It is understood that severe COVID-19 infection causes multi-organ dysfunction, and cardiac injury yields worse outcomes [16]. Trans-thoracic echocardiography is helpful in this group of patients but not routinely ordered to minimize the risk of disease transmission [17]. It enables bed side and non-invasive assessment of heart function and hemodynamic status of the patient [16]. Conventional echocardiography study can rule out obstructive problems (e.g., cardiac tamponade and pulmonary embolism) and hypovolemic shock (decreased cardiac output and collapsed IVC) [17,18,19,20]. In recent years, many studies observed that nearly 40% of severe sepsis patients developed a decline in left ventricular systolic and diastolic functions. In severe sepsis hyperdynamic status increases cardiac performance due to systemic inflammatory response. In later stages, hypoxia and inflammation cause myocardial suppression [20].
The main finding of this study was that COVID-19 negatively affects the RV as well as LV functions. Moreover, we found a strong correlation between right ventricular systolic pressure and elevated cardiac biomarkers, right ventricular dimensions as well as with newly recognized left ventricular systolic dysfunction. This finding confirmed the injurious effect of COVID-19 infection on myocardial performance. COVID-19 myocardial impact is not only on pulmonary artery pressure and right ventricular dimensions but also it harms left ventricular systolic functions which were directly correlated to high recording of right ventricular systolic pressure. The magnitude of rise of cardiac biomarkers was correlated to high right ventricular systolic pressure assessed by echocardiography, supporting the hypothesis of using either cardiac biomarkers or bed side imaging to predict right ventricular injury and consequently predicting worse outcome during hospital stay. In fact, the 3 patients who died in this study had LV dysfunction and elevated Troponin serum level. Patients with previous COVID-19 infection who were re-admitted by moderate or severe infection were more liable for de novo myocardial injury in terms of elevated pulmonary artery pressure.
These findings were in accordance with Barman et al. who showed a statistically positive correlation between RV diameter and troponin level, similarly left ventricular systolic functions showed a statistically significant negative correlation with troponin and RV systolic functions. In their linear regression model; Troponin, left ventricular ejection fraction, D-dimer, RA dimensions and PASP were independent predictors of RV dilatation [21].
Further evidence of RV involvement in COVID-19 was mentioned by D’Andrea et al., who reported a statistically significant association between RV dilation/systolic dysfunction and mortality in a cohort of 115 patients. Patients with RV dysfunction had signs of myocardial injury (elevated Troponin), more severe lung disease, and higher pulmonary artery pressure, suggesting increased afterload as the primary mechanism of RV dysfunction in patients with severe COVID-19 sepsis [22]. In line with these findings, Kim et al. released data from 510 patients who underwent echocardiography in three NY hospitals from March to May 2020 [20]. RV dilation was detected in 35% of the cohort, while RV systolic dysfunction was found in 15%. These changes were associated with higher levels of circulating biomarkers. RV abnormalities were associated with lower LVEF, and associated with higher pulmonary artery systolic pressure, supporting an increased pulmonary vascular load as the primary pathophysiological mechanism. In multivariate analysis, RV abnormalities independently predicted mortality (32% of the cohort) [23].
In this study, TAPSE as a marker of RV systolic functions did not show a statistically relevant correlation to PASP, despite the strong correlation between RV basal dimensions and PASP. This finding could be attributed to the diversity of factors influencing TAPSE measurements as LV systolic functions, ischemic etiology of heart failure and wall motion index of RV [24]. Another point, is the impact of TR jet severity on reproducibility of TAPSE, severe TR is a confounding factor when TAPSE is used to assess RV systolic functions [25].
Despite the crucial rule of bed side echocardiogram in evaluating RT ventricular functions and its impact in predicting patient course during his hospital stay, the decision to perform echocardiogram should be only when clinically warranted and with the use of full personal protective equipments to minimize virus transmission. Moreover, the need for follow up study for a COVID-19 patient should be based upon multidisciplinary treating team since the effect of COVID-19 on ventricular function might be extended to longer periods.