Spectrum of Cardiac Manifestations in COVID-19: A Systematic Echocardiographic Study

Abstract

Background: Information on the cardiac manifestations of coronavirus disease 2019 (COVID-19) is scarce. We performed a systematic and comprehensive echocardiographic evaluation of consecutive patients hospitalized with COVID-19 infection.

Methods: One hundred consecutive patients diagnosed with COVID-19 infection underwent complete echocardiographic evaluation within 24 hours of admission and were compared with reference values. Echocardiographic studies included left ventricular (LV) systolic and diastolic function and valve hemodynamics and right ventricular (RV) assessment, as well as lung ultrasound. A second examination was performed in case of clinical deterioration.

Results: Thirty-two patients (32%) had a normal echocardiogram at baseline. The most common cardiac pathology was RV dilatation and dysfunction (observed in 39% of patients), followed by LV diastolic dysfunction (16%) and LV systolic dysfunction (10%). Patients with elevated troponin (20%) or worse clinical condition did not demonstrate any significant difference in LV systolic function compared with patients with normal troponin or better clinical condition, but they had worse RV function. Clinical deterioration occurred in 20% of patients. In these patients, the most common echocardiographic abnormality at follow-up was RV function deterioration (12 patients), followed by LV systolic and diastolic deterioration (in 5 patients). Femoral deep vein thrombosis was diagnosed in 5 of 12 patients with RV failure.

Conclusions: In COVID-19 infection, LV systolic function is preserved in the majority of patients, but LV diastolic function and RV function are impaired. Elevated troponin and poorer clinical grade are associated with worse RV function. In patients presenting with clinical deterioration at follow-up, acute RV dysfunction, with or without deep vein thrombosis, is more common, but acute LV systolic dysfunction was noted in ≈20%.

Keywords: COVID-19; echocardiography; heart ventricles; thromboembolism.

Figure 1.

Patterns of cardiac disease in hospitalized patients with coronavirus disease 2019 (COVID-19). LV indicates left ventricular; and RV, right ventricular.

Figure 2.

Forest plots for association of imaging with outcome. A, Forest plot for association of imaging with clinical deterioration. Impact of left and right imaging parameters on clinical deterioration in patients with coronavirus disease 2019 (COVID-19) infection. B, Forest plot for association of imaging with mortality. Impact of left and right ventricular imaging parameters on mortality in patients with COVID-19 infection. AT indicates pulmonic acceleration time; EF, ejection fraction; RVEDA, right ventricular end-diastolic area; and SV, stroke volume.

Figure 3.

A patient with a sudden decrease in systolic function. Doppler interrogation of the mitral inflow (A and B), tissue Doppler of mitral annulus (C and D), and left ventricular (LV) outflow tract (LVOT) flow (E and F). Images on the left (A, C, and E) are at baseline. Images on the right (B, D, and F) were obtained 2 days later, after clinical deterioration and an increase in troponin level. Note the increase in E/e’ ratio, suggesting an increase in left filling pressure, and decrease in LV S’ and LVOT flow velocity, suggesting a decrease in stroke volume. Time bar scale is 40 milliseconds between every thin line and 200 milliseconds between every thick line.

Figure 4.

A patient with sudden right ventricular dysfunction with an acute rise in afterload. Doppler interrogation of mitral inflow (A and D), left ventricular (LV) outflow tract (LVOT) flow (B and E), and pulmonary flow acceleration time (C and F) in patients with right ventricular (RV) dysfunction and deep vein thrombosis. Top images (A–C) are at baseline; bottom images (D–F) are after clinical deterioration. Note that mitral inflow velocity decreases as a result of unloading of the LV by the failing RV and the mild decrease in LVOT velocity, suggesting a decrease in stroke volume caused by the underfilled LV. On the right, note the change in pulmonic flow acceleration time from symmetrical to early picking, suggesting an elevation in pulmonary vascular resistance. Time bar scale is 40 milliseconds between every thin line and 200 milliseconds between every thick line.