Cardiovascular involvement in COVID-19: not to be missed

Abstract In December 2019, a striking appearance of new cases of viral pneumonia in Wuhan led to the detection of a novel coronavirus (SARS-CoV2). By analyzing patients with severe manifestations, it became apparent that 20 to 35% of patients who died had preexisting cardiovascular disease. This finding warrants the important need to discuss the influence of SARS-CoV2 infection on the cardiovascular system and hemodynamics in the context of clinical management, particularly during mechanical ventilation. The SARS-CoV2 enters human cells through the spike protein binding to angiotensin-converting enzyme 2 (ACE2), which is important to cardiovascular modulation and endothelial signaling. As ACE2 is highly expressed in lung tissue, patients have been progressing to acute respiratory injury at an alarming frequency during the Coronavirus Disease (COVID-19) pandemic. Moreover, COVID-19 leads to high D-dimer levels and prothrombin time, which indicates a substantial coagulation disorder. It seems that an overwhelming inflammatory and thrombogenic condition is responsible for a mismatching of ventilation and perfusion, with a somewhat near-normal static lung compliance, which describes two types of pulmonary conditions. As such, positive pressure during invasive mechanical ventilation (IMV) must be applied with caution. The authors of this review appeal to the necessity of paying closer attention to assess microhemodynamic repercussion, by monitoring central venous oxygen saturation during strategies of IMV. It is well known that a severe respiratory infection and a scattered inflammatory process can cause non-ischemic myocardial injury, including progression to myocarditis. Early strategies that guide clinical decisions can be lifesaving and prevent extended myocardial damage. Moreover, cardiopulmonary failure refractory to standard treatment may necessitate the use of extreme therapeutic strategies, such as extracorporeal membrane oxygenation.

摘要 2019年12月，武汉出现多起病毒性肺炎新增病例，由此检出新型冠状病毒（SARS-CoV2）。通过分析重症患者，研究人员发现20%至35%的死亡患者既往存在心血管基础疾病。该发现凸显了在临床管理场景下探讨SARS-CoV2感染对心血管系统及血流动力学的影响的重要性，尤其在机械通气过程中。SARS-CoV2通过刺突蛋白结合血管紧张素转换酶2（ACE2）侵入人体细胞，该酶在心血管调节及内皮信号传导中发挥关键作用。由于ACE2在肺组织中高表达，在新型冠状病毒肺炎（COVID-19）大流行期间，患者急性呼吸损伤的进展速度令人警觉。此外，COVID-19可导致D-二聚体水平升高及凝血酶原时间延长，提示存在显著的凝血功能障碍。目前认为，过度的炎症及血栓形成状态会引发通气血流比例失调，同时静态肺顺应性近乎正常，这一特征对应两类肺部病变。因此，实施有创机械通气（IMV）时的正压通气策略需格外谨慎。本综述的作者呼吁，有必要进一步密切监测并评估血流动力学微改变，可通过在有创机械通气策略期间监测中心静脉血氧饱和度来实现。众所周知，重症呼吸道感染及弥散性炎症过程可引发非缺血性心肌损伤，甚至进展为心肌炎。能够指导临床决策的早期干预策略可挽救患者生命，并预防心肌进一步损伤。此外，经标准治疗无效的心肺衰竭患者，可能需要采用体外膜肺氧合等极端治疗手段。