Coronavirus and Cardiovascular Disease, Myocardial Injury, and Arrhythmia
Key result
Elevated troponin in severe COVID-19 strongly predicts higher in-hospital mortality alongside widespread cardiovascular injury.
Journal of the American College of Cardiology published a graphical abstract
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Why the study?
The cardiovascular system is broadly affected by SARS-CoV-2 infection, but the mechanisms underlying cardiovascular injury and their clinical sequelae require detailed description.
Key Points
- To describe the pathophysiology underlying cardiovascular injury, thromboembolic complications, and arrhythmias during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.
- Narrative review synthesizing mechanisms of SARS-CoV-2 cardiovascular damage, host immune responses, and renin-angiotensin system dysregulation.
- Summarized clinical evidence on troponin elevation, thromboembolism incidence, and myocardial involvement from published cohort studies and autopsy series.
- Myocardial injury, manifested by elevated cardiac troponin levels, occurs in approximately one-quarter of hospitalized patients and is associated with increased requirements for mechanical ventilation and higher in-hospital mortality.
- Cardiovascular damage is mediated through SARS-CoV-2 binding to angiotensin-converting enzyme 2 (ACE2), triggering dysregulation of the renin-angiotensin system, endothelial inflammation, and severe cytokinemia.
- In hospitalized cohorts, thromboembolic disease is frequent, including a 31% cumulative incidence of thrombotic complications (95% CI: 20% to 41%) in intensive care unit patients, with elevated D-dimer and fibrinogen tracking with higher mortality.
PICO
P
Population
COVID-19 and Cardiovascular Disease
E
Exposure / Comparator
COVID-19
Key expert perspectives
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“Myocardial injury results in detectable increases in serum troponin, varying degrees of ventricular dysfunction and relatively frequent cardiac arrhythmias. Whether these effects are simply associated with poor patient outcomes, including death, or directly contribute to patient mortality is as yet uncertain.”
Implication
COVID-19 frequently involves the cardiovascular system, resulting in myocardial injury, endotheliitis, microvascular thrombosis, and arrhythmias which portend a worse prognosis.
Abstract
The cardiovascular system is affected broadly by severe acute respiratory syndrome coronavirus 2 infection. Both direct viral infection and indirect injury resulting from inflammation, endothelial activation, and microvascular thrombosis occur in the context of coronavirus disease 2019. What determines the extent of cardiovascular injury is the amount of viral inoculum, the magnitude of the host immune response, and the presence of co-morbidities. Myocardial injury occurs in approximately one-quarter of hospitalized patients and is associated with a greater need for mechanical ventilator support and higher hospital mortality. The central pathophysiology underlying cardiovascular injury is the interplay between virus binding to the angiotensin-converting enzyme 2 receptor and the impact this action has on the renin-angiotensin system, the body’s innate immune response, and the vascular response to cytokine production. The purpose of this review was to describe the mechanisms underlying cardiovascular injury, including that of thromboembolic disease and arrhythmia, and to discuss their clinical sequelae.
Discussion
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Cite This Study
Giustino et al. (2020) conducted a review in COVID-19 and Cardiovascular Disease. COVID-19 was evaluated. Severe COVID-19 is associated with exuberant cytokinemia, endothelial inflammation, microvascular thrombosis, myocardial injury, and arrhythmias, with elevated cardiac troponin strongly predicting higher in-hospital mortality.