Subject: COVID-19
Subject: SARS-CoV-2
Subject: cardiovascular disease
Subject: cytokines
Subject: endothelial dysfunction
Subject: infection
Subject: inflammation
Subject: microcirculation
Subject: myocardial injury
Subject: post-acute COVID-19
Subject: thrombosis
Year: 2021
Type: Article
Title: Cardiovascular disease and COVID-19: a consensus paper from the ESC Working Group on Coronary Pathophysiology & Microcirculation, ESC Working Group on Thrombosis and the Association for Acute CardioVascular Care (ACVC), in collaboration with the European Heart Rhythm Association (EHRA)
Author: Cenko, Edina
Author: Badimon, Lina
Author: Bugiardini, Raffaele
Author: Claeys, Marc J
Author: De Luca, Giuseppe
Author: de Wit, Cor
Author: Derumeaux, Geneviève
Author: Dorobantu, Maria
Author: Duncker, Dirk J
Author: Eringa, Etto C
Author: Gorog, Diana A
Author: Hassager, Christian
Author: Heinzel, Frank R
Author: Huber, Kurt
Author: Manfrini, Olivia
Author: Milicic, Davor
Author: Oikonomou, Evangelos
Author: Padro, Teresa
Author: Trifunovic-Zamaklar, Danijela
Author: Vasiljevic-Pokrajcic, Zorana
Author: Vavlukis, Marija
Author: Vilahur, Gemma
Author: Tousoulis, Dimitris
Abstract: 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 SARS-CoV-2 and ACE2 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.
Publisher: Oxford University Press (OUP)
Relation: Cardiovascular research
Identifier: oai:repository.ukim.mk:20.500.12188/15463
Identifier: Cenko E, Badimon L, Bugiardini R, Claeys MJ, De Luca G, de Wit C, Derumeaux G, Dorobantu M, Duncker DJ, Eringa EC, Gorog DA, Hassager C, Heinzel FR, Huber K, Manfrini O, Milicic D, Oikonomou E, Padro T, Trifunovic-Zamaklar D, Vasiljevic-Pokrajcic Z, Vavlukis M, Vilahur G, Tousoulis D. Cardiovascular disease and COVID-19: a consensus paper from the ESC Working Group on Coronary Pathophysiology & Microcirculation, ESC Working Group on Thrombosis and the Association for Acute CardioVascular Care (ACVC), in collaboration with the European Heart Rhythm Association (EHRA). Cardiovasc Res. 2021 Sep 16:cvab298. doi: 10.1093/cvr/cvab298. Epub ahead of print. PMID: 34528075; PMCID: PMC8500019.
Identifier: http://hdl.handle.net/20.500.12188/15463Identifier: 10.1093/cvr/cvab298
Identifier: http://academic.oup.com/cardiovascres/advance-article-pdf/doi/10.1093/cvr/cvab298/40533236/cvab298.pdfIdentifier: http://academic.oup.com/cardiovascres/advance-article-pdf/doi/10.1093/cvr/cvab298/40533236/cvab298.pdf
