Lee Clement C E, Ali Kashan, Connell David, Mordi Ify R, George Jacob, Lang Elizabeth Msl, Lang Chim C
Division of Molecular & Clinical Medicine, School of Medicine, Ninewells Hospital & Medical School, University of Dundee, Dundee DD1 9SY, UK.
Diseases. 2021 Jun 29;9(3):47. doi: 10.3390/diseases9030047.
Coronavirus disease 2019 (COVID-19) has been reported to cause cardiovascular complications such as myocardial injury, thromboembolic events, arrhythmia, and heart failure. Multiple mechanisms-some overlapping, notably the role of inflammation and IL-6-potentially underlie these complications. The reported cardiac injury may be a result of direct viral invasion of cardiomyocytes with consequent unopposed effects of angiotensin II, increased metabolic demand, immune activation, or microvascular dysfunction. Thromboembolic events have been widely reported in both the venous and arterial systems that have attracted intense interest in the underlying mechanisms. These could potentially be due to endothelial dysfunction secondary to direct viral invasion or inflammation. Additionally, thromboembolic events may also be a consequence of an attempt by the immune system to contain the infection through immunothrombosis and neutrophil extracellular traps. Cardiac arrhythmias have also been reported with a wide range of implicated contributory factors, ranging from direct viral myocardial injury, as well as other factors, including at-risk individuals with underlying inherited arrhythmia syndromes. Heart failure may also occur as a progression from cardiac injury, precipitation secondary to the initiation or withdrawal of certain drugs, or the accumulation of des-Arg-bradykinin (DABK) with excessive induction of pro-inflammatory G protein coupled receptor B (BK1). The presenting cardiovascular symptoms include chest pain, dyspnoea, and palpitations. There is currently intense interest in vaccine-induced thrombosis and in the treatment of Long COVID since many patients who have survived COVID-19 describe persisting health problems. This review will summarise the proposed physiological mechanisms of COVID-19-associated cardiovascular complications.
据报道，2019冠状病毒病（COVID-19）可引发心血管并发症，如心肌损伤、血栓栓塞事件、心律失常和心力衰竭。多种机制——有些相互重叠，尤其是炎症和白细胞介素-6的作用——可能是这些并发症的潜在原因。报告的心脏损伤可能是由于心肌细胞受到病毒直接侵袭，随后血管紧张素II产生无对抗作用、代谢需求增加、免疫激活或微血管功能障碍所致。血栓栓塞事件在静脉和动脉系统中均有广泛报道，这引发了人们对其潜在机制的浓厚兴趣。这些可能是由于病毒直接侵袭或炎症继发的内皮功能障碍所致。此外，血栓栓塞事件也可能是免疫系统试图通过免疫血栓形成和中性粒细胞胞外陷阱来控制感染的结果。也有报道称心律失常与多种促成因素有关，从病毒直接心肌损伤到其他因素，包括患有潜在遗传性心律失常综合征的高危个体。心力衰竭也可能是心脏损伤的进展、某些药物开始或停用继发的病情加重，或去精氨酸缓激肽（DABK）积累并过度诱导促炎G蛋白偶联受体B（BK1）所致。出现的心血管症状包括胸痛、呼吸困难和心悸。目前，人们对疫苗诱导的血栓形成以及长期COVID的治疗兴趣浓厚，因为许多从COVID-19中康复的患者描述了持续存在的健康问题。本综述将总结COVID-19相关心血管并发症的拟议生理机制。
