103. Case Report: A Rare Cause of Postpartum Angina and Arrest – University of Maryland

CardioNerds (Amit Goyal & Daniel Ambinder) join University of Maryland cardiology fellows (Manu Mysore, Adam Zviman, and Scott Butler) for some cardiology and an Orioles game in Baltimore! They discuss a rare cause of postpartum angina and cardiac arrest due to coronary vasculitis. Program director Dr. Mukta Srivastava provides the E-CPR expert segment and a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Rick Ferraro with mentorship from University of Maryland cardiology fellow Karan Desai.

This case has been published in JACC Case Reports!

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Ep 103 Coronary Vasculitis University of Maryland
Episode graphic by Dr. Carine Hamo


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Patient Summary

A woman in her early 30s with a past medical history of Hashimoto’s thyroiditis and one prior miscarriage at <8 weeks presented with chest pain about 6 weeks postpartum from the birth of her third child. In the ED, she continued to report intermittent sharp chest discomfort and found to have a diastolic decrescendo murmur at the left upper sternal border and labs demonstrating a troponin-I of 0.07 ng/dL. Join the UMD Cardionerds for the incredible course and story of this young patient as we go through the differentia and approach to postpartum chest pain and ultimately arrive in a very rare diagnosis!   For a detailed course, enjoy the JACC case report.


Case Media

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Episode Schematics & Teaching


The CardioNerds 5! – 5 major takeaways from the #CNCR case

1. How Do We Evaluate Chest Pain in Younger Patients 

  • Start with the same things as everyone else!  Think broadly about the big three concerning etiologies of chest pain: Cardiac, Gastric, and Pulmonary (The excellent Clinical Problems Solvers 4+2+2 construct here is always a great resource. Find them at: https://clinicalproblemsolving.com/dx-schema-chest-pain/).   
  • Of course it is important to think about non-life threatening etiologies as well – esophageal spasm, gastric ulcer, rib fracture, skin lesion, among many others – given that high-risk chest pain is less likely in younger adults.  
  • While less common, acute coronary syndrome is not uncommon in young patients, as 23% of patients with MI present at age <55 years.  

2. What About Chest Pain in Women?  

  • As has been discussed on the Cardionerds podcast (Listen to episodes with Dr. Nanette Wenger, Dr Martha Gulati, and Dr. Leslie Cho), women generally present with acute coronary syndrome at a later age, with a higher burden of risk factors than men, and with greater symptom burden but are less likely to be treated with guideline-directed medical therapies, undergo cardiac catheterization and receive timely reperfusion. In one study of young patients with acute MI, women – 19% of cases overall – were less likely to undergo revascularization or receive guideline-directed therapy 
  • The construct of classifying chest pain as “typical” and “atypical” likely leads to misdiagnosis or delayed diagnosis of acute myocardial infarction in women. Rather, it is important to recognize that while symptoms may not be “typical” for angina, coronary disease can manifest in many different ways.  
  • While many women will presents with chest pain suggestive of angina, women are more likely than men to present with dyspnea, indigestion, weakness, nausea/vomiting and/or fatigue. Note, shoulder pain and arm pain are twice as predictive of an acute myocardial infarction diagnosis in women compared with men.  
  • Furthermore, while obstructive epicardial disease remains the primary cause of acute MI in young women, it is also important to keep other causes of chest pain such as MINOCA, SCAD (see the UCLA episode), peripartum cardiomyopathy (see the Penn and MCW episodes), or coronary vasculitis on the differential. While these etiologies are rare, they are disproportionately represented in young women.  

3. How do we think about categorizing vasculitis? 

  • Vasculitis is a broad term encompassing many forms of vessel wall (including arteries, veins or capillaries) inflammation.  This can be secondary to autoimmunity, infection, drug reaction, and malignancy to name a few underlying causes.  
  • Generally vasculitis is divided by large vessel (e.g., Takayasu, Giant Cell), medium vessel (e.g., Polyarteritis Nodosa), and small vessel etiologies (e.g., Granulomatosis with Polyangitis, Eosinophilic Granulomatosis with Polyangiitis, Microscopic Polyangitis, Immune-mediated Vasculitis, amongst others). This characterization follows the 2012 Revised International Chapel Hill Consensus Conference Nomenclature of Vasculitis.  
  • Other important categories includes variable vessel vasculitis (e.g., Behcet’s Disease, Cogan’s Syndrome) and vasculitis associated with systemic disease (e.g., Lupus vasculitis, Rheumatoid vasculitis, Sarcoid vasculitis).  

4. What Does Vasculitis Look Like in the Heart? 

  • While inflammation can occur throughout the heart – e.g., pericarditis or myocarditis – vasculitis in the heart refers specifically to inflammation of the coronary arteries. This is a relatively rare process, with <10% of vasculitis patients exhibiting cardiac involvement.  
  • Patients with coronary vasculitis rarely present with isolated coronary involvement and typically have systemic manifestations, such as constitutional symptoms in addition to cardiac symptoms (e.g., angina, heart failure, arrhythmia). Examination may reveal asymmetric pulses or BP readings between limbs and arterial bruits, with imaging revealing multi-organ infarcts without a clear embolic origin. Amongst the vasculitides, Takayasu Arteritis (TA) is one of the more frequent etiologies of coronary arteritis.  
  • In Takayasu Arteritis (TA), the affected arteries are typically the aorta and its major branches. In contrast to giant cell arteritis (GCA), TA is quite rare and tends to have onset <40 years age; however, for both diagnoses coronary involvement is rare. TA patients will typically have constitutional symptoms and may have diminished/absent arterial pulses often accompanied by bruits. Weakness of the arterial walls may lead to aneurysms and specifically aortic root aneurysm may result in aortic valve insufficiency. When involving the coronaries, there are three main type of TA lesions: stenosis or occlusion of the ostia/proximal segments (Type 1); diffuse or focal coronary vasculitis involving all the epicardial branches or focal areas (Type 2); coronary aneurysms (Type 3). 

5. What Are the Complications of Coronary Vasculitis?  

  • The consequences of coronary vasculitis are variable and much of the data we have comes from case reports. As in the case presented, severe coronary ischemia and its complications, including arrhythmia and cardiac arrest, are a major concern. However, cardiac arrest is rarely the first presentation of coronary vasculitis, especially if it is detected early. The manifestations of coronary vasculitis are also going to be dependent on the specific etiology of the arteritis.  
  • Amongst the medium vessel vasculitis and specifically polyarteritis nodosa, 15-20% of patients will have cardiac involvement, with major complications including heart failure, myocardial infarction, or arrhythmia.  
  • Amongst the small vessel vasculitis, eosinophilic granulomatosis with polyangiitis is the most common culprit for cardiac involvement, primarily secondary to eosinophilic toxicity. Cardiac involvement is a major cause of mortality and poor prognostic sign in EGPA. 

The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus.

We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director.

Cardionerds Cardiology Podcast Presents CardioNerds Case Report Series

References

  1. Kostner, M. J., & Warrington, K. J. (2019, March 13). Vasculitis of the Coronary Arteries. ACC.org. 
  2. Ward, E. V., Nazari, J., & Edelman, R. R. (2012). Coronary artery vasculitis as a presentation of cardiac sarcoidosis. Circulation125(6), e344-e346. 
  3. Awad, H. H., McManus, D. D., Anderson Jr, F. A., Gore, J. M., & Goldberg, R. J. (2013). Young patients hospitalized with an acute coronary syndrome. Coronary Artery Disease24(1), 54-60. 
  4. Bugiardini, R., Cenko, E. (2020). Sex differences in myocardial infarction deaths. Lancet, 396:72–73 
  5. DeFilippis, E.M., Collins, B.L., Singh A., et. al Women who experience a myocardial infarction at a young age have worse outcomes compared with men: the Mass General Brigham YOUNG-MI registry, European Heart Journal, ehaa662 
  6. Miloslavsky, E., & Unizony, S. (2014). The heart in vasculitis. Rheumatic Disease Clinics40(1), 11-26. 
  7. Mehta LS, Beckie TM, DeVon HA et al; American Heart Association Cardiovascular Disease in Women and Special Populations Committee of the Council on Clinical Cardiology, Council on Epidemiology and Prevention, Council on Cardiovascular and Stroke Nursing, and Council on Quality of Care and Outcomes Research. (2016) Acute Myocardial Infarction in Women: A Scientific Statement From the American Heart Association. Circulation. Mar 1;133(9):916-47. doi: 10.1161/CIR.0000000000000351.  

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94. Case Report: Altered Mental Status & Electrical Instability: DIGging through the Differential – University of Illinois at Chicago

CardioNerds (Amit Goyal & Karan Desai) join University of Illinois at Chicago cardiology fellows (Brody Slostad, Kavin Arasar, and Mary Rodriguez-Ziccardi) for a cup of tea from atop Hancock Tower! They discuss an illuminating case of altered mental status & electrical instability due to digitalis poisoning. Program director Dr. Alex Auseon and APD Dr. Mayank Kansal provide the E-CPR and a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai.  

Jump to: Patient summaryCase mediaCase teachingReferences

CardioNerds (Amit Goyal & Karan Desai) join University of Illinois at Chicago cardiology fellows (Brody Slostad, Kavin Arasar, and Mary Rodriguez-Ziccardi) for a cup of tea from atop Hancock Tower! They discuss an illuminating case of altered mental status & electrical instability due to digitalis poisoning. Program director Dr. Alex Auseon and APD Dr. Mayank Kansal provide the E-CPR and a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai.
Episode graphic by Dr. Carine Hamo

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Patient Summary

A woman in her late 80s with history of systemic arterial hypertension and dementia presented with 2 weeks of nausea, vomiting, confusion, and yellow-tinted vision. When she presented to the hospital, initial history was limited as her caregiver was unaware of her medications and medical history. An initial ECG showed isorhythmic A-V dissociation and scooping ST segments laterally. Given her clinical history, this raised the suspicion for Digoxin toxicity, and a serum digoxin level was significantly elevated. However, this was not a home medication for the patient, nor did she have access to it! Listen to the episode now as the UIC Cardionerds masterfully take us through this case that would surely stump Dr. House!  


Case Media

through the Differential

A. Initial ECG
B. CXR- Patchy opacities of the left lower lobe consistent with pulmonary edema and/or aspiration​ pneumonia.
C. Repeat ECG: AF with AV block, persistent scooped T waves​
D. Post arrest ECG: Flutter/fib with AV block, VERY LONG PAUSES up to 6 seconds
E. ECG post TVP: A flutter, slow V response (pacing picking up), intrinsic ventricular rate 20-40, PM set to 50 bpm
F. Most recent ECG: Normal sinus rhythm

TTE

Episode Schematics & Teaching

The CardioNerds 5! – 5 major takeaways from the #CNCR case

1) This episode featured a challenging case of digitalis toxicity. Cardionerds, what is the mechanism of action of cardiac glycosides?  

  • Cardiac Glycosides (such as digoxin, digitalis, and oubain), inhibit the myocardial Na/K ATPase pump. This leads to an increased concentration of intracellular sodium, which then drives the influx of calcium into cardiac myocytes via the Na/Ca exchanger. This increase in intracellular calcium leads to further calcium release from the sarcoplasmic reticulum making even more calcium available to bind to troponin, increasing contractility. 
  • In addition to their effect on inotropy, cardiac glycosides increase vagal tone, reducing SA node activity and slowing conduction through the AV node by increasing the refractory period 

2) The first published account of digitalis to treat heart failure dates back to the 18th century, when botanist and physician William Withering published “An account of the Foxglove and some of its medical uses with practical remarks on dropsy, and other diseases”. A lot has changed over the years; what are some of the uses of digoxin in the modern day?  

  • The DIG trial (1997) demonstrated a reduction in hospitalizations in patients with HFrEF treated with digoxin. However, no impact on mortality was shown. A major limitation from randomized trials of digoxin is the lack of contemporary background HF treatment (e.g., ARNI, SGLT2i, MRA, Device Therapy). Thus, its role in modern HFrEF management is typically limited to reducing hospitalizations in patients with persistent NYHA Class III or IV symptoms despite maximally tolerated guideline-directed medical therapy 
  • Digoxin can also be used for acute or chronic rate control in atrial fibrillation, and may be particularly useful in patients with RVR refractory to beta blockers/calcium channel blockers or in those patients who cannot tolerate these agents due to hypotension. Notably, data from the ARISTOTLE trial (2018) showed a significant mortality increase was seen in patients with a digoxin level ≥1.2 ng/ml, while no increase in mortality was seen with levels <0.9 ng/ml.  
  • Recent data from the small, randomized RATE-AF trial showed no difference in quality of life and similar heart rate control in older patients with permanent atrial fibrillation and heart failure symptoms. Thus, while the therapeutic window may be limited, there remains a role for digoxin in the treatment of HFrEF, Afib, or both. 

3) While digoxin can be given in HFrEF and/or AF, its use is limited by its side-effects and potential toxicity. What are the clinical manifestations of digitalis toxicity?  

  • Arrhythmia: Digitalis toxicity can cause virtually any atrial or ventricular arrhythmia. More to come in take-away #4! 
  • GI: Acute toxicity is associated with nausea, vomiting, abdominal pain. Meanwhile, chronic toxicity can be more subtle with less pronounced nausea, anorexia and weight loss developing over weeks to months.  
  • Neuro: Alterations in color vision (chromatopsia), particularly seeing a yellow hue, can be specific for digitalis poisoning. Headache, fatigue, lethargy and altered mental status can also occur.  

4) Lets dig a little deeper into digoxin induced arrhythmias; why is digoxin so arrhythmogenic, and what are the most common electrical manifestations?  

  • By inhibiting the  Na/K ATPase pump, digoxin increases intracellular sodium and calcium levels, as well as extracellular potassium. These electrolytes shifts, in addition to the increased parasympathetic activity, lead to Digoxin’s arrhythmogenicity.  
  • Generally, younger patients develop bradyarrythmias due to increased vagal tone, while older patients who may have pre-existing cardiac disease are more likely to develop tachyarrythmias.  
  • Influx of calcium into the cardiac myocyte leads to delayed afterdepolarizations in phase 4 of the ventricular action potential, which can trigger ventricular tachycardia.  
  • Digoxin also increases atrial pacemaker cell automaticity, leading to an increase in atrial arrythmias. This occurs via an increase in the slope of phase 4 of the pacemaker action potential (decreasing the time to depolarization), lowering the depolarization threshold, and increasing the resting potential. 
  • While ectopic atrial tachycardia with AV block and bidirectional VT are associated with digoxin toxicity, virtually any arrhythmia can be seen in digitalis toxicity. However, atrial fibrillation and flutter are less likely to be induced by digoxin toxicity.  

5) Now that we’ve established all the effects and side-effects of digoxin, lets wrap up with some points on treating cardiac glycoside toxicity! 

  • The mainstay of therapy for acute and/or severe digoxin toxicity is digoxin-specific antibody (Fab) fragments. Empiric treatment for adults with imminent cardiac arrest or ingestion of an unknown amount of digoxin consists of 10 vials, with each vial binding approximately 0.5mg of digoxin.  
  • Indications for Fab fragments aside from acute overdose include: 
    • Hemodynamically unstable arrythmias 
    • Hyperkalemia 
    • Evidence of end-organ damage from hypoperfusion 
  • Notably, the serum digoxin concentration alone does not dictate Fab fragment treatment. Additionally, in patients with severe renal impairment, Fab fragments may be ineffective and may provide a false sense of benefit. The manifestations of digoxin toxicity may improve initially in these patients given Fab; however, recurrent toxicity can occur weeks later as digoxin moves from peripheral tissues.  
  • While other cardiac glycosides have cross-reactivity with digoxin and can be treated with Fab fragments, dosing can be challenging due to lack of correlation between serum digoxin level and cardiac glycoside activity. 
  • Potassium homeostasis in digoxin toxicity is nuanced. Hyperkalemia, as a result of Na-K ATPase inhibition, is a predictor of mortality in acute toxicity. After Fab fragments are given, hyperkalemia is often rapidly corrected, and over-aggressive treatment of hyperkalemia in the setting of acute toxicity may ultimately lead to hypokalemia once Fab fragments are given.  

References

  1. Digitalis Investigation Group (1997). The effect of digoxin on mortality and morbidity in patients with heart failure. The New England journal of medicine, 336(8), 525–533. 
  2. Lopes, R. D., Rordorf, R., De Ferrari, G. M., et al. (2018). Digoxin and Mortality in Patients With Atrial Fibrillation. Journal of the American College of Cardiology, 71(10), 1063–1074.  
  3. Chen, J. Y., Liu, P. Y., Chen, J. H., & Lin, L. J. (2004). Safety of transvenous temporary cardiac pacing in patients with accidental digoxin overdose and symptomatic bradycardia. Cardiology, 102(3), 152–155. 
  4. Taboulet, P., Baud, F. J., Bismuth, C., & Vicaut, E. (1993). Acute digitalis intoxication–is pacing still appropriate?. Journal of toxicology. Clinical toxicology, 31(2), 261–273.  

The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus.

We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director.

Cardionerds Cardiology Podcast Presents CardioNerds Case Report Series

CardioNerds Case Reports: Recruitment Edition Series Production Team

90. Case Report: Atrioesophageal Fistula (AEF) Formation after Pulmonary Vein Isolation – Thomas Jefferson University Hospital

CardioNerds (Amit Goyal) joins Thomas Jefferson cardiology fellows (Jay Kloo, Preya Simlote and Sean Dikdan – host of the Med Lit Review podcast) for some amazing craft beer from Independence Beer Garden in Philadelphia! They discuss a fascinating case of atrioesophageal fistula (AEF) formation after pulmonary vein isolation (PVI). Dr. Daniel Frisch provides the E-CPR and program director Dr. Gregary Marhefka provides a message for applicants. Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai.  

Jump to: Patient summaryCase mediaCase teachingReferences

CardioNerds (Amit Goyal) joins Thomas Jefferson cardiology fellows (Jay Kloo, Preya Simlote and Sean Dikdan - host of the Med Lit Review podcast) for some amazing craft beer from Independence Beer Garden in Philadelphia! They discuss a fascinating case of atrioesophageal fistula (AEF) formation after pulmonary vein isolation (PVI). Dr. Daniel Frisch provides the E-CPR and program director Dr. Gregary Marhefka provides a message for applicants. Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai.
Episode graphic by Dr. Carine Hamo

The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus.

We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director.

CardioNerds Case Reports Page
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Support our educational mission by becoming a Patron!
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Patient Summary

A mid 60s male with relevant PMHx of paroxysmal atrial fibrillation presents to the ED with altered mental status after one week of mild chest pain. Given the long history of atrial fibrillation refractory to rate and rhythm control with diltiazem and flecainide, he underwent a pulmonary vein isolation 21 days prior to arrival. In the ED, T 39.4 and patient had a witnessed seizure requiring intubation for airway protection. Signs of hypoperfusion on labs, but white blood cell count not elevated. LP negative, but blood cultures positive for strep agalactiae. CT head with multiple tiny foci of intravascular air throughout the brain with MRI consistent with multiple areas of acute infarction. CTA of chest then obtained, which was notable for a small focus of air tracking along the esophagus. Taken together, findings most c/w atrial esophageal fistula causing sepsis and air emboli. Patient underwent surgical repair of left atrium and esophagus with a good outcome. 


Case Media

A. ECG: Normal sinus rhythm HR 105 bpm
B. CXR
C. CT head: Multiple tiny foci of air throughout bilateral cerebral hemispheres. Appearance is most suggestive of intravascular air, although it is unclear if it is venous, arterial or both.
D. MRI: 1. Restricted diffusion in bilateral cortical watershed zones, as well as in the posterior medial left cerebellar hemisphere, most consistent with recent infarctions.
E. CT Chest: A small focus of air tracking along the left mainstem bronchus anterior to the esophagus, may represent a small amount of pneumomediastinum versus air in an outpouching of the esophagus. No air tracking more cranially along the mediastinal soft tissues. No definite soft tissue defect in the esophagus.
F. Surgical repair of LA & Esophagus


Episode Schematics & Teaching

Coming soon!


The CardioNerds 5! – 5 major takeaways from the #CNCR case

Coming soon!


References

Coming soon!


CardioNerds Case Reports: Recruitment Edition Series Production Team

89. Case Report: Cardiac Arrest associated with Mitral Valve Prolapse with Mitral Annular Disjunction – Oregon Health & Science University

CardioNerds (Amit Goyal & Daniel Ambinder) join Oregon Health & Science University cardiology fellows (Miranda Merrill, Timothy Simpson, Kris Kumar, and Stacey Howell) for a riverside chat at the Portland waterfront! They discuss a case of cardiac arrest associated with mitral valve prolapse (MVP) with mitral annular disjunction (MAD). Dr. Punag Divanji provides the E-CPR and program director Dr. Hind Rahmouni provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident, Eunice Dugan, with mentorship from University of Maryland cardiology fellow Karan Desai.  

Jump to: Patient summaryCase mediaCase teachingReferences

CardioNerds (Amit Goyal & Daniel Ambinder) join Oregon Health & Science University cardiology fellows (Miranda Merrill, Timothy Simpson, Kris Kumar, and Stacey Howell) for a riverside chat at the Portland waterfront!  They discuss a case of cardiac arrest associated with mitral valve prolapse (MVP) with mitral annular disjunction (MAD). Dr. Punag Divanji provides the E-CPR and program director Dr. Hind Rahmouni provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident, Eunice Dugan, with mentorship from University of Maryland cardiology fellow Karan Desai.
Episode graphic by Dr. Carine Hamo

The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus.

We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director.

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Subscribe to our newsletter- The Heartbeat
Support our educational mission by becoming a Patron!
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Patient Summary

Coming soon!


Case Media

A. CXR
B. Rhythm Strips – ventricular fibrillation
C. ECG: 1st degree AVB (PR ~ 215), borderline RAD, Qtc ~460 msec, slight ant. convexity with inferior terminal T wave
D: TTE
E: TTE with Pickelhaube Spike seen in mitral valve prolapse
F-G: Cardiac MRI

TTE 1
TTE 2
TTE 3
Cardiac MRI

Episode Schematics & Teaching

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The CardioNerds 5! – 5 major takeaways from the #CNCR case

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References

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87. Case Report: Giant Coronary Aneurysm Presenting with Heart Failure – University of Hawaii

Aloha! CardioNerds (Amit Goyal & Karan Desai)  join University of Hawaii cardiology fellows (Isaac Mizrahi, Nath Limpruttidham, Nishant Trivedi, and Shana Greif) for some shaved iced on the Big Island’s north shore! They discuss a fascinating case of a patient presenting with decompensated heart failure found to have a giant coronary aneurysm. Program director Dr. Dipanjan Banerjee provides the E-CPR as well as a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai.  

Jump to: Patient summaryCase mediaCase teachingReferences

Aloha! CardioNerds (Amit Goyal & Karan Desai)  join University of Hawaii cardiology fellows (Isaac Mizrahi, Nath Limpruttidham, Nishant Trivedi, and Shana Greif) for some shaved iced on the Big Island's north shore! They discuss a fascinating case of a patient presenting with decompensated heart failure found to have a giant coronary aneurysm. Program director Dr. Dipanjan Banerjee provides the E-CPR as well as a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai.
Episode graphic by Dr. Carine Hamo

CardioNerds Case Reports Page
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Subscribe to our newsletter- The Heartbeat
Support our educational mission by becoming a Patron!
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Patient Summary

A man in his early 60s with history of hypertension, peripheral arterial disease, atrial fibrillation, and AAA s/p repair presented with subacute fatigue, palpitations, shortness of breath, and lower extremity edema. On exam he was warm and well perfused, though hypotensive, tachycardic with an irregular rhythm, and had an elevated JVP. ECG showed AF with RVR without evidence of acute MI, and troponin was negative. TTE revealed a reduced LVEF and WMA in the inferolateral walls with akinesis of the basal mid septum; additionally, two large extracardiac structures were noted, one with heterogenous echotexture in the AV groove, and a second with an echolucent interior adjacent to the RA.  

The patient underwent coronary angiography, showing a dilated and calcified proximal LAD with high grade stenosis adjacent to the first septal perforator, a ectatic LCX that supplied left to right collaterals, and a giant RCA aneurysm with TIMI 0 flow distally. CCTA confirmed these findings, showing thrombosed aneurysms of the LAD, LCX, and RCA. Interventional cardiology and cardiac surgery both evaluated the patient’s case, and determined that he was not a candidate for intervention. He was ultimately diuresed to euvolemia with significant improvement in symptoms, and plans to follow-up as an outpatient for heart transplant evaluation.  


Case Media

A. CXR
B. ECG: atrial fibrillation with RVR, left axis deviation, poor r wave progression
C. Wide complex tachycardia
D. CT chest demonstrating giant aneurysm

TTE
Coronary Angiography

Episode Schematics & Teaching

Coming soon!


The CardioNerds 5! – 5 major takeaways from the #CNCR case

1) This case featured a patient with a giant coronary aneurysm – how are coronary artery aneurysms defined and classified?  

  • Coronary artery aneurysms (CAA) are defined as a focal dilation of a coronary segment at least 1.5x the adjacent normal segment. Contrast this with coronary artery ectasia, which refers to a diffuse, as opposed to focal, coronary dilation.  
  • CAA morphology can be classified as either saccular (transverse > longitudinal diameter) or fusiform (transverse < longitudinal diameter). 
  • Giant CAA’s are >20mm in diameter. 
  • Aortocoronary saphenous vein graft aneurysms have distinct characteristics and natural history compared to native coronary aneurysms. These aneurysms tend to present late (e.g., > 10 years following CABG) and tend to be larger than native CAA. 
  • IVUS can help differentiate between a true aneurysm with preserved integrity of all 3 vessel layers (intima, media, and adventitia) and a pseudoaneurysm with loss of wall integrity and damage to the adventitia. 

2) Now that we have the language to define and classify coronary artery aneurysms, what are some causes these lesions?  

  • Atherosclerosis: lipid deposition, focal calcification, and fibrosis can weaken the vessel wall and predispose to subsequent coronary artery dilation. Up to 50% of CAAs are linked to arteriosclerosis.  
  • Autoimmune/inflammatory processes: Lupus and systemic vasculitis, such as Kawasaki’s disease and Takayasu arteritis, can all lead to CAAs. Vasculitic CAAs usually affect more than one artery.  
  • Connective Tissue Disease: Marfan’s syndrome and Ehlers-Danlos disease, for instance, are characterized by deficiencies in vessel wall integrity, leading to CAAs. 
  • Dynamic Wall StressEpisodic hypertension and vasoconstriction, such as that seen in frequent cocaine use, can lead to wall stress, endothelial damage, and coronary artery aneurysms.  
  • Direct Vessel Wall Injury: Intracoronary interventions, such as angioplasty, stent delivery, and brachytherapy, can cause shear wall stress that leads to CAAs.  
  • Infectious Causes: Direct vessel wall invasion or immune complex deposition can be seen in bacterial, mycobacterial, fungal, and syphilitic infections. Septic emboli from infectious endocarditis can also lead to mycotic coronary aneurysms.  
  • Genetic susceptibility: Certain HLA class II genotypes are susceptible to CAAs. This may be the underlying pathology in certain idiopathic and congenital CAAs.  

3) How do coronary artery aneurysms clinically present? 

  • Most CAAs are asymptomatic, and are found incidentally on coronary angiography or CCTA.  
  • Concomitant obstructive arteriosclerosis can cause angina or plaque rupture, and thrombosis in the aneurysm lumen can lead to distal embolization and myocardial infarction.  
  • Massive enlargement of CAAs and saphenous vein graft aneurysms can compress adjacent structures. 
  • CAA rupture is rare, though can cause cardiac tamponade.  
  • Stress-induced myocardial ischemia can also occur due to microvascular dysfunction  

4) How do we diagnosis and assess CAAs? 

  • Most CAAs are evaluated via coronary angiography, though a complete angiographic evaluation can be complicated by delayed antegrade contrast filling, segmental back flow, and contrast stasis. In giant aneurysms, a forceful and prolonged contrast injection is needed to avoid misinterpreting slow aneurysmal filling as thrombosis.  
  • IVUS can help differentiate between true aneurysms, pseudoaneurysms, and coronary segments with aneurysmal appearance due to plaque rupture or stenosis. Furthermore, IVUS can assist in sizing aneurysm and planning for potential PCI.  
  • Coronary CTA noninvasively allows for a more accurate assessment of aneurysm size and degree of thrombus than angiography. CCTA is particularly useful in patients with giant CAA as it can provide an understanding of mechanical complications of these aneurysms.  

5) How are coronary artery aneurysms managed?  

  • Notably, there is a lack of randomized and large-scale trial data to guide the treatment of CAAs; most recommendations are made on the basis of small case series and expert opinion.  
  • Medical Management: Given the association between CAA and arteriosclerosis, risk factor modification should be emphasized. The role of antiplatelet and anticoagulant agents is an area of ongoing debate, though there may be benefit in patients with multivessel ectasia. Furthermore, the context in which the patient presents (e.g., incidental finding vs. acute coronary syndrome) will guide the antiplatelet and/or anticoagulant strategy.  
  • Invasive (Percutaneous) Management: PCI of an aneurysmal vessel in the setting of acute MI is associated with lower rates of procedural success, and higher rates of distal embolization and no-reflow phenomenon. Additionally, these patients have higher rates of stent thrombosis and mortality. Given the higher thrombus burden in aneurysmal arteries, thrombectomy may be helpful in aiding PCI. Some case studies have additionally utilized intracoronary thrombolytics. Another strategy is a stent-assisted coil embolization technique in cases where covered stent placement is not possible due to tortuosity, calcification, or risk of side branch compromise. To date, there haven’t been covered stents specifically designed for CAAs, but stents have been used off-label. 
  • Surgical Management: The most common operative strategy is to open the aneurysm, suture the afferent and efferent vessels, and finish with bypass grafting if possible. Other operative strategies include aneurysm ligation, resection, or marsupialization with interposition graft.

References

  1. Thibodeau, J. T., & Drazner, M. H. (2018). The Role of the Clinical Examination in Patients With Heart Failure. JACC. Heart failure, 6(7), 543–551.  
  2. Abou Sherif, S., Ozden Tok, O., Taşköylü, Ö., et al. (2017). Coronary Artery Aneurysms: A Review of the Epidemiology, Pathophysiology, Diagnosis, and Treatment. Frontiers in cardiovascular medicine, 4, 24. 
  3. Kawsara, A., Núñez Gil, I. J., Alqahtani, F., et al. (2018). Management of Coronary Artery Aneurysms. JACC. Cardiovascular interventions, 11(13), 1211–1223.  
  4. Newburger, J. W., Takahashi, M., & Burns, J. C. (2016). Kawasaki Disease. Journal of the American College of Cardiology, 67(14), 1738–1749.  
  5. McCrindle, B. W., Rowley, A. H., Newburger, J. W., et al. (2017). Diagnosis, Treatment, and Long-Term Management of Kawasaki Disease: A Scientific Statement for Health Professionals From the American Heart Association. Circulation, 135(17), e927–e999.  

The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus.

We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director.

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86. Case Report: Histoplasmosis Pericarditis Complicated by Cardiac Tamponade – Georgetown University

CardioNerds (Amit Goyal & Daniel Ambinder) join Georgetown University/Washington Hospital Center cardiology fellows (Nitin Malik, AJ Grant, and Tsion Aberra) for some fresh Maryland blue crab cakes at the Georgetown waterfront in Washington, DC. They discuss a rare case of histoplasmosis pericarditis complicated by cardiac tamponade. Dr. Patrick Bering provides the E-CPR and program director Dr. Gaby Weissman provides a message for applicants. Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai.  

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CardioNerds (Amit Goyal & Daniel Ambinder) join Georgetown University/Washington Hospital Center cardiology fellows (Nitin Malik, AJ Grant, and Tsion Aberra) for some fresh Maryland blue crab cakes at the Georgetown waterfront in Washington, DC. They discuss a rare case of histoplasmosis pericarditis complicated by cardiac tamponade. Dr. Patrick Bering provides the E-CPR and program director Dr. Gaby Weissman provides a message for applicants. Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai.
Episode graphic by Dr. Carine Hamo

The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus.

We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director.

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Case Media

A. Left: Admission chest x-ray (PA film), which was overall unremarkable. Right: Chest x-ray from hospital day 12 – which revealed pulmonary edema with bilateral perihilar haziness, increased prominence of pulmonary vascularity, and small-moderate bilateral pleural effusions. Note increased size of cardiac silhouette. At the corresponding time, pericardial effusion (without tamponade) had been diagnosed.
B. EKG: Sinus tachycardia and low-voltage QRS complexes.
C. CT abdomen/pelvis on hospital day 14. Free air noted within the abdomen (left). Moderate pericardial effusion also incidentally appreciated (right).
D. Pulse-Wave Doppler of mitral inflow. Flow variation is present, but variation is less than <30%.
E. (A) Small bowel resection showing focal mucosal ulceration, serositis, and formation of a granuloma. (B) Transmural inflammation seen on small bowel resection. (C) Pathology of ileocecectomy showing focal histoplasmosis characterized by intracytoplasmic yeast-like forms (black circles)

Parasternal short axis view on echocardiogram showing a moderate pericardial effusion without diastolic septal flattening.
Apical view showing profound tachycardia but without chamber collapse. Ejection fraction was moderately reduced.
Parasternal short axis view on echocardiogram showing a moderate pericardial effusion with intermittent septal flattening.
Apical view showing early diastolic RV chamber collapse. 

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CardioNerds Case Reports: Recruitment Edition Series Production Team