Evidence map›Paper›PMID 28426714›Full record

ArticlePloS one2017

A genetic risk score for CAD, psychological stress, and their interaction as predictors of CAD, fatal MI, non-fatal MI and cardiovascular death.

Thomas Svensson, Mariusz Kitlinski, Gunnar Engström, Olle Melander

Abstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Role ofPharmaceutics · 2022
    Article
  2. Genetic Risk Score for Coronary Heart Disease: Review.Journal of personalized medicine · 2020
    Review
  3. Sub-Chronic Stress Exacerbates the Pro-Thrombotic Phenotype in BDNFInternational journal of molecular sciences · 2018
    Article
  4. Review
  5. Article
  6. Review
4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Thomas SvenssonDepartment of Clinical Sciences, Lund University, Malmö, Sweden.
Mariusz KitlinskiDepartment of Clinical Sciences, Lund University, Malmö, Sweden.
Gunnar EngströmDepartment of Clinical Sciences, Lund University, Malmö, Sweden.
Olle MelanderDepartment of Clinical Sciences, Lund University, Malmö, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPsychological stress is an independent risk factor for cardiovascular disease (CVD), but the mechanism by which stress is associated with CVD is not entirely understood. Although genetic factors are implied in both stress responsivity and cardiovascular reactivity, no studies to date have investigated their interactions with stress for cardiovascular end points. The objective was to elucidate the association and interactions between a genetic risk score (GRS), individual genetic variants and stress for three cardiovascular end points: coronary artery disease (CAD), fatal myocardial infarction (MI), non-fatal MI, and cardiovascular death. METHODS AND

findings18,559 participants from the Malmö Diet Cancer Study, a population-based prospective study, were included in the analyses. Cox proportional hazards regression models were used and adjusted for a large number of known predictors of cardiovascular end points. Mean follow-up time in years was 14.6 (CAD; n = 1938), 14.8 (fatal MI; n = 436), 14.8 (non-fatal MI; n = 1108), and 15.1 (cardiovascular death; n = 1071) respectively. GRS was significantly associated with increased risks of CAD (top quartile hazard ratio [HR], 1.72; 95% confidence interval [CI], 1.51-1.96), fatal MI (top quartile HR, 1.62; 95%CI, 1.23-2.15), non-fatal MI (top quartile HR, 1.55; 95%CI, 1.31-1.84), and cardiovascular death (top quartile HR, 1.29; 95%CI, 1.08-1.53). Stress was not independently associated with any end point and did not interact with GRS. Four individual genetic variants interacted unfavorably with stress for end points with mortality outcomes.

conclusionA GRS composed of 50 SNPs and predictive of CAD was found for the first time to also strongly predict fatal MI, non-fatal MI and cardiovascular death. A stress-sensitive component of the GRS was isolated on the basis of individual genetic variants that interacted unfavorably with stress.

Indexed as

Genetic Predisposition to DiseaseStress, PsychologicalAgedCoronary Artery DiseaseFemaleHumansMaleMiddle AgedMyocardial Infarction

Identifiers

PMID28426714
PMCPMC5398707

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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.