In the context of COVID-19, both patients with and without underlying cardiovascular comorbidities can develop cardiovascular complications secondary to SARS-CoV-2 infection. For example, Wang et al., reported that among 138 hospitalized patients with COVID-19 in Wuhan, China, cardiac injury, as evidenced by new ECG or echocardiographic abnormalities or elevated high-sensitivity cardiac troponin I, was present in 7.2% of all patients and 22% of patients who required intensive care unit (ICU) hospitalization (Wang, Hu, et al., 2020). Moreover, the National Health Commission of China reported that 12% of patients infected with SARS-CoV-2 and without known cardiovascular disease (CVD) had elevated troponin levels or cardiac arrest during hospitalization, 17% had coronary heart disease and 35% of patients had hypertension (Zheng, Ma, Zhang, & Xie, 2020; Zhou et al., 2020). However, there is accumulating evidence that COVID-19 patients with underlying CVD are at higher risk for developing severe complications (Huang et al., 2020; Wang, Hu, et al., 2020). For instance, older patients with underlying CVD who are infected with SARS-CoV-2 are more prone to become severely ill, develop cardiac injury or require intensive care (Guo et al., 2020; Shi et al., 2020). The death rate among patients with underlying CVD has been stated as 10.5%, which is much higher than that of the general population (Epidemiology Working Group for Ncip Epidemic Response & Prevention, 2020; Wu & McGoogan, 2020). Furthermore, according to an epidemiological study conducted in China, 4.2% of the confirmed cases and 22.7% of mortalities have cardiovascular comorbidities (Epidemiology Working Group for Ncip Epidemic Response & Prevention, 2020). Many COVID-19 patients suffer from persistent hypotension, myocardial injury, myocarditis, left ventricular dysfunction, arrhythmia and HF (Guan, et al., 2020; Guo et al., 2020; Inciardi et al., 2020; Zhou, Yu, et al., 2020). Importantly, cardiac biopsy samples collected from patients with COVID-19 demonstrated increased interstitial infiltration of mononuclear inflammatory cells providing extra evidence of myocarditis in COVID-19 patients (Xu et al., 2020). Therefore, cardiovascular damage secondary to COVID-19 is now drawing growing attention in clinical practice (Table 2 ) and the American College of Cardiology recently issued a clinical report to address the cardiovascular consequences of SARS-CoV-2 infection (Mohammad Madjid et al., 2020).
Table 2 Overview of COVID-19-associated cardiovascular complications.
COVID-19-induced cardiovascular injury Proposed mechanism of injury
• Acute myocarditis • Direct pathogen invasion
• Indirect cytokine storm
• Instability of coronary atherosclerotic plaques
• Coagulopathy
• Acute MI
• Hypertension
• Left ventricular dilation, hypertrophy and dysfunction
• Arrhythmias (long QT-syndrome, torsade de pointes) • Indirect inflammatory response (Cytokine storm)
• Worsening of heart failure • Indirect inflammatory response (Cytokine storm)
• Volume overload due to impaired sodium and water metabolism
• Disturbance of endothelial function
• Pyroptosis of cardiomyocytes • Hypoxemia
• Activation of the NLRP3 inflammasome
• Severe tachycardia, increased peripheral resistance, hypertension, increased myocardial oxygen requirements and ischemia • Pneumonia-induced increase in sympathetic activity