Cardiac Risk Factors for Stroke: A Comprehensive Mendelian Randomization Study.


Journal

Stroke
ISSN: 1524-4628
Titre abrégé: Stroke
Pays: United States
ID NLM: 0235266

Informations de publication

Date de publication:
04 2022
Historique:
pubmed: 17 12 2021
medline: 26 4 2022
entrez: 16 12 2021
Statut: ppublish

Résumé

Observational studies suggest an association of stroke with cardiac traits beyond atrial fibrillation, the leading source of cardioembolism. However, controversy remains regarding a causal role of these traits in stroke pathogenesis. Here, we leveraged genetic data to systematically assess associations between cardiac traits and stroke risk using a Mendelian Randomization framework. We studied 66 cardiac traits including cardiovascular diseases, magnetic resonance imaging-derived cardiac imaging, echocardiographic imaging, and electrocardiographic measures, as well as blood biomarkers in a 2-sample Mendelian Randomization approach. Genetic predisposition to each trait was explored for associations with risk of stroke and stroke subtypes in data from the MEGASTROKE consortium (40 585 cases/406 111 controls). Using multivariable Mendelian Randomization, we adjusted for potential pleiotropic or mediating effects relating to atrial fibrillation, coronary artery disease, and systolic blood pressure. As expected, we observed strong independent associations between genetic predisposition to atrial fibrillation and cardioembolic stroke and between genetic predisposition to coronary artery disease as a proxy for atherosclerosis and large-artery stroke. Our data-driven analyses further indicated associations of genetic predisposition to both heart failure and lower resting heart rate with stroke. However, these associations were explained by atrial fibrillation, coronary artery disease, and systolic blood pressure in multivariable analyses. Genetically predicted P-wave terminal force in V1, an electrocardiographic marker for atrial cardiopathy, was inversely associated with large-artery stroke. Available genetic data do not support substantial effects of cardiac traits on the risk of stroke beyond known clinical risk factors. Our findings highlight the need to carefully control for confounding and other potential biases in studies examining candidate cardiac risk factors for stroke.

Sections du résumé

BACKGROUND
Observational studies suggest an association of stroke with cardiac traits beyond atrial fibrillation, the leading source of cardioembolism. However, controversy remains regarding a causal role of these traits in stroke pathogenesis. Here, we leveraged genetic data to systematically assess associations between cardiac traits and stroke risk using a Mendelian Randomization framework.
METHODS
We studied 66 cardiac traits including cardiovascular diseases, magnetic resonance imaging-derived cardiac imaging, echocardiographic imaging, and electrocardiographic measures, as well as blood biomarkers in a 2-sample Mendelian Randomization approach. Genetic predisposition to each trait was explored for associations with risk of stroke and stroke subtypes in data from the MEGASTROKE consortium (40 585 cases/406 111 controls). Using multivariable Mendelian Randomization, we adjusted for potential pleiotropic or mediating effects relating to atrial fibrillation, coronary artery disease, and systolic blood pressure.
RESULTS
As expected, we observed strong independent associations between genetic predisposition to atrial fibrillation and cardioembolic stroke and between genetic predisposition to coronary artery disease as a proxy for atherosclerosis and large-artery stroke. Our data-driven analyses further indicated associations of genetic predisposition to both heart failure and lower resting heart rate with stroke. However, these associations were explained by atrial fibrillation, coronary artery disease, and systolic blood pressure in multivariable analyses. Genetically predicted P-wave terminal force in V1, an electrocardiographic marker for atrial cardiopathy, was inversely associated with large-artery stroke.
CONCLUSIONS
Available genetic data do not support substantial effects of cardiac traits on the risk of stroke beyond known clinical risk factors. Our findings highlight the need to carefully control for confounding and other potential biases in studies examining candidate cardiac risk factors for stroke.

Identifiants

pubmed: 34911345
doi: 10.1161/STROKEAHA.121.036306
pmc: PMC10510836
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

e130-e135

Subventions

Organisme : NINDS NIH HHS
ID : R01 NS105150
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS100178
Pays : United States

Références

Stroke. 2016 Mar;47(3):895-900
pubmed: 26786114
Am J Epidemiol. 2007 Sep 15;166(6):646-55
pubmed: 17615092
Stroke. 2017 May;48(5):1161-1168
pubmed: 28377383
Lancet Neurol. 2016 Feb;15(2):174-184
pubmed: 26708676
Nat Genet. 2018 Sep;50(9):1225-1233
pubmed: 29892015
Eur J Heart Fail. 2012 Feb;14(2):211-8
pubmed: 22200911
Circ Genom Precis Med. 2019 Mar;12(3):e002459
pubmed: 30919689
Wellcome Open Res. 2019 Nov 26;4:186
pubmed: 32760811
Nat Genet. 2018 Oct;50(10):1412-1425
pubmed: 30224653
Stroke. 1991 Aug;22(8):983-8
pubmed: 1866765
Nutr Metab Cardiovasc Dis. 2017 Jun;27(6):504-517
pubmed: 28552551
Stroke. 2018 Apr;49(4):980-986
pubmed: 29535268
Nat Genet. 2018 Apr;50(4):524-537
pubmed: 29531354
Stroke. 2007 Nov;38(11):2979-84
pubmed: 17901381
Nat Genet. 2018 May;50(5):693-698
pubmed: 29686387
Nature. 2018 Oct;562(7726):203-209
pubmed: 30305743
Circ Res. 2018 Feb 2;122(3):433-443
pubmed: 29212778

Auteurs

Simon Frerich (S)

Institute for Stroke and Dementia Research (S.F., R.M., M.K.G., M.D.), University Hospital, LMU Munich, Germany.

Rainer Malik (R)

Institute for Stroke and Dementia Research (S.F., R.M., M.K.G., M.D.), University Hospital, LMU Munich, Germany.

Marios K Georgakis (MK)

Institute for Stroke and Dementia Research (S.F., R.M., M.K.G., M.D.), University Hospital, LMU Munich, Germany.

Moritz F Sinner (MF)

Department of Cardiology (M.F.S.), University Hospital, LMU Munich, Germany.
German Centre for Cardiovascular Research (DZHK), partner site: Munich Heart Alliance, Germany (M.F.S.).

Steven J Kittner (SJ)

Department of Neurology (S.J.K.).

Braxton D Mitchell (BD)

Department of Medicine (B.D.M.), University of Maryland School of Medicine and Baltimore VAMC.

Martin Dichgans (M)

Institute for Stroke and Dementia Research (S.F., R.M., M.K.G., M.D.), University Hospital, LMU Munich, Germany.
Munich Cluster for Systems Neurology (SyNergy), Germany (M.D.).
German Centre for Neurodegenerative Diseases (DZNE), Munich, Germany (M.D.).

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH