Cardiovascular factors predicting poor outcome in COVID-19 patients.

We read with much interest the article “Pathophysiological characteristics and therapeutic approaches for pulmonary injury and cardiovascular complications of coronavirus disease 2019″ by Geng et al. published in your esteemed journal [1]. We believe that this topic is relevant and is constantly evolving with newer insights and details being published every day. We wanted to contribute the following details on cardiac involvement to this manuscript, which we believe will be an important addendum. We discuss the various cardiac pathophysiological factors contributing to mortality.

Pathophysiology

1.1. Mechanism

Even though multiple mechanisms of cardiac injury have been postulated, cytokine storm-related injury has been uniformly shown to predict several outcomes including acute respiratory distress syndrome, requirement of mechanical ventilation, severity of illness, and mortality. Patients with elevated inflammatory markers including C-reactive protein, ferritin, procalcitonin, D-Dimer, and IL-6 are consistently reported across patients with poor outcome [2].

1.2. Pathology

Involvement of myocardium and pericardium has been reported. Acute myocardial injury has been reported as the most common cardiac manifestation of COVID-19 and is reported in 8%-12% of patients [3,4]. In a recent review Buja et al. summarized the cardiac autopsy findings of 23 COVID-19 patients. They reported cardiomegaly in 57% (N = 13), evidence of individual cardiac myocyte injury in 35% (N = 8), lymphocytic pericarditis, and lymphocytic myocarditis in 13% (N = 3), 4% (N = 1) of patients respectively [5,6]. Myocardial involvement has been reported with elevated cardiac biomarkers, electrocardiography, echocardiography (ECHO), cardiac magnetic resonance imaging, and autopsy [5,7]. Among these, elevated cardiac biomarkers like creatinine phosphokinase, lactate dehydrogenase, and high-sensitive troponin have been consistently reported to predict disease severity. Studies have also shown that a high level, and a rising trend in high-sensitive troponin is predictive of poor outcome [2,8]. Presence of ST segment elevation, and ST-T changes have been reported to be higher among patients with severe illness. Among 19 patients presenting with ST segment elevation on EKG, coronary angiogram revealed the presence of coronary obstruction in only 8 patients, confirming a predominantly non-ischemic pattern of myocardial injury [9]. A recent study including 120 patients with COVID-19 showed that the presence of an enlarged right heart diameter, reduced right ventricular function, and right ventricular longitudinal strain pattern on ECHO were predictors of mortality. In another study, the development of a new wall motion abnormality reduced left ventricular ejection fraction, and an increased wall thickness, suggesting a possible myocarditis was statistically higher in patients with severe illness [10,11].

Pericardial involvement has been reported in less than 5% of patients. In a study by Li et al., computed tomography of chest identified the presence of pericardial effusion in 4.8% of patients. Interestingly presence of pericardial effusion was noted to be a predictor of poor outcome. ECHO-based studies have also shown that pericardial effusions of more than 5 mm in diameter were significantly higher among those who had severe disease [2,8].

Endocardial involvement has not been consistently reported yet. Patients with severe illness are more prone to have rhythm abnormalities and develop cardiogenic shock. However, involvement of valves, supporting structures including papillary muscles or the conduction system have not been reported. As mentioned by the authors IL-6-related papillary dysfunction is not yet been reported in the literature. Presence of pulmonary artery hypertension has been reported and has been found to be a predictor of a poor outcome [8,11].

We agree with the authors on older patients with diabetes being at higher risk of myocardial injury. The other reported potential contributors of myocardial injury have been hypertension, coronary artery disease, heart failure, and cerebrovascular disease. The presence of these comorbidities along with vitals at the time of presentation facilitates patient triage, disposition, and treatment methods. Clinical scores like National Early Warning Score have been used to standardize care across multiple facilities. These scores are neither predictors of myocardial injury nor of mortality [12].