Non-ST elevation myocardial infarction and post-stenting ventricular septal defect in the setting of viral myocarditis

A 58-year-old hypercholesterolemic male presented to the emergency room (ER) with palpitations, fatigue and shortness of breath. He was afebrile with an irregular heart rate (80–90 bpm), BP of 92/70 mmHg, respirations of 20/min, and an otherwise unremarkable physical examination. ECG showed atrial fibrillation (Afib) with mean heart rate of 80–90 bpm, left ventricular hypertrophy (LVH) and non-ischemic appearing ST elevation diffusely (Figure 1A), and he was admitted to the intensive care unit (ICU). Supplemental oxygen and intravenous fluids were given with excellent response. There were no signs or symptoms of infection. Troponin-I was 1,491.30 pg/mL. Transthoracic echo (TTE) showed mild LVH with normal left ventricular (LV) ejection fraction (EF) and segmental left anterior descending (LAD) territory hypokinesis with a normal pericardium. The working diagnosis was recent onset Afib with unstable angina. As an intermediate risk symptomatic patient, he underwent coronary computed tomography angiography (CCTA) (1). Despite controlled Afib, a 64-MDCT scan was diagnostic, and a coronary calcium score was 76 [62nd percentile, i.e., low probability of obstructive coronary artery disease (CAD)]. CCTA showed a partially calcified mild proximal LAD stenosis (CAD-RADS 2) (2) and a non-calcified moderate mid-LAD stenosis (CAD-RADS 3) (Figure 1B) (2). A resting mid-inferoseptal segment perfusion defect was seen, corresponding to the mid-LAD lesion (Figure 1C,D). Per guidelines (3), the patient underwent invasive conventional angiography (ICA) confirming the CCTA findings, and mid-LAD stenting was performed (Figure 1E-G). A septal perforator and a diagonal branch were occluded during stenting, causing hemodynamically instability and heart failure requiring pharmacological support. C-reactive protein (CRP) and troponin-I peaked at 20.8 mg/dL and 5,064 pg/mL, respectively. The magnitude of the troponin level seemed out of proportion to the CAD findings and he underwent cardiac MR (CMR) to exclude myocarditis. CMR demonstrated mild LV dysfunction (LVEF 49%) with mid-LAD territory hypokinesis and normal RV function with an LV stroke volume of 87 mL. Imaging at the mid ventricular inferoseptal segment suggested a small ventricular septal defect (VSD) (Figure 2, Figure 3 and Figure 4A-F), a CMR-calculated Qp:Qs of 1.2, mild mitral regurgitation, and a small pericardial and pleural effusion. Tissue characterization sequences suggested myocardial edema in the mid inferoseptal segment, with several late gadolinium enhancement (LGE) patterns: an ischemic area corresponding