The cardiovascular system is significantly affected in coronavirus disease-19 (COVID-19). Microvascular injury, endothelial dysfunction, and thrombosis resulting from viral infection or indirectly related to the intense systemic inflammatory and immune responses are characteristic features of severe COVID-19. Pre-existing cardiovascular disease and viral load are linked to myocardial injury and worse outcomes. The vascular response to cytokine production and the interaction between severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and angiotensin-converting enzyme 2 receptor may lead to a significant reduction in cardiac contractility and subsequent myocardial dysfunction. In addition, a considerable proportion of patients who have been infected with SARS-CoV-2 do not fully recover and continue to experience a large number of symptoms and post-acute complications in the absence of a detectable viral infection. This conditions often referred to as ‘post-acute COVID-19’ may have multiple causes. Viral reservoirs or lingering fragments of viral RNA or proteins contribute to the condition. Systemic inflammatory response to COVID-19 has the potential to increase myocardial fibrosis which in turn may impair cardiac remodelling. Here, we summarize the current knowledge of cardiovascular injury and post-acute sequelae of COVID-19. As the pandemic continues and new variants emerge, we can advance our knowledge of the underlying mechanisms only by integrating our understanding of the pathophysiology with the corresponding clinical findings. Identification of new biomarkers of cardiovascular complications, and development of effective treatments for COVID-19 infection are of crucial importance.

中文翻译：

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心血管疾病和 COVID-19：ESC 冠状动脉病理生理学和微循环工作组、ESC 血栓形成工作组和急性心血管护理协会 (ACVC) 与欧洲心律协会 (EHRA) 合作的共识文件

心血管系统在冠状病毒病 19 (COVID-19) 中受到显着影响。由病毒感染或与强烈的全身炎症和免疫反应间接相关的微血管损伤、内皮功能障碍和血栓形成是严重 COVID-19 的特征。预先存在的心血管疾病和病毒载量与心肌损伤和更坏的结果有关。血管对细胞因子产生的反应以及严重急性呼吸综合征冠状病毒-2 (SARS-CoV-2) 与血管紧张素转换酶 2 受体之间的相互作用可能导致心脏收缩力显着降低和随后的心肌功能障碍。此外，在没有检测到病毒感染的情况下，相当一部分感染 SARS-CoV-2 的患者没有完全康复，并继续出现大量症状和急性后并发症。这种通常被称为“急性 COVID-19 后”的情况可能有多种原因。病毒库或病毒 RNA 或蛋白质的挥之不去的片段会导致这种情况。对 COVID-19 的全身炎症反应有可能增加心肌纤维化，进而可能损害心脏重塑。在这里，我们总结了目前关于心血管损伤和 COVID-19 急性后遗症的知识。随着大流行的继续和新变种的出现，只有将我们对病理生理学的理解与相应的临床发现相结合，我们才能提高对潜在机制的了解。识别心血管并发症的新生物标志物以及开发针对 COVID-19 感染的有效治疗方法至关重要。