms including monoclonal antibodies, small molecules, and antisense oligonucleotides. Most data reported thus far relates to VTE prophylaxis in orthopedic surgery. However, ongoing/planned trials, like the PACIFIC and OCEANIC series, will look at factor XI inhibitors in the context of atrial fibrillation, stroke, and myocardial infarction. Comparator drugs in these studies include DOACs and enoxaparin.
Long-term impact for this class of investigational therapeutics remains to be seen, and cost will likely be a limiting factor in using these agents (especially as DOACs are anticipated to go generic in 5-10 years). However, early data seems promising! [19, 20].
References – Anticoagulation Pharmacology
January CT, Wann LS, Calkins H, et al. 2019 AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society in Collaboration With the Society of Thoracic Surgeons [published correction appears in Circulation. 2019 Aug 6;140(6):e285]. Circulation. 2019;140(2):e125-e151. doi:10.1161/CIR.0000000000000665
Eikelboom JW, Connolly SJ, Brueckmann M, et al. Dabigatran versus warfarin in patients with mechanical heart valves. N Engl J Med. 2013;369(13):1206-1214. doi:10.1056/NEJMoa1300615
Wang TY, Svensson LG, Wen J, et al. Apixaban or Warfarin in Patients with an On-X Mechanical Aortic Valve. NEJM Evid 2023;May 6:[Epub ahead of print]. doi:10.1056/EVIDoa2300067
Pengo V, Hoxha A, Andreoli L, et al. Trial of Rivaroxaban in AntiPhospholipid Syndrome (TRAPS): Two-year outcomes after the study closure. J Thromb Haemost. 2021;19(2):531-535. doi:10.1111/jth.15158
Woller SC, Stevens SM, Kaplan D, et al. Apixaban compared with warfarin to prevent thrombosis in thrombotic antiphospholipid syndrome: a randomized trial. Blood Adv. 2022;6(6):1661-1670. doi:10.1182/bloodadvances.2021005808
Martin KA, Beyer-Westendorf J, Davidson BL, Huisman MV, Sandset PM, Moll S. Use of direct oral anticoagulants in patients with obesity for treatment and prevention of venous thromboembolism: Updated communication from the ISTH SSC Subcommittee on Control of Anticoagulation. J Thromb Haemost. 2021;19(8):1874-1882. doi:10.1111/jth.15358
Ellenbogen MI, Ardeshirrouhanifard S, Segal JB, Streiff MB, Deitelzweig SB, Brotman DJ. Safety and effectiveness of apixaban versus warfarin for acute venous thromboembolism in patients with end-stage kidney disease: A national cohort study. J Hosp Med. 2022;17(10):809-818. doi:10.1002/jhm.12926
Chen A, Stecker E, A Warden B. Direct Oral Anticoagulant Use: A Practical Guide to Common Clinical Challenges. J Am Heart Assoc. 2020;9(13):e017559. doi:10.1161/JAHA.120.017559
Connolly SJ, Ezekowitz MD, Yusuf S, et al. Dabigatran versus warfarin in patients with atrial fibrillation [published correction appears in N Engl J Med. 2010 Nov 4;363(19):1877]. N Engl J Med. 2009;361(12):1139-1151. doi:10.1056/NEJMoa0905561
Patel MR, Mahaffey KW, Garg J, et al. Rivaroxaban versus warfarin in nonvalvular atrial fibrillation. N Engl J Med. 2011;365(10):883-891. doi:10.1056/NEJMoa1009638
Granger CB, Alexander JH, McMurray JJ, et al. Apixaban versus warfarin in patients with atrial fibrillation. N Engl J Med. 2011;365(11):981-992. doi:10.1056/NEJMoa1107039
Giugliano RP, Ruff CT, Braunwald E, et al. Edoxaban versus warfarin in patients with atrial fibrillation. N Engl J Med. 2013;369(22):2093-2104. doi:10.1056/NEJMoa1310907
Okumura K, Akao M, Yoshida T, et al. Low-Dose Edoxaban in Very Elderly Patients with Atrial Fibrillation. N Engl J Med. 2020;383(18):1735-1745. doi:10.1056/NEJMoa2012883
Dewilde WJ, Oirbans T, Verheugt FW, et al. Use of clopidogrel with or without aspirin in patients taking oral anticoagulant therapy and undergoing percutaneous coronary intervention: an open-label, randomised, controlled trial. Lancet. 2013;381(9872):1107-1115. doi:10.1016/S0140-6736(12)62177-1
Cannon CP, Bhatt DL, Oldgren J, et al. Dual Antithrombotic Therapy with Dabigatran after PCI in Atrial Fibrillation. N Engl J Med. 2017;377(16):1513-1524. doi:10.1056/NEJMoa1708454
Gibson CM, Mehran R, Bode C, et al. Prevention of Bleeding in Patients with Atrial Fibrillation Undergoing PCI. N Engl J Med. 2016;375(25):2423-2434. doi:10.1056/NEJMoa1611594
Lopes RD, Heizer G, Aronson R, et al. Antithrombotic Therapy after Acute Coronary Syndrome or PCI in Atrial Fibrillation. N Engl J Med. 2019;380(16):1509-1524. doi:10.1056/NEJMoa1817083
Kumbhani D, Cannon C, Beavers C, et al. 2020 ACC Expert Consensus Decision Pathway for Anticoagulant and Antiplatelet Therapy in Patients With Atrial Fibrillation or Venous Thromboembolism Undergoing Percutaneous Coronary Intervention or With Atherosclerotic Cardiovascular Disease. J Am Coll Cardiol. 2021 Feb, 77 (5) 629–658. https://doi.org/10.1016/j.jacc.2020.09.011
Nopp S, Kraemmer D, Ay C. Factor XI Inhibitors for Prevention and Treatment of Venous Thromboembolism: A Review on the Rationale and Update on Current Evidence. Front Cardiovasc Med. 2022;9:903029. Published 2022 May 12. doi:10.3389/fcvm.2022.903029
Greco A, Laudani C, Spagnolo M, et al. Pharmacology and Clinical Development of Factor XI Inhibitors. Circulation. 2023;147(11):897-913. doi:10.1161/CIRCULATIONAHA.122.062353
1 hr 4 min
December 27, 2023352. Case Report: The Culprit in the Pillbox – University of Kansas
CardioNerds (Dr. Amit Goyal) join Dr. Anureet Malhotra, Dr. John Fritzlen, and Dr. Tarun Dalia from the University of Kansas School of Medicine for some of Kansas City’s famous barbeque. They discuss a case of Hydroxychloroquine induced cardiomyopathy. Notes were drafted by Dr. Anureet Malhotra, Dr. John Fritzlen, and Dr. Tarun Dalia. Expert commentary was provided by Dr. Pradeep Mammen. The episode audio was edited by Dr. Akiva Rosenzveig.
Drug-induced cardiomyopathy remains an important and under-recognized etiology of cardiomyopathy and heart failure. Hydroxychloroquine is a disease-modifying antirheumatic drug used for various rheumatological conditions, and its long-term use is well-known to have toxic effects on cardiac muscle cells. Multiple cardiac manifestations of these drugs have been identified, the most prominent being electrophysiological disturbances.
In this episode, we discuss a biopsy-proven case of hydroxychloroquine-induced cardiotoxicity with detailed histopathological and imaging findings. We develop a roadmap for the diagnosis of hydroxychloroquine-induced cardiomyopathy and discuss the various differentials of drug-induced cardiomyopathy. We highlight the importance of clinical monitoring and early consideration of drug-induced toxicities as a culprit for heart failure.
“To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all.” – Sir William Osler. CardioNerds thank the patients and their loved ones whose stories teach us the Art of Medicine and support our Mission to Democratize Cardiovascular Medicine.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Case Media – Hydroxychloroquine induced cardiomyopathy
Pearls – Hydroxychloroquine induced cardiomyopathy
Continued decline in left ventricular systolic function despite appropriate guideline directed medical therapy should prompt a thorough evaluation for unrecognized etiologies and warrants an early referral to advanced heart failure specialists.
Transthoracic echocardiogram is a valuable non-invasive screening tool for suspected pulmonary hypertension, but right heart catheterization is required for definitive diagnosis.
Cardiac MRI can be used for better characterization of myocardial tissue and can aid in the evaluation of patients with non-ischemic cardiomyopathy.
Hydroxychloroquine (HCQ) is a commonly used DMARD that remains an underrecognized etiology of cardiomyopathy and heart failure. In addition to ophthalmological screening, annual ECG, as well as echocardiography screening for patients on long-term HCQ therapy, should be considered in patients at risk for cardiovascular toxicity, including those with pre-existing cardiovascular disease, older age, female sex, longer duration of therapy, and renal impairment.
Management of hydroxychloroquine-associated cardiomyopathy consists of discontinuing hydroxychloroquine and standard guideline-directed medical therapy for heart failure. HCQ cardiomyopathy may persist despite medical therapy, and advanced therapy options may have to be considered in those with refractory heart failure.
Show Notes – Hydroxychloroquine induced cardiomyopathy
What are the various cardiotoxic effects of hydroxychloroquine (HCQ) and the mechanism of HCQ-mediated cardiomyopathy?
One of the most frequently prescribed disease-modifying antirheumatic drugs (DMARDs), HCQ is an immunomodulatory and anti-inflammatory agent that remains an integral part of treatment for a myriad of rheumatological conditions. Its efficacy is linked to inhibiting lysosomal antigen processing, MHC-II antigen presentation, and TLR functions.8 The known cardiac manifestations of HCQ-induced toxicity include conduction abnormalities, ventricular hypertrophy, hypokinesia, and lastly, cardiomyopathy.
Conduction Abnormalities – by binding to and inhibiting the human ether-à-go-go-related gene (hERG) voltage-gated potassium channel, also known as Ikr channel, HCQ can lead to prolongation of corrected QT (QTc) interval. This can lead to an increased risk of drug-induced Torsades de pointes and other lethal ventricular arrhythmias.
Cardiomyopathy – HCQ is a lipophilic drug that easily permeates myocytes and binds to lysosomal phospholipids, leading to lysosomal accumulation of phospholipids. Furthermore, by increasing the pH of the lysosome, HCQ inhibits lysosomal enzymes, which interferes with lysosomal function and exocytosis, leading to an acquired lysosomal storage disorder. This results in myofibrillar disorganization, atrophy, and fibrosis, which may lead to cardiomyopathy. Risk factors for the development of cardiotoxicity are thought to be pre-existing cardiovascular disease, older age, female sex, longer duration of therapy, and renal impairment. 8
Extracardiac side effects – With long term use, HCQ can also lead to ocular toxicity, neuropathy, and myopathy with similar pathogenesis as cardiotoxicity, i.e., acquired lysosomal storage disorder.
What are the histopathological findings of HCQ induced Cardiomyopathy?
HCQ causes an acquired lysosomal storage disorder due to the inhibition of constitutive autophagy present in normal cardiac myocytes. On histopathology, this presents itself as cytoplasmic vacuoles, lamellar bodies and curvilinear inclusion bodies in cytoplasm that can be visualized with electron microscopy. Of these findings, curvilinear bodies are thought to be pathognomonic for HCQ induced cardiotoxicity. On histopathology, these findings can resemble inherited lysosomal storage disorders including Anderson- Fabry disease except for the presence of curvilinear bodies. 9
What is the differential diagnosis for HCQ induced cardiomyopathy?
Differentials of HCQ mediated cardiomyopathy include storage disorders like Fabry disease, adult-onset Pompe disease (acid maltase deficiency), and Danon disease. Many drug-induced myopathies such as amiodarone, rituximab, prednisone, cocaine, cobalt, and several chemotherapeutic agents can also resemble HCQ mediated cardiotoxicity.
Furthermore, amyloidosis, sarcoidosis and myocarditis also merit consideration as they can lead to restrictive physiology and present similar echocardiographic findings. They can be differentiated using advanced cardiac imaging such as cardiac MRI and histopathological findings on endomyocardial biopsy.
How can Cardiac MRI (CMR) assist in the work up of non-ischemic cardiomyopathy?
CMR can enhance visualization of cardiac structures that may be poorly seen on echocardiogram due to location or poor acoustic windows. CMR also uniquely provides detailed tissue characterization. CMR can be used for assessing many pathologies, including aortic disease, coronary artery disease, cardiomyopathies, pericardial disease, and congenital heart disease. 4 CMR is also considered the gold standard for assessing cardiac function and can be used to assess valvular pathologies with flow assessment.
Late gadolinium enhancement (LGE) refers to the discrimination of regions of scar, necrosis, or inflammation from normal tissue by the prolonged retention of gadolinium-based contrast agents. The pattern of LGE, as well as T1 and T2 mapping, aid in tissue characterization and accurate diagnosis. Key take-home points are as follows:
The presence of LGE in a coronary distribution can support the diagnosis of prior myocardial infarction and aid in the assessment of myocardial viability.
LGE in the mid-wall and sub-epicardium of the LV is characteristic of viral myocarditis. In addition, T1 mapping helps estimate the extracellular volume, and T2 weighted imaging can show myocardial edema in patients with myocarditis.
In amyloidosis, the classic CMR findings include thick LV walls, valves, and interatrial septum and the presence of a pericardial effusion. They may also have the existence of amyloid protein in the myocardial interstitium associated with characteristic patterns of circumferential subendocardial LGE.
What is the management of HCQ induced cardiomyopathy?
Diagnosis – HCQ cardiomyopathy diagnosis requires a high level of suspicion. A detailed history is an essential first step. CMR can aid in tissue characterization and is a helpful non-invasive tool. Definitive diagnosis can be established by obtaining an endomyocardial biopsy, given its distinctive histopathological findings, and ruling out close mimics of HCQ-induced cardiotoxicity.
Treatment – the potentially reversible nature of HCQ cardiomyopathy makes early diagnosis and discontinuation of the offending drug the mainstays of treatment along with guideline directed medical therapy for heart failure. Recovery is variable and may take months or even years for LV function to improve. In some cases, there may be partial or no recovery, requiring advanced therapies evaluations.
References – Hydroxychloroquine induced cardiomyopathy
Greiner S, Jud A, Aurich M, et al. Reliability of Noninvasive Assessment of Systolic Pulmonary Artery Pressure by Doppler Echocardiography Compared to Right Heart Catheterization: Analysis in a Large Patient Population. Journal of the American Heart Association.2014;3(4).10.1161/JAHA.114.001103
Augustine DX, Coates-Bradshaw LD, Willis J, et al. Echocardiographic assessment of pulmonary hypertension: a guideline protocol from the British Society of Echocardiography. Echo research and practice. 2018;5(3):G11-G24. 10.1530/ERP-17-0071
Page RL, O’Bryant CL, Cheng D, et al. Drugs That May Cause or Exacerbate Heart Failure. Circulation. 2016;134(6).https://doi.org/10.1161/CIR.0000000000000426
Kramer CM. Role of Cardiac MR Imaging in Cardiomyopathies. Journal of Nuclear Medicine. 2015;56(Supplement_4):39S45S.10.2967/jnumed.114.142729.
Joyce E, Fabre A, Mahon N. Hydroxychloroquine cardiotoxicity presenting as a rapidly evolving biventricular cardiomyopathy: key diagnostic features and literature review. European Heart Journal Acute Cardiovascular Care. 2013;2(1):77-83. https://doi.org/10.1177/2048872612471215
Ezzeddine FM, Giudicessi JR, Maleszewski JJ, Lin PT, Borlaug BA, Geske JB. Unmasking Hydroxychloroquine Cardiotoxicity in a Patient With Heart Failure and Chronotropic Incompetence. JACC: Case Reports. 2021;3(7):997-1001. https://doi.org/10.1016/j.jaccas.2021.03.003
Humbert M, Kovacs G, Hoeper MM, et al. 2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension. European Heart Journal. Published online August 26, 2022. https://doi.org/10.1093/eurheartj/ehac237
Bansal P, Goyal A, Cusick A, et al. Hydroxychloroquine: a comprehensive review and its controversial role in coronavirus disease 2019. Annals of Medicine. 2020;53(1):117-134. 10.1080/07853890.2020.1839959.
Roos JM, Aubry MC, Edwards WD. Chloroquine cardiotoxicity: Clinicopathologic features in three patients and comparison with three patients with Fabry disease. Cardiovascular Pathology. 2002;11(5):277-283. https://doi.org/10.1016/s1054-8807(02)00118-7
24 min
December 20, 2023351. Case Report: The Tall Tail Heart: Angioleiomyoma – The Christ Hospital
CardioNerds meet with fellows from The Christ Hospital, Drs. Hanad Bashir, Hyunsoo Chung, and Dalia Aziz to discuss the following case that highlights angioleiomyoma:
A 60-year-old woman with a past medical history significant for breast cancer (on tamoxifen) presented as a transfer to our facility for a clot-in-transit. She had initially presented to the outside hospital after progressive dyspnea on exertion and recent syncope. She was found on an echocardiogram to have a right atrial mass spanning into the right ventricle. CTA of the chest and abdomen/pelvis demonstrated extensive thrombus burden spanning from the IVC into the right ventricle. She was transferred to our facility for intervention.
Endovascular attempts were unsuccessful, at which point she underwent surgical thrombectomy. Gross examination of the mass revealed a cylindrical shape, homogeneous tan color, rubbery soft tissue, measuring 25.5 cm in length and 2.3 cm in diameter. Histology confirmed the presence of angioleiomyoma. A second, smaller mass (5.2cm long and 4mm in diameter) was removed from under the tricuspid valve, with histology consistent with leiomyoma. Estrogen receptor and progesterone receptor staining were strongly positive, leading to the discontinuation of tamoxifen. Given the presence of uterine fibroids identified on the CT scan, there was concern about a uterine origin. A hysterectomy is planned for her in the near future.
Expert commentary is provided by Dr. Wojciech Mazur. Episode audio was edited by student Dr. Adriana Mares.
“To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all.” – Sir William Osler. CardioNerds thank the patients and their loved ones whose stories teach us the Art of Medicine and support our Mission to Democratize Cardiovascular Medicine.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here.
CardioNerds Case Reports Page
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll
CardioNerds Journal Club
Subscribe to The Heartbeat Newsletter!
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Case Media – The Tall Tail Heart: Angioleiomyoma – The Christ Hospital
Pearls – The Tall Tail Heart: Angioleiomyoma – The Christ Hospital
Although evaluation of cardiac mass by echocardiography can provide information such as size, location, and morphology, adjunctive cross-sectional imaging may be used depending on the need for further temporal resolution (CT) or tissue characterization via cardiac MRI (CMR). If suspicious for elevated metabolic activity, there should be consideration of FDG-PET.

Tamoxifen (a selective estrogen receptor modulator) is an agent used for breast cancer therapy. However, its use has been associated with endometrial hyperplasia, uterine fibroids, endometrial and uterine malignancy. Increased risk of malignancy has been seen more often in post-menopausal women and is dose and time-dependent.

Clot in transient is a mobile thrombus, typically within the right heart structures. It is estimated to occur in 4-18% of patients with pulmonary embolism and is associated with elevated morbidity and mortality. Treatment includes surgical embolectomy, endovascular embolectomy, systemic thrombolysis, catheter-directed thrombolysis, or systemic anticoagulation.

Angioleiomyoma is a rare benign pericystic tumor that most commonly affects the extremities. There are case reports of other affected sites, including the uterus. Invasion into the cardiac structures is exceedingly rare.

The only established treatment for angioleiomyoma is surgical resection.
Show Notes – The Tall Tail Heart: Angioleiomyoma – The Christ Hospital
Syncope
Syncope is a transient loss of consciousness secondary to reduced blood flow to the brain. Often, certain presentations are mislabeled as syncope, such as seizure disorders, posttraumatic loss of consciousness, and cataplexy.
An organized diagnostic approach should be used to reduce hospital admissions and medical costs and increase diagnostic accuracy.
Syncope can be divided into five general subgroups.
1) Neurally mediated reflex syncope (carotid sinus syndrome, vasovagal)
2) Orthostatic syncope
3) Cardiac arrhythmias
4) Structural cardiac and pulmonary causes
5) Cerebrovascular disorders.
Initial evaluation should include thorough H&P, including orthostatic vitals and ECG. If diagnosis remains uncertain after initial evaluation, patients’ syncope should be risk stratified into three groups: high, intermediate, and low risk.
Additionally, the 2017 ACC/AHA/HRS guidelines stratify patient risk based on short-term (<30 days) and long-term (>30 days) morbidity and mortality based on initial examination and history.
Patients presenting with high-risk and short-term syncope features should be immediately hospitalized for further diagnostic testing and treatment. High-risk features are usually indicative of underlying cardiovascular causes that could lead to sudden death; this includes but is not limited to life-threatening arrhythmias and acute coronary syndrome.
Risk stratification also determines the selection of diagnostic tests. When underlying cardiac etiology is suspected, diagnostic tests such as echocardiography, CT angiography, cardiac magnetic resonance, electrophysiology study, exercise stress testing, and coronary angiography may be valuable in establishing timely diagnosis in high-risk patients.
Choice of study modality varies greatly based on patient presentation and risk factors. In contrast to patients presenting with high-risk syncope, low-risk patients are discharged home with re-assurance and follow-up.
Strategy for Intracardiac Masses
First, take into account the patient’s age at the time of presentation, as certain medical conditions like rhabdomyomas and fibromas are more commonly observed among pediatric patients.
Second, assess the likelihood from an epidemiological perspective and consider the clinical probability. For instance, if a patient has recently experienced an anterior wall myocardial infarction and exhibits an akinetic ventricular apex, the presence of a cardiac mass during echocardiography could indicate the possibility of an intracardiac thrombus.
Third, factor in the location of the tumor. If the mass is detected on the valves, potential diagnoses to consider include thrombus or vegetation. While masses within the heart chambers might still indicate thrombus, it’s also important to contemplate other possibilities, such as myxomas, lymphomas, and metastases.
Fourth, delve into the tissue characteristics of the mass using additional diagnostic imaging methods like cardiac magnetic resonance imaging.
Imaging Modalities for Intracardiac Masses
Transthoracic echocardiography (TTE) is readily available and non-invasive. Transesophageal echocardiography (TEE) offers insights into size, shape, attachment site, extension, and hemodynamic effects. Ultrasound-enhancing agents in echocardiography help differentiate various masses. Thrombi and benign tumors display a non or low-enhancing pattern. Malignancies and highly vascular tumors display a hyperenhancing pattern. Doppler velocities aid in assessing the hemodynamic impact.
Cardiac MRI (CMR) is invaluable in the assessment of cardiac masses. In addition to anatomy, dimensions, and mass consistency, using different signal sequences like T1, T2, early and late gadolinium enhancement differentiate tissue characteristics and unveil fatty presence, necrosis, bleeding, inflammation, and vascularity within a mass.
Cardiac CT provides high spatial and temporal resolution, multiplanar image reconstruction, and rapid acquisition. The broad field of view allows for the evaluation of the chest, lung tissue, vascular structures, and potential masses within the chest. Cardiac CT can be used to detect calcifications within the mass, although it has less soft tissue resolution compared with CMR.
FDG-PET/CT can help gauge tumors’ metabolic activity. When CT alone doesn’t decisively determine benign or malignant nature, PET/CT steps in, aiding in malignancy diagnosis and guiding biopsy locations, staging, and cancer therapy planning.
Cardiac tumors
Cardiac tumors can be categorized into primary and secondary tumors.
Secondary tumors, arising from metastasis, are more prevalent and often stem from cancers like melanoma, breast, or lung cancer.
Secondary tumors can lead to issues like pericardial effusion with or without cardiac tamponade, myocardial infiltration, obstruction, or embolization. Primary tumors include benign (about 80%) and malignant (about 20%) types.
Malignant tumors are mainly sarcomas, such as angiosarcomas and rhabdomyosarcomas.
Benign tumors encompass myxomas, gelatinous masses with scattered myxoma cells; papillary fibroelastomas, frond-like masses typically on valves; lipomas, composed of fat cells; fibromas, containing fibroblasts and mostly found in the left ventricle; and rhabdomyomas, made of maldeveloped cardiac myocytes and often seen in ventricles. Other rare tumors include Purkinje cell tumors. However, the latter three mentioned are more common in children.
Clot-in-transit
Clot-in-transit (CIT) is the presence of mobile echogenic material in the right atrium or ventricle as seen on ultrasound.
Right heart clots are classified into three types based on their morphology:
Type A (common and carries a high risk of pulmonary embolization)
Type B (assumed to originate from the atrium or ventricle)
Type C (rare and migratory, resembling cardiac myxomas)
Intervention options for CIT include catheter-based thrombolysis, systemic (IV) thrombolysis, surgical/endovascular embolectomy, and anticoagulation therapy.
Catheter-based thrombolysis involves high-frequency ultrasound exposure, catheter-directed thrombolysis, mechanical thrombectomy, and endovascular clot suction. It has a high success rate but may not work for bulky thrombi.
Surgical embolectomy is recommended for hemodynamically unstable patients with CIT and provides an opportunity to address right-to-left heart communication. It requires substantial surgery and cardiopulmonary bypass.
In cases of concomitant CIT and pulmonary embolism (PE), simultaneous treatment is essential to prevent further PE episodes.
Anticoagulants are an option for patients in whom surgery is contraindicated, but they do not affect existing clots and may lead to bleeding or thrombus fragmentation.
Systemic thrombolysis can improve right ventricular function, reduce pulmonary hypertension, and dissolve clots in multiple locations but carries a risk of thrombus embolization as well as bleeding complications.
Management plans for CIT should consider individual patient factors like hemodynamic stability, right heart function, patent foramen ovale (PFO), and malignancy.
There are no definitive guidelines. As a result, treatment decisions should be made on a case-by-case basis. An algorithm for CIT treatment may be helpful in clinical decision-making. PE response teams (PERT) are invaluable for complex decision making.
Angioleiomyoma
These are rare, benign tumors that are classified as pericytic (perivascular) soft tissue tumors.
There appears to be no consensus on incidence and prevalence, though there have been reports of this tumor accounting for around 5% of benign soft tissue tumors. Women are more affected than men. The age of diagnosis tends to be in the 4th to 6th decade.
They typically arise in the extremities, particularly the lower extremities. However, the prevalence of uterine, cardiac, and major vascular deposition (IVC) is unknown.
Typically, when present in the extremities, patients complain of discomfort due to the nodules. That said, location and size will determine symptoms. Pulmonary angioleiomyomas causing dyspnea have been reported. If involving the uterus, patients may present with menorrhagia, abdominal pain, and abdominal mass. Those masses can be submucosal, intramural, subserosal. As in this case, excessive burden in the IVC and right heart can lead to hemodynamic limitations, ultimately leading to symptoms of dyspnea and syncope.
There is no agreement on the pathophysiology of this tumor. However, there are hypotheses, including trauma to the area, venous stasis, and hormonal factors causing the propagation of abnormal cell growth. Proposed histological types include capillary type (narrow vessels interlaced with thick fascicles of smooth muscles), venous type (thick vessels interspersed with fascicles of smooth muscle), and cavernous type (widened vessels with less smooth muscles).
Although echo, CT, and MRI imaging could help evaluate the characteristics of this mass, pathology is required for a definitive diagnosis.
The mainstay treatment is surgical excision of the tumor. This has been effective in preventing recurrence. However, in this case, the treating team should be cognizant of any potential medications leading to the proliferation of this tumor.
Benign metastasizing leiomyoma
The origins of the tumor are typically uterine leiomyomas. These are inherently mitotically inactive smooth muscle cells without atypia, which have migrated to extra-uterine sites.
Although rare, these are mostly seen in patients of reproductive age and frequently involve the lungs, whereby it is called pulmonary benign metastasizing leiomyoma.
Patients may present with incidental extra-uterine leiomyoma found on exam. If there is hemodynamic change in the cardiac chambers or if involving the lungs, patients may present with symptoms including dyspnea, cough, and chest discomfort.
There is evidence to suggest chromosome deletions, particularly in 19q and 22q, may predispose leiomyomas to metastatic potential.
When present in the lung, this needs to be differentiated from pulmonary lymphangioleiomyomatosis (LAM), which on histology demonstrates perivascular epithelioid cells along bronchial interstitium.
Leiomyomas beyond the uterus have been classified as intravenous, benign metastasizing, diffuse peritoneal, retroperitoneal, and parasitic. Incidence is approximately 0.25% to 0.4% for those with leiomyomas.
For patients with symptomatic disease, resection of the leiomyoma, anti-hormonal agents, and anti-angiogenesis agents can be used for tumor treatment.
References –
Schaal SF, Nelson SD, Boudoulas H, Lewis RP. Syncope. Curr Probl Cardiol. 1992 Apr;17(4):205-64. doi: 10.1016/0146-2806(92)90002-6. PMID: 1563273.
Writing Committee Members; Shen WK, Sheldon RS, Benditt DG, Cohen MI, Forman DE, Goldberger ZD, Grubb BP, Hamdan MH, Krahn AD, Link MS, Olshansky B, Raj SR, Sandhu RK, Sorajja D, Sun BC, Yancy CW. 2017 ACC/AHA/HRS guideline for the evaluation and management of patients with syncope: A report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Heart Rhythm. 2017 Aug;14(8):e155-e217. doi: 10.1016/j.hrthm.2017.03.004. Epub 2017 Mar 9. PMID: 28286247.
Sutton R, Ricci F, Fedorowski A. Risk stratification of syncope: Current syncope guidelines and beyond. Auton Neurosci. 2021 Dec 23;238:102929. doi: 10.1016/j.autneu.2021.102929. Epub ahead of print. PMID: 34968831.
Motwani M, Kidambi A, Herzog BA, Uddin A, Greenwood JP, Plein S. MR imaging of cardiac tumors and masses: a review of methods and clinical applications. Radiology. 2013 Jul;268(1):26-43. doi: 10.1148/radiol.13121239. PMID: 23793590.
Tyebally S, Chen D, Bhattacharyya S, Mughrabi A, Hussain Z, Manisty C, Westwood M, Ghosh AK, Guha A. Cardiac Tumors: JACC CardioOncology State-of-the-Art Review. JACC CardioOncol. 2020 Jun 16;2(2):293-311. doi: 10.1016/j.jaccao.2020.05.009. PMID: 34396236; PMCID: PMC8352246.
Lopez-Mattei JC, Lu Y. Multimodality Imaging in Cardiac Masses: To Standardize Recommendations, The Time Is Now! JACC Cardiovasc Imaging. 2020 Nov;13(11):2412-2414. doi: 10.1016/j.jcmg.2020.04.009. Epub 2020 Jun 17. PMID: 32563655
Patel AN, Amrutiya RJ, Manvar BN. A Proposed Approach for the Management of Clot-in-Transit. Cureus. 2022 Aug 27;14(8):e28481. doi: 10.7759/cureus.28481. PMID: 36176887; PMCID: PMC9512516.
Hu Y, Ren S, Tan S, Chen C, Wang X, Liang Q, Yu F, Liu W. Angioleiomyoma of the pulmonary artery: a case report and literature review. J Cardiothorac Surg. 2020 Aug 28;15(1):230. doi: 10.1186/s13019-020-01275-z. PMID: 32859240; PMCID: PMC7456385.
Sikora-Szczęśniak DL. Uterine angioleiomyoma – a rare variant of uterine leiomyoma: review of literature and case reports. Prz Menopauzalny. 2016 Nov;15(3):165-169. doi: 10.5114/pm.2016.63496. Epub 2016 Nov 15. PMID: 27980528; PMCID: PMC5137480.
Zhang JZ, Zhou J, Zhang ZC. Subcutaneous Angioleiomyoma: Clinical and Sonographic Features With Histopathologic Correlation. J Ultrasound Med. 2016 Aug;35(8):1669-73. doi: 10.7863/ultra.15.06056. Epub 2016 Jul 1. PMID: 27371376.
Kang BS, Shim HS, Kim JH, Kim YM, Bang M, Lim S, Park GM, Lee TY, Ha ND, Kwon WJ. Angioleiomyoma of the Extremities: Findings on Ultrasonography and Magnetic Resonance Imaging. J Ultrasound Med. 2019 May;38(5):1201-1208. doi: 10.1002/jum.14798. Epub 2018 Sep 12. PMID: 30208227.
Kumar S, Hasan R, Maddukuri SB, Mathew M. Angiomyoma presenting as a painful subcutaneous mass: a diagnostic challenge. BMJ Case Rep. 2014 Oct 16;2014:bcr2014206606. doi: 10.1136/bcr-2014-206606. PMID: 25323285; PMCID: PMC4202094.
Morimoto Y, Sato M, Yamada A, Gan K. Large right ventricle cardiac leiomyoma metastasis from uterine leiomyoma. BMJ Case Rep. 2022 Dec 8;15(12):e252389. doi: 10.1136/bcr-2022-252389. PMID: 36593619; PMCID: PMC9743285.
Galvin SD, Wademan B, Chu J, Bunton RW. Benign metastasizing leiomyoma: a rare metastatic lesion in the right ventricle. Ann Thorac Surg. 2010 Jan;89(1):279-81. doi: 10.1016/j.athoracsur.2009.06.050. PMID: 20103256.
Pacheco-Rodriguez G, Taveira-DaSilva AM, Moss J. Benign Metastasizing Leiomyoma. Clin Chest Med. 2016 Sep;37(3):589-95. doi: 10.1016/j.ccm.2016.04.019. Epub 2016 Jun 25. PMID: 27514603.
Barnaś E, Książek M, Raś R, Skręt A, Skręt-Magierło J, Dmoch-Gajzlerska E. Benign metastasizing leiomyoma: A review of current literature in respect to the time and type of previous gynecological surgery. PLoS One. 2017 Apr 20;12(4):e0175875. doi: 10.1371/journal.pone.0175875. PMID: 28426767; PMCID: PMC5398563.
Mustafa A, Obholz J, Ghanim M, Congello S. Clot in Transit: Therapy via Peripherally Inserted Central Catheter Line. Cureus. 2022 Jan 28;14(1):e21691. doi: 10.7759/cureus.21691. PMID: 35237484; PMCID: PMC8882343.
38 min
December 19, 2023350. GLP-1 Agonists: Mechanisms to Applications with Dr. Dennis Bruemmer
Calling all those with a passion for cardiovascular prevention! In this episode of the CardioNerds Cardiovascular Prevention Series, we take a deep dive into the world of glucagon-like peptide-1 (GLP-1) receptor agonists. Along the way, you’ll hear about the biology of the GLP-1 molecule and its related peptides, learn more about how GLP-1 agonists promote glycemic control, weight loss, and cardiometabolic health, and explore the current body of literature supporting the individualized application of these medications to patients with diabetes, obesity, and/or ASCVD.
Join Dr. Christian Faaborg-Andersen (CardioNerds Academy Fellow and Internal Medicine Resident at MGH), Dr. Gurleen Kaur (Director of the CardioNerds Internship, Chief of House Einthoven, and Internal Medicine resident at BWH), and Dr. Rick Ferraro (CardioNerds Academy House Faculty and Cardiology Fellow at JHH) for a wide-ranging discussion on GLP-1 and GIP agonists with Dr. Dennis Bruemmer (Cardiologist and Director of the Center for Cardiometabolic Health in the section of Preventive Cardiology at the Cleveland Clinic).
Show notes were drafted by Dr. Christian Faaborg-Andersen. Audio editing was performed by CardioNerds Academy Intern, student Dr. Tina Reddy.
This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Novo Nordisk. See below for continuing medical education credit.
Claim CME for this episode HERE.
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Pearls and Quotes – GLP-1 Agonists: Mechanisms to Applications
The selection and dosing of GLP-1 and GIP agonists (GLP-1s and GIPs) depends on their intended use as an anti-glycemic or anti-obesity agent.
The cardiovascular benefits of GLP-1s and GIPs may be independent of improvements in glycemic control, and in part be driven by reduction in inflammation, a key driver of arterial plaque formation.
In patients with comorbid coronary artery disease, obesity, and diabetes, GLP-1 agonists and SGLT-2 inhibitors should be used as first-line agents, over metformin.
Tirzepatide is a dual agonist that activates GIP and GLP-1 receptors. GIP is highly expressed in the brain, which may mediate satiety, promote energy expenditure, and enhance peripheral glucose metabolism.
Caution should be used with GLP-1 agonists in patients with long-standing diabetes complicated by gastroparesis, as well as incompletely treated diabetic retinopathy.
GI upset is not uncommon with GLP-1/GIP agonists, and switching to a different agonist is unlikely to help.
Show notes – GLP-1 Agonists: Mechanisms to Applications
What are the mechanisms of action by which GLP-1 and GIP controls blood sugar and body weight?
Glucagon-like peptide-1 (GLP-1) is an endogenous hormone that is secreted in response to an oral glucose load. It promotes insulin release, inhibits glucagon secretion, and slows gastric emptying via the brain-intestine axis, leading to satiety. GLP-1 agonists are medications that mimic the effect of this hormone and, on average, lower hemoglobin A1C by 0.8% to 1.5%. These medications include semaglutide, liraglutide, and dulaglutide.
Glucose-dependent insulinotropic polypeptide (GIP) is also an endogenous hormone, similarly secreted by the body in response to an oral glucose load such as a meal. GIP is highly expressed in the arcuate nucleus and hypothalamus, which may mediate satiety, promote energy expenditure, and enhance peripheral glucose metabolism. Tirzepatide is a dual GLP-1/GIP agonist.
What is the role of GLP-1/GIP agonists in patients with overweight/obesity and/or type 2 diabetes? How does the dosing of GLP-1/GIP medications change with their intended disease target?
The STEP-1 trial showed that once-weekly semaglutide led to a net 15% weight loss in non-diabetic, obese/overweight patients. The SELECT trial builds on these results, showing that once-weekly semaglutide resulted in a 20% reduction in the primary composite endpoint of cardiovascular death, nonfatal myocardial infarction, or nonfatal stroke in patients with pre-existing cardiovascular disease and BMI ≥ 27kg/m2. Other notable trials in this space include the LEADER trial (liraglutide), the SUSTAIN-6 trial (semaglutide), and the REWIND trial (dulaglutide).
The dosing of GLP-1 agonists depends on their intended use as either an anti-glycemic or anti-obesity agent. For weight management, the current FDA-approved therapies are semaglutide 2.4mg weekly and liraglutide 3mg daily. For diabetes, the approved medications are semaglutide 2mg weekly, dulaglutide 4.5mg weekly, and tirzepadite 15mg weekly.
What are the cardiometabolic benefits of GLP-1/GIP agonist therapy, beyond glycemic control and/or weight loss? When are GLP-1/GIP agonists considered first-line therapy?
The cardiovascular benefits of GLP-1s may be independent of improvements in glycemic control, and in part be driven by reductions in inflammation and cytokine response driving plaque formation in the arterial wall. In the SELECT trial, once weekly 2.4mg semaglutide led to a 20% reduction in MACE in non-diabetic, obese/overweight patients with established ASCVD.
In patients with comorbid coronary artery disease, obesity, and diabetes, national guidelines recommend GLP-1 agonists and SGLT-2 inhibitors as first-line agents, over metformin.
How does tirzepatide differ from GLP-1 agonists?
Tirzepetide is a dual GLP-1/GIP agonist. GIP is highly expressed in the arcuate nucleus and hypothalamus, which may mediate satiety, promote energy expenditure, and enhance peripheral glucose metabolism.
The SURMOUNT trial showed 20% net weight loss with tirzepatide in patients with overweight/obesity, nearly as effective as metabolic surgery.
What are the absolute and relative contraindications to GLP-1/GIP agonist therapy?
GLP-1/GIP agonists are contraindicated in patients with a personal or family history of medullary thyroid cancer.
Caution should be used in patients with long-standing diabetes with neuropathy and gastroparesis, as well as incompletely treated diabetic retinopathy.
Gallstone pancreatitis should not be considered a contraindication to GLP-1/GIP therapy after cholecystectomy, though a history of recent pancreatitis should give one pause in prescribing a GLP-1/GIP agonist.
GLP-1 agonists should not be prescribed for type 1 diabetes, during pregnancy, or with breastfeeding.
What are the most common side effects of GLP-1 agonists?
GI upset is the most common side effect with GLP-1/GIP agonist therapy, and the incidence of these side effects is similar between tirzepadite and semaglutide in randomized control trials.
References – GLP-1 Agonists: Mechanisms to Applications
Wilding JPH, Batterham RL, Calanna S, et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity. N Engl J Med. 2021;384(11):989-1002. doi:10.1056/NEJMoa2032183 https://pubmed.ncbi.nlm.nih.gov/33567185/
Marso SP, Daniels GH, Brown-Frandsen K, et al. Liraglutide and Cardiovascular Outcomes in Type 2 Diabetes. N Engl J Med. 2016;375(4):311-322. doi:10.1056/NEJMoa1603827 https://pubmed.ncbi.nlm.nih.gov/27295427/
Marso SP, Bain SC, Consoli A, et al. Semaglutide and Cardiovascular Outcomes in Patients with Type 2 Diabetes. N Engl J Med. 2016;375(19):1834-1844. doi:10.1056/NEJMoa1607141 https://pubmed.ncbi.nlm.nih.gov/27633186/
Gerstein HC, Colhoun HM, Dagenais GR, et al. Dulaglutide and cardiovascular outcomes in type 2 diabetes (REWIND): a double-blind, randomised placebo-controlled trial. Lancet. 2019;394(10193):121-130. doi:10.1016/S0140-6736(19)31149-3 https://pubmed.ncbi.nlm.nih.gov/31189511/
44 min
December 17, 2023349. Case Report: Into the Thick of It – An Unusual Cause of Hypertrophic Cardiomyopathy – Cleveland Clinic
CardioNerds cofounder Dr. Amit Goyal and cardiology fellows from the Cleveland Clinic (Drs. Alejandro Duran Crane, Gary Parizher, and Simrat Kaur) discuss the following case: A 61-year-old man presented with symptoms of heart failure and left ventricular hypertrophy. He was given a diagnosis of obstructive hypertrophic cardiomyopathy. He eventually underwent septal myectomy, mitral valve replacement, aortic aneurysm repair, and aortic valve replacement with findings of Fabry’s disease on surgical pathology. The case discussion focuses on the differential diagnosis for LVH and covers Fabry disease as an HCM mimic. Expert commentary was provided by Dr. Angelika Ewrin. The episode audio was edited by student Dr. Diane Masket.
“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.
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Case Media – An Unusual Cause of Hypertrophic Cardiomyopathy – Cleveland Clinic
Pearls – An Unusual Cause of Hypertrophic Cardiomyopathy – Cleveland Clinic
Left ventricular hypertrophy is a cardiac manifestation of several different systemic and cardiac processes, and its etiology should be clarified to avoid missed diagnosis and treatment opportunities.
Fabry disease is a rare, X-linked inherited disease that can present cardiac and extra-cardiac manifestations, the former of which include hypertrophic cardiomyopathy, conduction defects, coronary artery disease, conduction abnormalities, arrhythmias, and heart failure.
The diagnosis of Fabry disease includes measurement of alpha-galactosidase enzyme activity as well as genetic testing to evaluate for pathogenic variants or variants of unknown significance in the GLA gene. Family members of patients diagnosed with Fabry disease should be screened based on the inheritance pattern.
Multimodality imaging can be helpful in the diagnosis of Fabry disease. Echocardiography can show left ventricular hypertrophy (LVH), reduced global strain, aortic and mitral valve thickening, and aortic root dilation with associated mild to moderate aortic regurgitation. Cardiac MRI can show hypertrophy of papillary muscles, mid-wall late gadolinium enhancement and low-native T1 signal.
The treatment of Fabry disease involves a multi-disciplinary approach with geneticists, nephrologists, cardiologists, nephrologists, and primary care doctors. Enzyme replacement therapy can delay the progression of cardiac disease.
Show Notes – An Unusual Cause of Hypertrophic Cardiomyopathy – Cleveland Clinic
What are the causes of left ventricular hypertrophy?
LVH is extremely common. It is present in 15-20% of the general population, and is more common in Black individuals, the elderly, obese or hypertensive individuals, with most cases being secondary to hypertension and aortic valve stenosis. In general terms, it is helpful to divide the causes of LVH into three main groups: high afterload states, obstruction to LV ejection, and intrinsic myocardial problems. Increased afterload states include both primary and secondary hypertension and renal artery stenosis. Mechanical obstruction includes aortic stenosis, subaortic stenosis, and coarctation of the aorta. Lastly, several intrinsic problems of the myocardium can cause LV hypertrophy, such as athletic heart with physiological LVH, hypertrophic cardiomyopathy with or without outflow obstruction, and infiltrative or storage diseases such as cardiac amyloidosis, Fabry’s disease, or Danon disease, among others.
How does Fabry disease present?
Fabry disease is present in all races and is an X-linked lysosomal storage disorder caused by pathogenic variants in the GLA gene that result in reduced alpha-galactosidase enzyme activity, leading to accumulation of lysosomal globotriaosylceramide (Gb3) globotriaosylsphingosine (lyso-Gb3) in affected tissues, including the heart, kidneys, vasculature, and peripheral nervous system. The reported incidence of this disease is said to be between 1 in 40,000 and 1 in 117,000 individuals, but screening in newborns suggests that this incidence may be underestimated, as it is present in up to 1 in 8,800 newborns. Depending on the variant of the mutation or the presence of mosaicism in females, the disease can have variable expression with early-onset presentations in the classical form or late-onset presentations in individuals who have residual a-galactosidase enzyme activity.
Fabry disease can have multiple cardiac and extracardiac manifestations. Accumulation of Gb3 occurs in all cell types of the heart, including smooth muscle cells of the endothelium, myocytes, conduction cells, and valvular fibroblasts. Accumulation of glycosphingolipids also leads to biochemical changes in cell function that lead to apoptosis, cellular necrosis, inflammation, and altered membrane ion channel properties that may lead to increased conduction velocities. In the myocardium, cell damage produces LVH and diastolic dysfunction. Damage to endothelial cells leads to coronary artery disease and myocardial ischemia. Together, these changes may eventually lead to myocardial fibrosis and systolic dysfunction. Involvement of the conduction cells can manifest as conduction abnormalities and ventricular arrhythmias. Other electrocardiographic findings are a short PQ interval or chronotropic incompetence. Aortic remodeling in FD has been well described and often presents as sinus of Valsalva dilatation or ascending aortic aneurysm, which in turn may lead to secondary aortic regurgitation.
Extracardiac manifestations of Fabry disease include neuropathy, gastrointestinal symptoms, angiokeratomas, cornea verticillata (golden-brown or gray discoloration of the corneal epithelium), hypohidrosis and exercise intolerance, proteinuria and renal failure, juvenile or cryptogenic stroke, hearing loss, chronic white matter hyperintensities in brain MRI, and lymphedema.
How is Fabry disease diagnosed?
Diagnosis of Fabry disease should be suspected in patients with unexplained LVH, especially when there are any extracardiac red flags. LVH presents in more than half of men and more than a third of women after the third decade of life. Other electrocardiographic findings besides high QRS voltages may include inferolateral negative T-waves, short PQ intervals, and a reduced P wave duration. The diagnosis is confirmed through genetic testing that may identify pathogenic variants as well as variants of unknown significance. Enzymatic level activities should be measured as well for confirmation. Absent or reduced alpha-galactosidase activity levels coupled with pathogenic variants in genetic testing confirm a diagnosis of FD. Variants of uncertain significance might require confirmation by endomyocardial biopsy and by lyso-Gb3 level assessment.
What is the role of cardiovascular imaging in the diagnosis of Fabry disease?
Multimodality imaging may be helpful in the diagnosis and staging of FD. Echocardiography typically reveals LVH with disproportionate hypertrophy of the papillary muscles, loss of base-to-apex circumferential strain gradient, and right-ventricular hypertrophy with normal systolic function. There may also be abnormal thickening of the aortic and mitral valves. Global longitudinal strain and speckle tracking may allow for early detection of cardiac involvement in patients with pathogenic variants.
Cardiac MRI (CMR) may help with tissue characterization. Typical CMR findings of FD include late gadolinium enhancement (LGE), initially in the basal inferolateral wall, and low native T1 signal intensity, likely reflecting glycosphingolipid myocardial storage and occurring before the development of significant LVH. Tissue characterization by CMR also allows for staging of FD cardiomyopathy in different and progressive stages of accumulation, with progressive lowering of T1 signal intensity; inflammation and hypertrophy, with low T1, initial LVH, and T2 mapping showing inflammation in the basal inferolateral segment associated with LGE; and fibrosis, with increasing T1 values or pseudo-normalization and LGE with wall thinning in the basal inferolateral segment.
What is the management for Fabry disease?
The main objective in the treatment of FD is prevention of disease progression and end-organ damage. The mainstay of therapy is enzyme replacement therapy (ERT) with agalsidase-alfa or beta intravenous injections every other week. Agalsidase-alfa is produced in human cell lines, while the beta form of the enzyme is produced by recombinant DNA technology using mammalian cells.
ERT is indicated in patients with late-onset FD who have the presence of laboratory, histological, or imaging evidence of injury to the heart, kidney, or central nervous system. It can delay the progression of cardiac disease and reduce the cardiovascular event rate in patients with FD.
Another available pharmacological agent is the chaperone agent migalastat, which can be helpful for specific genetic variants of FD by stabilizing the translated form of alpha-galactosidase. This chaperone agent is given in oral tablets every other day. There is ongoing development of novel therapies for FD with second-generation ERTs, substrate reduction therapies, and gene and mRNA therapies.
References – An Unusual Cause of Hypertrophic Cardiomyopathy – Cleveland Clinic
Weidemann F, Strotmann JM, Niemann M, et al. Heart Valve Involvement in Fabry Cardiomyopathy. Ultrasound in Medicine and Biology. 2009;35(5):730-735. doi:10.1016/j.ultrasmedbio.2008.10.010
Pieroni M, Moon JC, Arbustini E, et al. Cardiac Involvement in Fabry Disease: JACC Review Topic of the Week. Journal of the American College of Cardiology. 2021;77(7):922-936. doi:https://doi.org/10.1016/j.jacc.2020.12.024
Barbey F, Qanadli SD, Juli C, et al. Aortic remodelling in Fabry disease. European heart journal. 2010;31(3):347-353. doi:10.1093/eurheartj/ehp426
Chimenti C, Morgante E, Tanzilli G, et al. Angina in fabry disease reflects coronary small vessel disease. Circulation Heart failure. 2008;1(3):161-169. doi:10.1161/CIRCHEARTFAILURE.108.769729
Linhart A, Germain DP, Olivotto I, et al. An expert consensus document on the management of cardiovascular manifestations of Fabry disease. European Journal of Heart Failure. 2020;22(7):1076-1096. doi:https://doi.org/10.1002/ejhf.1960
Tower-Rader A, Jaber WA. Multimodality Imaging Assessment of Fabry Disease. Circulation Cardiovascular imaging. 2019;12(11):e009013. doi:10.1161/CIRCIMAGING.119.009013
Germain DP, Charrow J, Desnick RJ, et al. Ten-year outcome of enzyme replacement therapy with agalsidase beta in patients with Fabry disease. Journal of Medical Genetics. 2015;52(5):353 LP – 358. doi:10.1136/jmedgenet-2014-102797
Pieroni M, Moon JC, Arbustini E, et al. Cardiac Involvement in Fabry Disease: JACC Review Topic of the Week. J Am Coll Cardiol. 2021;77(7):922-936. doi:10.1016/J.JACC.2020.12.024
Maron BJ, Desai MY, Nishimura RA, et al. Diagnosis and Evaluation of Hypertrophic Cardiomyopathy: JACC State-of-the-Art Review. J Am Coll Cardiol. 2022;79(4):372-389. doi:10.1016/J.JACC.2021.12.002
Bornstein AB, Rao SS, Marwaha K. Left Ventricular Hypertrophy. StatPearls [Internet] Treasure Island (FL). Published online August 8, 2022. Accessed April 1, 2023. https://www.ncbi.nlm.nih.gov/books/NBK557534/
51 min
December 08, 2023348. Case Report: An Interesting Intersection of Cardiology and Hematology/Oncology – Guthrie Robert Packer Hospital
CardioNerds (Daniel Ambinder) joins Dr. Priyanka Ghosh and Dr. Ahmad Lone from the Guthrie Robert Packer Hospital for a day in the Finger Lakes region of New York. They discuss the following case. A 35-year-old man with nonspecific symptoms of headache, fatigue, and chest wall pain was found to have elevated troponin levels, elevated inflammatory markers, EKG with inferior and anterolateral ST depressions, and no obstructive coronary artery disease on cardiac catheterization. His peripheral eosinophilia, cardiac MRI results, and bone marrow biopsy revealed eosinophilic myocarditis from acute leukemia with eosinophilia. This episode discusses this rare type of myocardial inflammation, its potential causes, and the diagnostic workup with the mention of how this patient was ultimately treated for his acute leukemia and myocarditis. Expert commentary is provided by Dr. Saurabh Sharma. Audio editing by CardioNerds academy intern, student doctor Pace Wetstein.
“To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all.” – Sir William Osler. CardioNerds thank the patients and their loved ones whose stories teach us the Art of Medicine and support our Mission to Democratize Cardiovascular Medicine.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Case Media – Guthrie Robert Packer Hospital
Pearls – Guthrie Robert Packer Hospital
Myocarditis, especially eosinophilic myocarditis, requires a high level of clinical suspicion.
Eosinophilic myocarditis should be considered in a patient presenting with chest pain, normal coronary arteries, and pronounced eosinophilia levels.
Causes of eosinophilic myocarditis can vary, and diagnosis requires a thorough, detailed history, which cannot be determined many times.
Treatment of eosinophilic myocarditis focuses on the underlying etiology, acute management, and therapy for concomitant heart failure or cardiomyopathy.
Consider the whole-patient and cardiac manifestations of non-cardiac illnesses.
Show Notes – Guthrie Robert Packer Hospital
What is eosinophilic myocarditis?
Eosinophilic myocarditis is a type of myocardial inflammation involving eosinophilic cell infiltration and an entity that is likely under-recognized. It requires a high level of suspicion as, many times, patients may not initially present with peripheral eosinophilia, which may develop over the course of their disease process. The presentation can vary from mild cardiac injury to fulminant cardiogenic shock depending on the degree of infiltration and concurrent other organ involvement. The presentation can include heart failure symptoms as well as electrical conduction abnormalities.
How is eosinophilic myocarditis diagnosed?
Eosinophilic myocarditis is diagnosed by a thorough history including new medications, exposures, travel, prior allergy history, physical exam, lab work including a complete blood count differential, inflammatory markers, cardiac biomarkers, and cardiac diagnostics which should include a 12-lead ECG and transthoracic echocardiogram as well as potentially cardiac MRI and/or endomyocardial biopsy.
What are the causes of eosinophilic myocarditis?
The causes of eosinophilic myocarditis include medication-induced, hypersensitivity reactions, infections, malignancy, and immune-mediated disorders such as eosinophilic granulomatosis with polyangiitis and hypereosinophilic syndromes. The hypersensitivity subtype has been reported to be the most common cause. Potential offending medications can include antibiotics, sulfonamides, anticonvulsants, anti-inflammatory medications, and diuretics.
What is the treatment for eosinophilic myocarditis?
Treatment for eosinophilic myocarditis is multi-faceted, including focusing on the etiology and withdrawal of any potential offending agents, management of the acute clinical presentation, and treatment of any concomitant heart failure or cardiomyopathy. Immunosuppressive therapy has been controversial; however, many case reports have successfully used methylprednisolone, and some patients with cardiogenic shock from eosinophilic myocarditis have received therapy with azathioprine.
References
Al Ali AM, Straatman LP, Allard MF, Ignaszewski AP. Eosinophilic myocarditis: case series and review of literature. Can J Cardiol. 2006 Dec;22(14):1233-7. doi: 10.1016/s0828-282x(06)70965-5. PMID: 17151774; PMCID: PMC2569073.
Takkenberg JJ, Czer LS, Fishbein MC, Luthringer DJ, Quartel AW, Mirocha J, Queral CA, Blanche C, Trento A. Eosinophilic myocarditis in patients awaiting heart transplantation. Crit Care Med. 2004 Mar;32(3):714-21. doi: 10.1097/01.ccm.0000114818.58877.06. PMID: 15090952.
Morimoto S, Kubo N, Hiramitsu S, Uemura A, Ohtsuki M, Kato S, Kato Y, Sugiura A, Miyagishima K, Mori N, Yoshida Y, Hishida H. Changes in the peripheral eosinophil count in patients with acute eosinophilic myocarditis. Heart Vessels. 2003 Sep;18(4):193-6. doi: 10.1007/s00380-003-0721-0. PMID: 14520487.
Burke AP, Saenger J, Mullick F, Virmani R. Hypersensitivity myocarditis. Arch Pathol Lab Med. 1991 Aug;115(8):764-9. PMID: 1863186.
Fozing T, Zouri N, Tost A, Breit R, Seeck G, Koch C, Oezbek C. Management of a patient with eosinophilic myocarditis and normal peripheral eosinophil count: case report and literature review. Circ Heart Fail. 2014 Jul;7(4):692-4. doi: 10.1161/CIRCHEARTFAILURE.114.001130. PMID: 25028351.
Brambatti M, Matassini MV, Adler ED, Klingel K, Camici PG, Ammirati E. Eosinophilic Myocarditis: Characteristics, Treatment, and Outcomes. J Am Coll Cardiol. 2017 Nov 7;70(19):2363-2375. doi: 10.1016/j.jacc.2017.09.023. PMID: 29096807.
Cheung CC, Constantine M, Ahmadi A, Shiau C, Chen LYC. Eosinophilic Myocarditis. Am J Med Sci. 2017 Nov;354(5):486-492. doi: 10.1016/j.amjms.2017.04.002. Epub 2017 Apr 6. PMID: 29173361.
Aggarwal A, Bergin P, Jessup P, Kaye D. Hypersensitivity myocarditis presenting as cardiogenic shock. J Heart Lung Transplant. 2001 Nov;20(11):1241-4. doi: 10.1016/s1053-2498(01)00313-8. PMID: 11704488.
Kounis NG, Zavras GM, Soufras GD, Kitrou MP. Hypersensitivity myocarditis. Ann Allergy. 1989 Feb;62(2):71-4. PMID: 2645814.
Li H, Dai Z, Wang B, Huang W. A case report of eosinophilic myocarditis and a review of the relevant literature. BMC Cardiovasc Disord. 2015 Feb 26;15:15. doi: 10.1186/s12872-015-0003-7. PMID: 25887327; PMCID: PMC4359588.
32 min

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