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The coronavirus disease-2019 (COVID-19) pandemic has dramatically disrupted cardiovascular disease fellowship training. Significant reductions in cardiac volumes and simultaneous reassignment of physicians, including to COVID-19–centric services, have led to educational challenges in fellowship

Acute Chagas disease reactivation (CDR) after cardiac transplantation is a well-known phenomenon in endemic countries of Central and South America and Mexico, but is rare outside of those countries. In this report, we describe a case of a 49 year old male who presented 25 weeks after heart transplant with clinical features concerning for acute rejection, including malaise, anorexia, weight loss, and fever. His immunosuppression therapy included tacrolimus, mycophenolate, and prednisone. An endomyocardial biopsy revealed lymphocytic and eosinophilic inflammation, myocyte damage, and rare foci of intracellular organisms consistent with Trypanosoma cruzi amastigotes. The patient had no known history of Chagas disease. Upon additional questioning, the patient endorsed bites from reduviid bugs during childhood in El Salvador. Follow-up serum PCR testing was positive for T. cruzi DNA. Tests for other infectious organisms and donor specific antibodies were negative. This case illustrates the striking clinical and histologic similarities between acute cellular rejection and acute CDR with cardiac involvement in heart transplant patients, and thus emphasizes the importance of pre-transplant testing for Chagas in patients with epidemiologic risk factors.

Just as Hippocrates vowed his life to practicing the highest standards of medicine, cardiovascular disease fellowship program directors strive not only to provide comprehensive training for our fellows, but also to support them for long-term success in both professional and personal lives. Pregnancy

Background: Pulmonary hypertension (PH) is commonly reported in patients with end-stage renal disease (ESRD), and is associated with early graft failure and death in kidney transplant recipients. Calcifications of the lung, pulmonary vessels, heart, and kidney are frequently observed with ESRD, the consequence of secondary hyperparathyroidism. It follows that pulmonary artery vasculopathy, notably from extraosseous calcification, may contribute to PH. A popular, but unestablished, theory is that the stiffened pulmonary artery is unable to accommodate elevations in right ventricular stroke volume caused by arteriovenous (AV) hemodialysis shunts. We hypothesized that extraosseous calcification is related to PH in patients evaluated for kidney transplantation, and that the association is largely driven by AV shunts. Methods: Established in 2006, the UNC Cardiorenal Registry offers ongoing enrollment to all patients with stage 4 or 5 chronic kidney disease (CKD) referred for pretransplant cardiac evaluation. Pulmonary artery systolic pressure (PASP) was derived from routine echocardiograms within 6 months of the registry visit. All echocardiograms followed a standardized protocol, and were interpreted by the same cardiologist. PH was defined by a tricuspid regurgitant jet velocity >2.8 m/s, corresponding to a PASP >40 mmHg. Classification of grade 2 diastolic dysfunction (impaired left ventricular relaxation with elevated left atrial pressure) required a transmitral E/A ratio ≥ 0.8, and a transmitral to myocardial relaxation E/e’ ratio ≥ 15. Mitral annular calcification (MAC) was visually assessed, and considered evidence of extraosseous calcification. Associations between MAC and PH were analyzed with logistic regression, adjusted for age, sex, BMI, diastolic dysfunction, mitral regurgitation, left atrial dilation, and hematocrit. Results: From 2006-2013, 795 registry patients were screened preoperatively by echocardiography. Most were male (56%) and black (61%) with a mean age of 56 years. The majority (74%) received dialysis (13% peritoneal, 61% hemodialysis), for an average 2.8 years prior to the registry visit. PH, MAC, and AV shunts were present in 17%, 28%, and 62%; respectively. Relative to patients without MAC, those with MAC had higher odds of PH (OR adj =1.80; 95% CI: 1.17 – 2.78), which was not impacted by adjustment for AV shunts (OR adj = 1.78; 95% CI: 1.15 – 2.76). Further adjustment for years of dialysis modestly attenuated the association (OR adj = 1.55; 95% CI: 0.99 – 2.43). Conclusion: MAC is associated with higher odds of PH in severe CKD, irrespective of factors associated with PASP in the general population (age, sex, BMI), sources of pulmonary congestion (diastolic dysfunction, mitral regurgitation, and left atrial dilation), and causes of hyperdynamic circulation (hematocrit). The association is independent of hemodialysis shunts and dialysis vintage.

Pulmonary arterial hypertension (PAH) is a panvasculopathy that affects the distal pulmonary arteries and leads to restricted blood flow. This increased afterload leads to adaptive mechanisms of the right ventricle, with eventual failure once it can no longer compensate. Pulmonary hypertension from associated conditions, most importantly left heart disease, i.e. heart failure, can also lead to the same sequela. Patients often experience early vague symptoms of dyspnea and exercise intolerance, and thus PH can elude clinicians until right heart failure symptoms predominate. Evidence-based treatment options with pulmo-nary vasodilators are available for those with PAH and should be employed early. It is essential that patients be accurately categorized by their etiology of PH, as treatment strategies differ, and can potentially be dangerous if employed in the wrong clinical scenario.

Atrial fibrillation (AF) is exceedingly common in patients with heart failure (HF), as they share common risk factors. Rate control is the cornerstone of treatment for AF; however, restoration of sinus rhythm should be considered when more than minimal symptoms are present. Life-threatening ventricular arrhythmias are responsible for the primary mode of death in patients with NYHA I, II, or III HF. Although implantable cardioverter defibrillators protect against sudden cardiac arrest, many patients will present with VT or ICD shocks. Antiarrhythmic drug therapy beyond beta-blocker therapy remains fundamental to the termination of acute VT and the prevention of ICD shocks.

Heart failure with preserved ejection fraction (HFpEF) is a complex clinical syndrome based on traditional heart failure symptoms with documentation of increased left ventricular filling pressures and preserved left ventricular ejection fraction. The exact mechanisms that induce HFpEF are not known. End-diastolic ventricular stiffness does not seem to be acting alone. Substantial mortality exists compared with healthy age-matched controls, as well as significant health care expenditures on hospitalizations and readmissions. This article reviews the epidemiology, pathophysiology, and treatment of heart failure with preserved ejection fraction (HFpEF). Current practice guidelines focus on remedying volume overload, aggressively controlling hypertension, and treatment of comorbid conditions that contribute to decompensation.