Coronavirus disease 2019 and cardiovascular disease

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus behind the coronavirus disease 2019 (COVID-19) pandemic, is a type of RNA virus that is nonsegmented. Cardiovascular diseases (CVDs) increase the mortality risk of patients. In this review article, we overview the existing evidence regarding the potential mechanisms of myocardial damage in coronavirus disease 2019 (COVID-19) patients. Having a comprehensive knowledge of the cardiovascular damage caused by SARS-CoV-2 and its underlying mechanisms is essential for providing prompt and efficient treatment, ultimately leading to a reduction in mortality rates. Severe COVID-19 causes acute respiratory distress syndrome and shock in patients. In addition, awareness regarding COVID-19 cardiovascular manifestations has increased, including the adverse impact on prognosis with cardiovascular involvement. Angiotensin-converting enzyme 2 receptor may play a role in acute myocardial injury caused by SARS-CoV-2 infection. COVID-19 patients experiencing heart failure may have their condition exacerbated by various contributing factors and mechanisms. Increased oxygen demand, myocarditis, stress cardiomyopathy, elevated pulmonary pressures, and venous thrombosis are potential health issues. The combination of these factors may lead to COVID-19-related cardiogenic shock, resulting in acute systolic heart failure. Extracorporeal membrane oxygenation (ECMO) and left ventricular assist devices (LVADs) are treatment options when inotropic support fails for effective circulatory support. To ensure effective COVID-19-related cardiovascular disease (CVD) surveillance, it is crucial to closely monitor the future host adaptation, viral evolution, and transmissibility of SARS-CoV-2, given the virus's pandemic potential.

Keywords: Angiotensin-converting enzyme 2 receptor; Cardiovascular disease; Coronavirus disease 2019.

Figure 1

Proposed functions of host cell molecules for interaction with SARS-CoV-2. SARS-CoV-2 enters cells by binding its spike proteins to ACE2 receptors and priming with TMPRSS2 proteases. CyPA and SARS-CoV-2 N protein can promote entry via CD147. GRP78, normally a chaperone in the ER, can promote entry when transported to the cell membrane. The acidic environment in intracellular vesicles facilitates viral replication. CyPA regulates inflammation and cardiovascular processes. SARS-CoV-2: Severe acute respiratory syndrome coronavirus 2, ACE2: Angiotensin-converting enzyme 2, TMPRSS2: Transmembrane serine protease 2, ER: Endoplasmic reticulum

Figure 2

Endothelial cell damage, thromboinflammation, and VSMC injury in COVID-19. VSMC: Vascular smooth muscle cell, COVID-19: Coronavirus disease 2019

Figure 3

Possible mechanisms of myocardial injury in COVID-19. SARS-CoV-2 infection of the myocardium depends on ACE-2 receptors and leads to cardiomyopathy, dysfunction, and heart failure. Viral RNA is detected in autopsied heart samples, with significant macrophage infiltration. ACE-2 downregulation impairs cardioprotective effects, leading to TNF-α production and myocardial damage. Elevated inflammatory markers and troponin levels support the idea of a severe inflammatory response causing damage. SARS activates TGF-β signaling, inducing fibrosis and potentially causing cardiac damage. Interferon-mediated responses and exaggerated cytokine response from T-cells contribute to myocardial dysfunction. CD147 may provide an alternative route for SARS-CoV-2 entry besides ACE2. CD147 expression is regulated by reactive oxygen species and cytokines and is associated with hypertension, obesity, and cardiomyopathy. Cyclophilins, such as CyPA, may also promote entry through CD147. Other alternative receptors include CD209 L and CD209. SARS-CoV-2: Severe acute respiratory syndrome coronavirus 2, ACE2: Angiotensin-converting enzyme 2, TMPRSS2: Transmembrane serine protease 2, ER: Endoplasmic reticulum