Cardiac Damage After SARS-CoV2 Infection.

COVID-19 is a viral disease that can manifest acutely in the respiratory tract and other organs. In this study, we aimed to investigate potential long-term damage to the heart from COVID-19. For this study, we divided 97 consecutive unselected COVID-19 patients aged 18-80 years at a cardiology practice in Cologne, Germany, into two groups based on the severity of their infection. We performed a resting ECG and a resting transthoracic echocardiography three and six months after SARS-CoV2 infection. The key discriminator determining disease severity was bed confinement or hospital admission. Group 1 included patients with less severe COVID-19, whereas group 2 contained more severe cases. Heart rate as the primary ECG endpoint was lower by a statistically significant amount for the entire study population (p=0.024), subdivided by gender (p <0.001, p <0.001) and in group 1 p =0.003 compared to three months. QTc time and repolarization disturbances as primary ECG endpoints and the echocardiographic primary endpoints, left ventricular ejection fraction, and left ventricular end-diastolic diameter (LVEDD), showed no relevant difference between the subgroups at three and six months or between the measurements taken at each point. In contrast, LVEDD normalized to body surface area was statistically significantly lower at six months in women in group 1 compared to group 2 (p=0.048) and in the overall study population at six months compared with the data after three months (p=0.034). E/E' was statistically lower at six months than at three months in the whole population (p=0.004) and in women (p=0.031). All measured echocardiographic and electrocardiographic mean values were within the normal range in all groups and follow-up controls. Overall, the prospective study conducted showed no significant evidence of long-term cardiac damage from COVID-19 disease, as evidenced by electrocardiographic and echocardiographic examinations at three and six months after infection.