SARS-CoV-2 infection is associated with increased risk of late cardiovascular outcomes

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A new study by researchers from Oregon Health & Science University, Cleveland Clinic Lerner Research Institute and the Chicago Medical School at Rosalind Franklin University have in a new study found that either symptomatic or asymptomatic SARS-CoV-2 infection is associated with increased risk of late cardiovascular outcomes and has causal effect on all-cause mortality in a late post-COVID-19 period.

The study findings were published on a preprint server and are currently being peer reviewed. https://www.medrxiv.org/content/10.1101/2021.12.27.21268448v1

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) uses angiotensin- converting enzyme 2 (ACE2) as the receptor-binding domain.[1] Cardiac myocytes express ACE2, which makes the heart a target organ in the novel coronavirus disease 2019 (COVID- 19).[2]

The COVID-19 pandemic has revealed heterogenous cardiovascular manifestations of infection, which likely contribute to the high case fatality rate in COVID-19.[3]

Myocardial injury in COVID-19 can be caused by both direct injury to cardiac myocytes as well as secondary effects from the systemic inflammation and hypercoagulable state seen in acute infection. Cardiovascular manifestations of COVID-19 include acute myocardial infarction, stress cardiomyopathy, myocarditis, heart failure (HF), pulmonary embolism, and cardiac arrhythmias.[3]

Furthermore, COVID-19 patients with known cardiovascular disease (CVD) and other risk factors including age, hypertension, diabetes, obesity, kidney disease, and respiratory system disease are more likely to require critical care and have a higher mortality rate.[4]

Post-acute or “long” COVID-19 has been described in patients with persistent symptoms or complications after the end of the acute phase of infection.[5, 6] The virulence and transmissibility of the SARS-CoV-2 virus and ongoing difficulties with public health policies and compliance challenges the ability to control COVID-19. As the virus mutates, it continues circulating throughout the globe.[7]

Acute COVID-19 cardiovascular manifestations have been described in great depth.[8, 9, 10] However, the impact of COVID-19 on long-term cardiovascular outcomes remains unknown.[10] Furthermore, previous studies have had limitations, such as selection bias and absence of a control.

Thus, it is essential to study the incidence, manifestations, and risk factors of post-acute outcomes that either symptomatic or asymptomatic SARS-CoV-2 infection poses on cardiovascular health.

The COVID-19 pandemic disrupted the delivery of standard cardiovascular care[11] which led to increased cardiovascular mortality in populations presumably unexposed to the SARS- CoV-2 virus.[12, 13]

On the other hand, SARS-CoV-2 infection can be asymptomatic, and, thus, undiagnosed without testing. It remains unknown if the SARS-CoV-2 infection (either symptomatic or asymptomatic) is associated with a risk of long-term cardiovascular events, as compared to verified absence of the SARS-CoV-2 infection.

Furthermore, while higher than expected all-cause mortality during the pandemic has been recognized,[14] it is unclear whether either asymptomatic or symptomatic SARS-CoV-2 infections may have played a causal role.

To address these knowledge gaps, we prospectively designed and conducted a retrospective double- cohort study to determine: (1) absolute (attributable) risk, (2) relative conditional risk, and (3) causal inference effect of either symptomatic or asymptomatic SARS-CoV-2 infection on post- acute (late) cardiovascular events and all-cause mortality.

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