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.