This study focused on the potential cardiac involvement of SARS-CoV‑2 virus. It was based on laboratory parameters as well as electro- and echocardiographic values to determine the impact of SARS-CoV‑2 virus on heart tissues. The conducted investigations confirmed the relationship between the presence of acute cardiac injury and COVID-19.
The authorsʼ patients experienced myocardial injuries (45% of the study group): myocardial necrosis was suggested by increased troponin T levels, and myocardial functional disturbance by elevated NT-proBNP, as well as disturbed left ventricular systolic and diastolic function. In addition to these findings, the existence of enhanced inflammatory biomarkers such as CRP, ferritin, and FLCs suggested that myocardial injury may be caused by inflammatory myocardial processes. NT-proBNP showed significant correlation with the length of hospital management and the severity of pulmonary CT findings.
The electrocardiographic findings in these patients, such as ST elevation without reciprocal ST depression in the absence of acute coronary artery insult, and the conduction disturbances suggest further evidence of myocarditis, most likely due to direct viral invasion or immune-mediated myocardial injury. The presence of myocardial interstitial oedema in acute viral myocarditis can lead to disturbance of both systolic and diastolic function, which was detected in 25% of the patients. Patients with myocarditis can show pulmonary hypertension in the acute course. Other compensatory mechanisms, such as right ventricular hypertrophy, need weeks or months to develop. The thrombogenic nature of COVID-19 may have led to peripheral pulmonary vasculature insults with acute elevated pulmonary pressure. This theory cannot be excluded, even though no central pulmonary embolisms were detected on thorax CT.
The results of univariate Cox proportional hazards analysis for laboratory biomarkers or echocardiographic parameters, possibly due to relatively small sample size, showed no significant independent prognostic value for mortality in the present COVID patients.
The myocardium may be infected by a wide variety of viruses [15, 16]. In patients with moderate to severe heart failure (EF <45%) and inflammation in the Marburg registry, 42.1% were virus-positive .
In 2006, a study of patients diagnosed with SARS revealed that tachycardia was the most common finding (72%) beside hypotension (50%), bradycardia (15%), transient cardiomegaly (11%), and transient paroxysmal atrial fibrillation in only one patient (0.8%) as a result of direct cardiac injury in the absence of underlying heart disease . Another group aimed to characterize cardiac manifestations in the 2009 influenza pandemic (H1N1). In all, 46% of patients showed evidence of myocardial injury. Of 28 patients in whom an echocardiogram was clinically indicated, 20 had left ventricular systolic dysfunction. Of these, 14 patients were diagnosed as having myocarditis, with most (12 patients) developing this early on . Fulminant myocarditis caused by the H1N1 strain of influenza was also reported . Various studies described myocarditis related to other influenza forms [20,21,22]. Further reports linked MERS coronavirus (MERS-CoV) to myocarditis and severe left ventricular systolic dysfunction . Furthermore, an animal model study clearly stated that viral RNA could be seen in cardiac tissue, implying direct cardiac pathology .
Shi et al. conducted a single-center cohort study at Wuhan University, China, and retrospectively included a total of 416 hospitalized patients with COVID-19. Approximately 82 patients (19.7%) were reported to have cardiac injury. A higher mortality rate (p < 0.001) was noticed in patients with cardiac injury (51.2%) than those without cardiac injury (4.5%) . To evaluate the association of underlying CVD and myocardial injury with fatal outcomes in COVID-19 patients, Guo et al. conducted a retrospective single-center study. Of a total of 187 patients with confirmed COVID-19, 52 (27.8%) patients exhibited myocardial injury as indicated by elevated troponin T levels . Likewise, myocardial injury proved by troponin T elevation was determined in 45% of the present cohort. Similar to the current study, the authors did not observe any significant correlation between troponin T and NT-proBNP in relation to mortality .
Case reports have depicted the cardiac involvement of COVID-19 infection. The diagnosis of myocarditis was established upon troponin T and NT-proBNP elevation and was confirmed in one case through echocardiography and in the other with cardiac MRI [26, 27]. Another group from New York, USA, identified ST-segment elevation in 18 patients infected with COVID-19. Noncoronary myocardial injury was noted in 10 patients indicating myo/pericarditis .
The authors did not detect any ventricular arrhythmias or sudden cardiac death (SCD) in patients under monitor surveillance. The proportion of SCD caused by myocarditis has been reported as ranging from 1% to 14% of all SCD [29, 30].
Elevation of FLC kappa and lambda in the current patient cohort suggests that the clones of B lymphocytes and plasma cells that produce FLCs may be activated in COVID-19 patients, although the number of lymphocytes were decreased. However, there were contradictory observations of FLC in heart failure, which may partly reflect the different FLC assays used [31, 32].