Left ventricular assessment by 3D-echocardiography in post-COVID-19 syndrome

Abstract

Background
COVID-19 is a disease that affects multiple organs and is believed to have an impact on the function of the heart muscle. Initial findings from hospitalized COVID-19 patients indicate the presence of myocardial injury characterized by increased levels of high-sensitive troponin. The causes of myocardial damage are diverse and not completely comprehended.


Methods
A three-dimensional echocardiogram (3DE) accurately measures the volume of the left ventricle (LV) and its function, both globally and regionally. It eliminates the subjective nature of two-dimensional echocardiography (2DE) when evaluating irregularities in the movement of the LV walls. This study sought to assess the left ventricular systolic function in 150 individuals who had recovered from COVID-19 and were experiencing post-COVID symptoms such as dyspnea, palpitation, or chest discomfort using 3DE.


Results
Our investigation revealed a notable statistical correlation (p-value of > 0.001) between patients who had post-COVID-19 syndrome and reported enduring symptoms such as shortness of breath, or chest discomfort, and various 3D echocardiographic strain patterns (the mean GLS% in the cases group was − 16.06 ± 4.36, whereas in the control group it was − 17.9 ± 2.57). Subclinical myocardial dysfunction, as shown by a decrease in left ventricular global longitudinal strain (LV-GLS), is common in over 85% of patients with post-COVID-19 syndrome. However, more commonly observed indicators of left ventricular (LV) function, such as lower ejection fraction (EF) and anomalies in wall motion, were less frequently found.


Conclusion
Our study findings suggest that persons who developed symptoms such as difficulty breathing, rapid heartbeat, or chest pain following their recovery from COVID-19 exhibited a reduction in left ventricular global longitudinal strain (LV-GLS) as measured by three-dimensional echocardiography (3DE). Ongoing research is focused on determining the mechanism of heart damage in COVID-19 infection.