Relation Among Right Ventricular Dysfunction, Lung Damage, and Mortality in Patients With COVID-19

We read with interest the paper by Li et al. (1), which evaluated the prognostic value of speckle-tracking echocardiography derived right ventricular longitudinal strain (RVLS) in 120 hospitalized patients with coronavirus disease 2019 (COVID-19). The authors confirmed that impaired RVLS was associated with the mortality, but 3 key issues deserve further consideration.

First, a confounding bias. Right ventricular (RV) function is closely linked with afterload. The same is applicable for RVLS, which is modulated by afterload. Although RV dysfunction can be induced by direct COVID-19 damage, a more likely scenario is that it results from severe lung damage, including the development of acute respiratory distress syndrome and pulmonary hypertension. As the authors showed, there was no association between the cardiac enzyme (creatine kinase myocardial band, High-sensitivity Troponin I, and B-type natriuretic peptide) and RVLS, but patients with impaired RVLS had more tricuspid regurgitation and higher pulmonary artery systolic pressure than those without impaired RVLS. As such, given the small number of events, it becomes impossible, in our view, to claim with certainty that RVLS is independently associated with outcomes in this sick group of patients without properly accounting for the health of the right-side unit (2). This includes incorporating the right chamber size (larger in nonsurvivors), pulmonary pressures (greater in nonsurvivors), tricuspid regurgitation severity, and RV systolic function. Given the small number of events, the authors could at minimum evaluate the impact of the RV-PA coupling, which takes into account RV systolic performance at a given degree of afterload and which has been shown in several other cohorts to be prognostically important (3,4).

Second, the incremental prognostic value of RVLS over the comprehensive clinical assessment including known risk factors is also unclear, which given a likely type II error (underpowered), becomes less apparent. A case in point is baseline cardiovascular disease, which has a significant hazard ratio in the univariate analysis (2.93) and is shown by many other publications in this COVID-19 population to be associated with worse outcomes, but “loses” its significance in the overfitted multivariate model (3 variables for 18 events).

Last, RVLS is highly dependent on adequate image quality, which can be challenging in this group of sick patients, at times in the intensive care unit on mechanical ventilation or in supine or prone position, all of which make echocardiographic imaging quality decrease. In fact, the authors excluded 24 (16%) of the initial 150 patients, due to suboptimal image quality analysis for RVLS. Could other parameters of RV size/function be assessed besides RVLS in these excluded patients?

The study by Li et al. (1) is an important first step in the assessment of RV dysfunction in patients with COVID-19, and we commend them for exploring new parameters of RV performance. However we believe that a more balanced perspective of their findings is necessary, because we do not know the additional value of RVLS over the other clinical and echocardiographic parameters, which can be assessed more easily and possibly without direct potential exposure to COVID-19. Further studies are needed before this parameter could be used to improve the risk stratification.