Thriveni Sanagala

The presence of myocardial injury in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) infection is common. The cardiac complications of SARS-CoV2 infection are varied and distinguishing between them can be complicated. A 55-year-old man with recent diagnosis of SARS-CoV2 infection presented with chest pain, syncope, and was found to have saddle pulmonary embolism (PE). Marked elevation in cardiac enzymes prompted a coronary angiogram which was normal. Cardiac MRI revealed late gadolinium enhancement (LGE) in the anterolateral wall consistent with myocardial infarction (MI). He was diagnosed with paradoxical embolism causing MI. The differential for elevated cardiac enzymes is wide in patients with SARS-CoV2 infection. This case illustrates that sometimes multiple diagnoses exist, and that a high index of suspicion is required to continue work-up.

RV pacing (RVP), even with preserved atrioventricular (AV) synchrony, may lead to left atrial (LA) enlargement and atrial fibrillation. However, inciting events are unknown. We hypothesized that RVP acutely impairs LA function by mechanisms affecting atrial contraction and/or ventricular diastole. LA function in ICD patients (n = 31, LVEF ≤ 40%) and controls (n = 14, LVEF > 50%) was contrasted between intrinsic conduction versus RVP during asynchronous (ICD, n = 17, control, n = 7), and synchronous (ICD, n = 14, control, n = 14) pacing at long (LAVd, 107 ±16 ms) and short (SAVd, 31 ± 5 ms) AV delays. LA maximal volume (LA(Max)), minimal volume (LA(Min)), and emptying fraction {LA(EmF) = (LA(Max) -LA(Min))/LA(Max)} were measured echocardiographically. Six-segment mean mitral annular tissue doppler E' (global E') assessed diastolic recoil during baseline and LAVd. In the ICD group, LA(Min) increased by 42% (P < 0.0009) during VVI, by 31% (P = 0.0002) during SAVd, and by 17% (P < 0.0007) during LAVd. LA(EmF) decreased by 44% (P < 0.0008), 27% (P < 0.0001), and by 15% (P = 0.003) during VVI, SAVd, and LAVd respectively. LA(Max) was unaltered. Global E' was reduced by 12%. In control, LA(Min) increased and LA(EmF) decreased significantly during VVI (82 and 58%) and SAVd (46 and 41%), but not during LAVd. In patients with LV dysfunction, RVP acutely impaired LA emptying, and increased minimal volume, most prominently when atrial contraction was impeded (VVI, DDD-SAVd) but also when completed (DDD-LAVd), indicating impaired diastolic recoil as an important mechanism. When LV function was normal, similar changes were present when atrial filling is impeded (VVI, SAVd), but not when completed (LAVd).