Abstract
Infection with the novel severe acute respiratory coronavirus-2 (SARS-CoV2) results in COVID-19, a disease primarily affecting the respiratory system to provoke a spectrum of clinical manifestations, the most severe being acute respiratory distress syndrome (ARDS). A significant proportion of COVID-19 patients also develop various cardiac complications, among which dysfunction of the right ventricle (RV) appears particularly common, especially in severe forms of the disease, and which is associated with a dismal prognosis. Echocardiographic studies indeed reveal right ventricular dysfunction in up to 40% of patients, a proportion even greater when the RV is explored with strain imaging echocardiography. The pathophysiological mechanisms of RV dysfunction in COVID-19 include processes increasing the pulmonary vascular hydraulic load and others reducing RV contractility, which precipitate the acute uncoupling of the RV with the pulmonary circulation. Understanding these mechanisms provides the fundamental basis for the adequate therapeutic management of RV dysfunction, which incorporates protective mechanical ventilation, the prevention and treatment of pulmonary vasoconstriction and thrombotic complications, as well as the appropriate management of RV preload and contractility. This comprehensive review provides a detailed update of the evidence of RV dysfunction in COVID-19, its pathophysiological mechanisms, and its therapy.
Highlights
Since the first cases of infection with the novel severe acute respiratory coronavirus-2(SARS-CoV2) in December 2019, more than 160 million cases of COVID-19 and 3.3 million deaths worldwide have been reported
right ventricle (RV) dysfunction is a known complication associated with various forms of acute respiratory distress syndrome (ARDS), its prevalence appears elevated in the setting of COVID-19 ARDS
Echocardiographic studies have shown that RV dysfunction in COVID-19 may take the form of a specific radial, instead of longitudinal dysfunction, and that it is commonly accompanied by RV dilation due to pressure overload
Summary
Since the first cases of infection with the novel severe acute respiratory coronavirus-2. (SARS-CoV2) in December 2019, more than 160 million cases of COVID-19 and 3.3 million deaths worldwide have been reported (as of 12 May 2021). While the primary clinical manifestations of COVID-19 involve the respiratory tract, it has become evident that SARS-CoV2 provokes a systemic disease with multiorgan involvement. Among the extrapulmonary manifestations of COVID-19, a number of cardiac complications have been described, including myocarditis, taksotsubo cardiomyopathy, arrhythmias, or acute coronary syndromes. Dysfunction of the right ventricle (RV) has emerged as a common feature of COVID-19, most significantly in patients with acute respiratory distress syndrome (ARDS), responsible for the majority of casualties in COVID19. Several pathophysiological processes set in motion during the infection with SARS-CoV2 permit us, at least partly, to explain the frequent occurrence of RV dysfunction in this condition. The aim of the present comprehensive review is to provide an update of the relevant literature pertaining to the clinical presentation, the pathophysiology, and the therapeutic management of RV dysfunction in COVID-19
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