Cardiovascular disease (CVD) is the most common co-morbidity associated with COVID-19 and the fatality rate in COVID-19 patients with CVD is highest compared to other comorbidities, such as hypertension and diabetes. Preliminary data suggest that COVID-19 may also cause or worsen cardiac injury in infected patients through multiple mechanisms such as ‘cytokine storm’, endotheliosis, thrombosis, lymphocytopenia etc. Autopsies of COVID-19 patients reveal an infiltration of inflammatory mononuclear cells in the myocardium, confirming the role of the immune system in mediating cardiovascular damage in response to COVID-19 infection and also suggesting potential causal mechanisms for the development of new cardiac pathologies and/or exacerbation of underlying CVDs in infected patients. In this review, we discuss the potential underlying molecular mechanisms that drive COVID-19-mediated cardiac damage, as well as the short term and expected long-term cardiovascular ramifications of COVID-19 infection in patients.

心血管疾病 (CVD) 是与 COVID-19 相关的最常见的合并症，与高血压和糖尿病等其他合并症相比，患有 CVD 的 COVID-19 患者的死亡率最高。初步数据表明，COVID-19 还可能通过“细胞因子风暴”、内皮增生、血栓形成、淋巴细胞减少等多种机制，导致或加重感染患者的心脏损伤。对 COVID-19 患者的尸检显示，心肌中有炎性单核细胞浸润。 ，证实了免疫系统在介导应对 COVID-19 感染的心血管损伤中的作用，并提出了感染患者出现新的心脏病和/或潜在 CVD 恶化的潜在因果机制。在这篇综述中，我们讨论了导致 COVID-19 介导的心脏损伤的潜在分子机制，以及 COVID-19 感染对患者的短期和预期的长期心血管影响。