TY - JOUR
TI - 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)
AU - Cenko, Edina
AU - Badimon, Lina
AU - Bugiardini, Raffaele
AU - Claeys, Marc
AU - J.
AU - De Luca, Giuseppe
AU - de Wit, Cor
AU - Derumeaux, Genevieve and
AU - Dorobantu, Maria
AU - Duncker, Dirk J.
AU - Eringa, Etto C.
AU - Gorog,
AU - Diana A.
AU - Hassager, Christian
AU - Heinzel, Frank R.
AU - Huber, Kurt
AU - and Manfrini, Olivia
AU - Milicic, Davor
AU - Oikonomou, Evangelos and
AU - Padro, Teresa
AU - Trifunovic-Zamaklar, Danijela and
AU - Vasiljevic-Pokrajcic, Zorana
AU - Vavlukis, Marija
AU - Vilahur, Gemma and
AU - Tousoulis, Dimitris
JO - Cardiovascular Research
PY - 2021
VL - 117
TODO - 14
SP - 2705-2729
PB - Oxford University Press
SN - 0008-6363, 1755-3245
TODO - 10.1093/cvr/cvab298
TODO - Cardiovascular disease; COVID-19; SARS-CoV-2; cytokines; inflammation;
Infection; endothelial dysfunction; microcirculation; thrombosis;
Myocardial injury; post-acute COVID-19
TODO - 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.
ER -