SORA

Advancing, promoting and sharing knowledge of health through excellence in teaching, clinical practice and research into the prevention and treatment of illness

Genetically Determined Platelet Count and Risk of Cardiovascular Disease.

Gill, D; Monori, G; Georgakis, MK; Tzoulaki, I; Laffan, M (2018) Genetically Determined Platelet Count and Risk of Cardiovascular Disease. Arterioscler Thromb Vasc Biol, 38 (12). pp. 2862-2869. ISSN 1524-4636 https://doi.org/10.1161/ATVBAHA.118.311804
SGUL Authors: Gill, Dipender Preet Singh

[img]
Preview
PDF Published Version
Available under License Creative Commons Attribution.

Download (345kB) | Preview

Abstract

Objective- Cardiovascular disease, including coronary artery disease (CAD) and ischemic stroke, is the leading cause of death worldwide. This Mendelian randomization study uses genetic variants as instruments to investigate whether there is a causal effect of genetically determined platelet count on CAD and ischemic stroke risk. Approach and Results- A genome-wide association study of 166 066 subjects was used to identify instruments and genetic association estimates for platelet count. Genetic association estimates for CAD and ischemic stroke were obtained from genome-wide association studies, including 60 801 CAD cases and 123 504 controls, and 60 341 ischemic stroke cases and 454 450 controls, respectively. The inverse-variance weighted meta-analysis of ratio method Mendelian randomization estimates was the main method used to obtain estimates for the causal effect of genetically determined platelet count on risk of cardiovascular outcomes. We found no significant Mendelian randomization effect of genetically determined platelet count on risk of CAD (odds ratio of CAD per SD unit increase in genetically determined platelet count, 1.01; 95% CI, 0.98-1.04; P=0.60). However, higher genetically determined platelet count was causally associated with an increased risk of ischemic stroke (odds ratio, 1.07; 95% CI, 1.04-1.11; P<1×10-5), including all major ischemic stroke subtypes. Similar results were obtained in sensitivity analyses more robust to the inclusion of pleiotropic genetic variants. Conclusions- This Mendelian randomization study found evidence that higher genetically determined platelet count is causally associated with higher risk of ischemic stroke.

Item Type: Article
Additional Information: © 2018 The Authors. Arteriosclerosis, Thrombosis, and Vascular Biology is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited.
Keywords: blood platelet, cardiovascular diseases, coronary artery disease, myocardial infarction, stroke, Blood Platelets, Brain Ischemia, Coronary Artery Disease, Female, Genetic Association Studies, Genetic Predisposition to Disease, Humans, Male, Mendelian Randomization Analysis, Myocardial Infarction, Phenotype, Platelet Count, Polymorphism, Single Nucleotide, Predictive Value of Tests, Risk Assessment, Risk Factors, Stroke, Blood Platelets, Humans, Brain Ischemia, Myocardial Infarction, Genetic Predisposition to Disease, Platelet Count, Risk Assessment, Risk Factors, Predictive Value of Tests, Phenotype, Polymorphism, Single Nucleotide, Female, Male, Coronary Artery Disease, Stroke, Genetic Association Studies, Mendelian Randomization Analysis, Cardiovascular System & Hematology, 1103 Clinical Sciences, 1102 Cardiorespiratory Medicine and Haematology
SGUL Research Institute / Research Centre: Academic Structure > Infection and Immunity Research Institute (INII)
Journal or Publication Title: Arterioscler Thromb Vasc Biol
ISSN: 1524-4636
Language: eng
Dates:
DateEvent
December 2018Published
11 October 2018Published Online
24 September 2018Published Online
Publisher License: Creative Commons: Attribution 4.0
Projects:
Project IDFunderFunder ID
UNSPECIFIEDWellcome TrustUNSPECIFIED
PubMed ID: 30571169
Go to PubMed abstract
URI: https://openaccess.sgul.ac.uk/id/eprint/112798
Publisher's version: https://doi.org/10.1161/ATVBAHA.118.311804

Actions (login required)

Edit Item Edit Item