Discussion:
This article aims to evaluate cardiac involvement including cardiac biomarkers, echocardiographic findings as well as cardiovascular complications in patients with COVID-19,and to explore the association of cardiac impairment and short-term outcome.
Advanced age has been reported as a predictor of mortality in SARS, MERS and COVID- 19[2, 4, 5]. There is no doubt that older age was a correlation of adverse outcome in this study(P< 0.05). The effect of myocardial injury on adverse outcomes and/or in-hospital mortality has been reported in the recent literature[1]. In the current study, 33.5% patients exhibited myocardial injury as demonstrated by elevation of hs-TnI levels, and the incidence of myocardial injury in critical patients was significantly higher than that in non-critical patients (74.2% vs 12.0%). Multivariate analysis showed that increased baseline hs-TnI level was one of the independent risk factors for adverse outcomes. The rapid increasing level of BNP, LDH and HBDH in the late stage of illness in fatal cases suggested that myocardial injury played a greater role in the fatal outcome of COVID-19. The recent study found that the in-hospital mortality was higher in patients with elevated TNT level than that in patients with normal TNT level (59.6% vs 8.9%)[6]. It has been reported that cardiovascular system was affected by multiple possible mechanisms. On the one hand, direct SARS-CoV-2 infection of the myocytes causing active myocarditis might also contribute to the impairment in myocardial function. A case report in which a patient infected with SARS-CoV-2, without a history of cardiovascular disease, experienced acute myocarditis manifested as increased wall thickness,diffuse biventricular hypokinesis and severe left ventricular dysfunction, with the cardiac MRI findings showing marked biventricular myocardial interstitial edema and the slow gadolinium washout[7].On the other hand, balance between coronary perfusion and cardiac metabolic was disturbed by cytokine storm. The release of inflammatory cytokines may lead to the increased metabolic needs of peripheral tissues and organs including cardiac tissue, accompanied by coronary artery spasm or coronary microvascular dysfunction with decreased coronary blood flow, decreased oxygen supply, destabilization of coronary plaque, and microthrombogenesis[8]. In our study cohort, critical patients demonstrated higher level of Inflammatory biomarkers including C-reactive protein , procalcitonin , Interleukin-2 receptor, α-tumor necrosis factor ,and interleukin-6 than non-critical patients. To a certain degree, it partly explained probable cause for five patients in this cohort complicating by acute myocardial infarction after infected with SARS-CoV-2. The atherosclerotic plaques of coronary arteries are prone to rupture because their inflammatory activity is intensified in the systemic inflammatory response[9].
There are few literatures referred to the echocardiographic signs in patients with COVID-19. The enlargement of right atrium, right ventricle and pulmonary hypertension may be related to the severity of pulmonary lesions and acute respiratory distress syndrome (ARDS). ARDS and severe lung injury impact cardiac hemodynamics through pulmonary vascular dysfunction, which frequently manifest pulmonary hypertension and RV overload caused by inflammatory factors, hypoxia-induced mediators, hypercapnia-induced vasoconstriction, thrombosis, and pulmonary vascular remodeling[10]. However, the effect of pulmonary hypertension on the prognosis of patients with ARDS is controversial. Squara et al. [11] reported that fatal cases had a higher mean pulmonary artery pressure in a study of 586 patients with ARDS. On the contrary, Osman et al.[12] found that right heart failure /pulmonary hypertension didn’t have effect on adverse outcome in patients with ARDS. However, in our cohort, increased pulmonary artery systolic pressure was also one of the independent risk factors for adverse outcomes. In addition to being associated with the cytokine storm damage to the lung, the myocardial ischemia leading to the hypoperfusion of the right ventricle may be also the cause of pulmonary hypertension. The COVID-19 has been reported resembled the severe acute respiratory syndrome coronavirus (SARS-CoV) which caused an outbreak in 2003. Siu-fung Yiu et al. observed echocardiographic reversible, subclinical diastolic left ventricular impairment without systolic involvement in a cohort of acute SARS infection irrespective of the severity of their disease[13]. A lower mean left ventricular ejection fraction (LVEF) was found in patients who required mechanical ventilation. In line with their findings, the critical patients in our cohort demonstrated lower median LVEF than non-critical patients. However, no significant pulmonary hypertension was found in their study. Researchers speculated that the temporary changes in the echocardiographic parameters in the acute phase might be caused by the cytokine storm resulting from an excessive host immune response to SARS virus infection[14]. However, the changes in the echocardiographic parameters were generally nonspecific, a more severe impairment of left ventricular function in patients with COVID-19, like the 22 patients with cardiac disfunction with LVEF <50%,may suggest an exacerbation of the underlying heart disease or the presence of other secondary causes of left ventricular impairment. Segmental wall motion abnormalities occurred in patients with history of coronary heart disease and/or complications of myocardial infarction in the course of disease. Pericardial effusion was more likely to be related to systemic inflammatory reaction and wall thickening was more likely to be related to pre-existing cardiovascular disease such as hypertension or other metabolic diseases impaired the myocardium. Nevertheless, echocardiographic signs didn’t exhibit the typical myocarditis change.