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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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Patient Summary

A man in his mid-50s with alcohol use disorder, cirrhosis, atrial fibrillation, and alpha thalassemia complicated by iron overload presented with hematemesis. He was tachycardic and hypotensive. Labs were notable for Hgb 8.1 (baseline of 10.2), INR 1.3, lactate 4.2, and ferritin 4660. He was started on IV PPI and octreotide. Course was complicated initially by Afib with RVR with hypotension. Subsequently, the patient developed unstable VT requiring CPR. Post-code EKG showed inferolateral ST elevations. Troponin-I rose from 19 to 225 and his pressor requirement continued to increase despite resolution of his GIB. TTE showed LVEF 42% with new inferolateral wall motion abnormalities, normal RV systolic function, severe mitral regurgitation, and small pericardial effusion. After treatment of his GIB by IR and GI, he underwent an urgent LHC which showed 30% stenosis in proximal LAD, 70% in LADD2, and 95% in distal RCA. Coronary spasm was noted in all vessels. Intracoronary nitroglycerin and nicardipine were administered with significant improvement in spasm and resolution of STE on EKG. Vasopressors were quickly weaned off after. He was eventually stabilized, extubated, and started on an oral nitrate and calcium channel blocker. Repeat TTE showed normalized systolic function without any wall motion abnormalities.  

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Case Media

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Episode Schematics & Teaching

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

1. What are the cardiac manifestations of hemochromatosis? 
   • Cardiac hemochromatosis encompasses cardiac dysfunction from either primary or secondary hemochromatosis. Initially, hemochromatosis leads to diastolic dysfunction and arrhythmias. In later stages, it can lead to dilated cardiomyopathy.  
   • Diagnosis of iron overload is established by elevated transferrin saturation (>55%) and elevated serum ferritin (>300 ng/mL). Genetic testing for mutations in the HFE gene should be pursued. 
   • Cardiac MRI with measurement of T2* relaxation times is the diagnostic test of choice as it can both detect and quantify myocardial iron overload. The iron content in the myocardial tissue is inversely proportional to the time constant of decay for relaxation time. Thus the higher the iron content, the shorter T2* relaxation time.  
     
2. What are the causes of ST-segment elevation on EKG besides acute plaque rupture or vasospasm? 
   • Pericarditis: in acute pericarditis, ST elevation can be seen diffusely in all leads, with PR segment depression (except lead aVR +/- V1). The diffuse ST elevations are due to involvement of subepicardial layer of the ventricular wall. The PR depressions are due to involvement of the subepicardial layer of the atrial wall.  
   • Stress CM: The ECG findings of stress cardiomyopathy may be indistinguishable from STEMI secondary to acute plaque rupture. 
   • Brugada syndrome: >2 mm ST-segment elevation in the right precordial leads followed be a negative T wave can be seen in patients with Type 1 Brugada. Type 2 and Type 3 Brugada will have STE as well but with different morphologic criteria.  
   • Electrolyte abnormalities: hyperkalemia can sometimes cause ST elevation. Other EKG findings of hyperkalemia include widened QRS, tall and peaked T waves, low-amplitude or lack of P waves, high grade AV Block, sine wave, and/or ventricular fibrillation or PEA. 
   • Pulmonary embolism: the classic EKG features of PE are S1Q3T3 with signs of RV strain (RBBB, RAD) though these are neither sensitive or specific. Sometimes, ST elevation in aVR and right-sided precordial are seen in massive PE due to RV overload, dilation, and/or ischemia (see the Cedars-Sinai episode for more details!).  
   • Cardioversion: striking ST-segment elevation, often >10mm, can be seen after cardioversion but only lasts 1-2 minutes.  
   • Raised ICP: can mimic acute myocardial infarction with widespread T-wave inversions +/- STE (or depression). Other non-cardiac causes, albeit rare causes, include significant gastrointestinal visceral distension, pneumonia, and pancreatitis.  
     
3. What are the two types of ischemic mitral regurgitation (IMR)? 
   • IMR is often a complication of ischemic heart disease and is associated with a worse prognosis across a variety of settings. Ischemic MR can occur due to a primary cause (e.g., abnormality of the valve apparatus and specifically papillary muscle rupture) or secondary cause (e.g., acutely from ischemia and chronically from a complex pathophysiologic changes).  
   • In chronic IMR, regional and/or global LV systolic dysfunction and ventricular remodeling can cause restricted leaflet motion. There can be outward papillary muscle displacement and when this happens, mitral leaflet coaptation moves apically away from the mitral annulus. Further, scarring of the papillary muscles may produce further mitral leaflet tethering and LV dilation can lead to mitral annular dilation. The posterior mitral annulus may contract less as well (which contributes to as much as 25% of the closure of the mitral orifice during systole). The ultimate results is poor leaflet coaptation and mitral regurgitation.  
   • MR secondary to papillary muscle rupture after an acute MI will almost certainly require surgery; while secondary MR from acute ischemia will often respond to revascularization. The treatment of chronic ischemic MR is a topic for another Cardionerds Episode so stay tuned!  
     
4. What’s the pathogenesis of coronary vasospasm? 
   • In coronary vasospasm, the coronary arteries – and specifically the vascular smooth muscle layer – constricts due to various causes including emotional distress, changes in sympathetic tone, cocaine, or cigarette smoking, leading to myocardial ischemia.  
   • The causes and mechanisms of coronary vasospasms are still poorly understood but there are a few potential mechanisms proposed. 
     • Autonomic nervous system: increase in sympathetic tone can induce coronary vasospasms. Vasospasms more commonly occur at night during rapid eye movement sleep, when a reduction in vagal activity is associated with an increase in adrenergic activity.  
     • Inflammation: chronic inflammation and cigarette smoking are shown to be associated with vasospasm. Patients with vasospasm are found to have elevated hs-CRP, IL-6, and peripheral WBC.  
     • Other mechanisms have also been proposed including smooth muscle cell hypercontractility, oxidative stress, and genetics 
       
5. What’s the treatment for coronary vasospasm? 
   1. Any factor that may precipitate coronary vasospasm, especially smoking, should be avoided. There are additionally certain medications that should be avoided including non-selective beta blockers like propranolol and triptans.  
   2. For medical treatment, long-acting calcium channel blockers can be used, especially taken at nighttime when attacks of coronary vasospasm are frequent 
   3. Long-acting nitrates can also be added to prevent recurrent attacks if calcium channel blockers alone are inadequate 

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References

1. Gulati, V., Harikrishnan, P., Palaniswamy, C., Aronow, W. S., Jain, D., & Frishman, W. H. (2014). Cardiac involvement in hemochromatosis. Cardiology in review, 22(2), 56–68. 
2. Wang, K., Asinger, R. W., & Marriott, H. J. (2003). ST-segment elevation in conditions other than acute myocardial infarction. The New England journal of medicine, 349(22), 2128–2135.  
3. Báez-Ferrer, N., Izquierdo-Gómez, M. M., Marí-López, B., Montoto-López, J., Duque-Gómez, A., García-Niebla, J., Miranda-Bacallado, J., de la Rosa Hernández, A., Laynez-Cerdeña, I., & Lacalzada-Almeida, J. (2018). Clinical manifestations, diagnosis, and treatment of ischemic mitral regurgitation: a review. Journal of thoracic disease, 10(12), 6969–6986.  
4. Hung, M. J., Hu, P., & Hung, M. Y. (2014). Coronary artery spasm: review and update. International journal of medical sciences, 11(11), 1161–1171.  
5. Slavich, M., & Patel, R. S. (2016). Coronary artery spasm: Current knowledge and residual uncertainties. International journal of cardiology. Heart & vasculature, 10, 47–53.  

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CardioNerds Case Reports: Recruitment Edition Series Production Team

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