José Rozado , Ana Ayesta , César Morís , Pablo Avanzas
{"title":"COVID-19患者心血管疾病的病理生理学。缺血、血栓形成和心脏功能障碍","authors":"José Rozado , Ana Ayesta , César Morís , Pablo Avanzas","doi":"10.1016/S1131-3587(20)30028-5","DOIUrl":null,"url":null,"abstract":"<div><p>Cardiovascular complications are highly prevalent in patients with COVID-19 and frequently lead to hospitalization, death and long-term morbidity. This article describes the principle pathophysiological mechanisms involved in the development of these complications. After the initial viremia, viralinvasión and replication occurs in the lungs, accompanied by immune system activation, cytokine release and the induction of a proinflammatory state, with sepsis and multiorgan failure. Myocardial injury could be due to the direct effect of viralinvasión and a local inflammatory response or to the indirect effect of inappropriate systemic inflammation involving a cytokine storm. Furthermore, the development of a prothrombotic state, together with vascular disease due to the virus, could trigger ischemic and thrombotic events secondary to microvascular damage or to the destabilization of pre-existing atheromatous plaque. New research is needed to reveal the pathophysiological mechanisms underlying these cardiovascular events and to support the development of effective new treatments.</p></div>","PeriodicalId":34926,"journal":{"name":"Revista Espanola de Cardiologia Suplementos","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1131-3587(20)30028-5","citationCount":"12","resultStr":"{\"title\":\"Fisiopatología de la enfermedad cardiovascular en pacientes con COVID-19. Isquemia, trombosis y disfunción cardiaca\",\"authors\":\"José Rozado , Ana Ayesta , César Morís , Pablo Avanzas\",\"doi\":\"10.1016/S1131-3587(20)30028-5\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Cardiovascular complications are highly prevalent in patients with COVID-19 and frequently lead to hospitalization, death and long-term morbidity. This article describes the principle pathophysiological mechanisms involved in the development of these complications. After the initial viremia, viralinvasión and replication occurs in the lungs, accompanied by immune system activation, cytokine release and the induction of a proinflammatory state, with sepsis and multiorgan failure. Myocardial injury could be due to the direct effect of viralinvasión and a local inflammatory response or to the indirect effect of inappropriate systemic inflammation involving a cytokine storm. Furthermore, the development of a prothrombotic state, together with vascular disease due to the virus, could trigger ischemic and thrombotic events secondary to microvascular damage or to the destabilization of pre-existing atheromatous plaque. New research is needed to reveal the pathophysiological mechanisms underlying these cardiovascular events and to support the development of effective new treatments.</p></div>\",\"PeriodicalId\":34926,\"journal\":{\"name\":\"Revista Espanola de Cardiologia Suplementos\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2020-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/S1131-3587(20)30028-5\",\"citationCount\":\"12\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Revista Espanola de Cardiologia Suplementos\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1131358720300285\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Revista Espanola de Cardiologia Suplementos","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1131358720300285","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
Fisiopatología de la enfermedad cardiovascular en pacientes con COVID-19. Isquemia, trombosis y disfunción cardiaca
Cardiovascular complications are highly prevalent in patients with COVID-19 and frequently lead to hospitalization, death and long-term morbidity. This article describes the principle pathophysiological mechanisms involved in the development of these complications. After the initial viremia, viralinvasión and replication occurs in the lungs, accompanied by immune system activation, cytokine release and the induction of a proinflammatory state, with sepsis and multiorgan failure. Myocardial injury could be due to the direct effect of viralinvasión and a local inflammatory response or to the indirect effect of inappropriate systemic inflammation involving a cytokine storm. Furthermore, the development of a prothrombotic state, together with vascular disease due to the virus, could trigger ischemic and thrombotic events secondary to microvascular damage or to the destabilization of pre-existing atheromatous plaque. New research is needed to reveal the pathophysiological mechanisms underlying these cardiovascular events and to support the development of effective new treatments.
期刊介绍:
Revista Española de Cardiología, is an international scientific journal dealing with cardiovascular medicine. Revista Española de Cardiología, the official publication of the Spanish Society of Cardiology, publishes research articles related to cardiovascular diseases. Articles are published in Spanish for the paper edition and in both Spanish and English in the electronic edition, which is available on the Internet. Regular sections include original articles reporting clinical or basic research, brief reports, review articles, editorials and letters to the Editor.