Electrophysiology in the Era of Coronavirus Disease 2019

Collateral tissue injury and the inflammatory process that follows cause vasodilatation, endothelial permeability, and leucocyte recruitment leading to further pulmonary damage, hypoxaemia and cardiovascular stress.3,4 Several recent studies have demonstrated a deleterious impact on the cardiovascul...

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Veröffentlicht in:Arrhythmia & electrophysiology review 2020-11, Vol.9 (3), p.167-170
Hauptverfasser: Kanthasamy, Vijayabharathy, Schilling, Richard
Format: Artikel
Sprache:eng
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Zusammenfassung:Collateral tissue injury and the inflammatory process that follows cause vasodilatation, endothelial permeability, and leucocyte recruitment leading to further pulmonary damage, hypoxaemia and cardiovascular stress.3,4 Several recent studies have demonstrated a deleterious impact on the cardiovascular system including acute myocardial injury, acute myocarditis, cardiomyopathies, arrhythmias, sudden cardiac death and cardiac arrest.5,6 Angiotensin-converting enzyme 2 (ACE2) acts as a host receptor, facilitating entry of the SARS-CoV-2 infection into human cells, and is expressed in lung alveolar epithelial, heart, vascular and gastrointestinal tract cells.7,8 Even though it is not certain at this time, ACE2 host receptor involvement may account for the clinical presentations with cardiovascular complications, such as myocarditis, arrhythmia and cardiogenic shock. [...]extremely raised D-dimer levels are found in patients affected with COVID-19, with a substantial proportion affected with venous and arterial thromboembolism.13,15 There is no clear evidence as to whether all patients with the combination of severe COVID-19, new-onset AF and very high D-dimer would benefit from therapeutic anticoagulation irrespective of CHA2DS2VASc score due to the additional risk of thromboembolism associated with COVID-19. [...]either dose reduction or monitoring of plasma levels is essential to minimise the risk of bleeding.16–18 There is a small amount of emerging literature on the incidence of ventricular arrhythmias. COVID-19 can also cause diarrhoea, malabsorption, acute kidney injury and electrolyte imbalance, which may pose a risk of ventricular and atrial arrhythmias.21–23 In addition, there is an increased risk of MI during the acute phase in patients with cardiac comorbidities, secondary to supply/demand imbalance, plaque rupture, severe hypoxia causing myocyte necrosis or arterial embolism due to hypercoagulable state, which can trigger malignant ventricular arrhythmias.24–26 Risk of Sudden Cardiac Death There are no specific data on patients with channelopathies or inherited cardiomyopathies and COVID-19.
ISSN:2050-3369
2050-3377
DOI:10.15420/aer.2020.32