ArticleCardiovascular toxicology2025
COVID-19 Predisposition Inherently Increases Cardiovascular Risk Before SARS-CoV-2 Infection.
Article in Cardiovascular toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Association of COVID-19 with risks of all-cause and cause-specific mortality post-infection: A UK Biobank cohort study.New microbes and new infections · 2026Article
- Large-Scale Disease-Wide Association Study Identified Predisposition Links Between Influenza and Cardiovascular Diseases.Cardiovascular toxicology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
As COVID-19 transitions to an endemic stage, its long-term impacts on health, particularly cardiovascular disease (CVD), remain significant. While prior studies have focused on cardiovascular complications following SARS-CoV-2 infection, the question of inherent cardiovascular risk associated with genetic predisposition to COVID-19 has been less explored. This study investigates whether individuals genetically predisposed to COVID-19 may also be at higher risk for CVD, independent of actual infection. Using Mendelian randomization (MR) analysis with data from pre-pandemic, SARS-CoV-2-naive populations, this study assessed the impact of genetic susceptibility to COVID-19 on various CVD outcomes across 18 distinct cohorts. This approach allowed us to simulate COVID-19 predisposition without infection, providing insights into cardiovascular risks associated solely with genetic susceptibility. These findings reveal a significant association between genetic predisposition to COVID-19 and elevated risks for several CVD outcomes, particularly hypertensive heart disease. Notably, individuals with a genetic profile linked to severe COVID-19 (hospitalization-prone) showed a marked increase in risk for hypertensive heart disease. These findings suggest a shared genetic architecture that predisposes individuals to both COVID-19 and cardiovascular risks, irrespective of viral exposure. COVID-19 susceptibility, thus, may act as a "natural stress test," revealing latent cardiovascular vulnerabilities. This connection implies that individuals predisposed to severe COVID-19 may have inherently higher cardiovascular risks, even without SARS-CoV-2 infection. This study highlights the value of COVID-19 susceptibility as a novel marker for assessing CVD risk, enabling timely preventive strategies and mitigating future CVD burden in the post-COVID-19 era. Moreover, this study highlights disease predisposition as a "black box" until clinical onset. While COVID-19 demands an external viral trigger for acute onset, cardiovascular disease unfolds much more slowly, requiring prolonged exposure to detrimental lifestyle and genetic factors. Together, their intersection illustrates how acute environmental triggers and chronic disease processes can converge to influence overall health outcomes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.