Etiopathogenetic Particularities and Prognostic Impact of Right Ventricular Involvement in COVID-19-Related Acute Respiratory Distress Syndrome.

To the Editor:

I read with great interest the study by Chotalia et al (1) published in a recent issue of Critical Care Medicine, which provides further important data concerning the still insufficiently considered impact of coronavirus disease 2019 (COVID-19)–related right ventricular (RV) dysfunction on the therapeutic approaches to COVID-19 and patient survival.

The high occurrence rate of extensive pulmonary thrombotic microangiopathy associated with more severe hypoxemic respiratory failure, increased resistance in the pulmonary circulation, and frequent afterload mismatch-induced RV failure is a distinctive feature of COVID-19–related acute respiratory distress syndrome (CARDS) and also a main cause for the particularly high mortality related with severe infections (2). Early detection of hospitalized patients with evidence of increasing RV hemodynamic overloading can facilitate the selection of the most appropriate management (e.g., RV protective ventilation, anticoagulation, pulmonary vasodilation, extracorporeal membrane oxygenation, etc.), which can be decisive for their survival. Chotalia et al (1) demonstrated that even simple parameters measurable by conventional transthoracic echocardiography (TTE) can be useful for detection of RV dilation and systolic dysfunction. The authors also found that the RV phenotype characterized by cavity dilation (RV/left ventricular end-diastolic area ratio > 0.6) and systolic impairment (RV fractional area change [RVFAC] < 0.35%) was independently associated with mortality (1).

Unfortunately, Chotalia et al (1) did not include the prevalence and severity of tricuspid regurgitation (TR) in their study. This would have been important because greater than or equal to moderate TR was already found associated with increased odds for 30-day mortality in hospitalized patients with COVID-19 (3). Assessment of TR severity is also important because TR can induce misleading RVFAC and tricuspid annular peak systolic excursion (TAPSE) changes. By facilitating the RV free wall transversal and longitudinal motion, which will increase RVFAC and TAPSE (correspondingly to the increased blood volume leaving the RV in systole), TR can lead to an overestimation of RV systolic function (2).

The distinctively severe ventilation-perfusion mismatch with life-threatening hypoxemia resulting from pulmonary endothelial damage that promotes small vessel thrombosis and impairs the pulmonary vasoregulation can become the key problem already in early CARDS stages (4). Elevated pulmonary arterial systolic pressure appeared detectable by echocardiography in up to 70% of hospitalized COVID-19 patients and the prevalence of pulmonary hypertension in ventilated patients with CARDS was found four times higher compared with COVID-19 patients without the need for mechanical ventilation (2, 5). RV dilation was also detectable in about 30–70% of the hospitalized patients with COVID-19, and assessment of RV pulmonary artery coupling by echocardiography revealed a significant uncoupling in up to 50% of the patients necessitating intensive care (4). Additional monitoring of changes in the pulmonary circulation could be therefore particularly helpful in hospitalized patients with COVID-19. Nevertheless, TTE is generally still underused in monitoring of hospitalized COVID-19 patients and, if it is used, the importance of the right-sided heart involvement is often underestimated. Hospitals where 65% of the patients with COVID-19 receive TTE that focuses on both ventricles like that in Birmingham (1) are still rather rare. Full implementation of bedside TTE focused on the right-sided heart, which is currently still underused, could facilitate more personalized management and treatment of hospitalized patients and can contribute toward reducing the high mortality associated with severe acute respiratory syndrome coronavirus 2 infection.