Literature DB >> 24474739

Mendelian randomization of blood lipids for coronary heart disease.

Michael V Holmes1, Folkert W Asselbergs2, Tom M Palmer3, Fotios Drenos4, Matthew B Lanktree5, Christopher P Nelson6, Caroline E Dale7, Sandosh Padmanabhan8, Chris Finan9, Daniel I Swerdlow9, Vinicius Tragante10, Erik P A van Iperen11, Suthesh Sivapalaratnam12, Sonia Shah13, Clara C Elbers14, Tina Shah9, Jorgen Engmann9, Claudia Giambartolomei13, Jon White13, Delilah Zabaneh13, Reecha Sofat9, Stela McLachlan15, Pieter A Doevendans16, Anthony J Balmforth17, Alistair S Hall17, Kari E North18, Berta Almoguera19, Ron C Hoogeveen20, Mary Cushman21, Myriam Fornage22, Sanjay R Patel23, Susan Redline23, David S Siscovick24, Michael Y Tsai25, Konrad J Karczewski26, Marten H Hofker27, W Monique Verschuren28, Michiel L Bots29, Yvonne T van der Schouw29, Olle Melander30, Anna F Dominiczak8, Richard Morris31, Yoav Ben-Shlomo32, Jackie Price15, Meena Kumari9, Jens Baumert33, Annette Peters33, Barbara Thorand33, Wolfgang Koenig34, Tom R Gaunt35, Steve E Humphries36, Robert Clarke37, Hugh Watkins38, Martin Farrall38, James G Wilson39, Stephen S Rich40, Paul I W de Bakker41, Leslie A Lange42, George Davey Smith35, Alex P Reiner43, Philippa J Talmud36, Mika Kivimäki44, Debbie A Lawlor35, Frank Dudbridge7, Nilesh J Samani6, Brendan J Keating45, Aroon D Hingorani9, Juan P Casas46.   

Abstract

AIMS: To investigate the causal role of high-density lipoprotein cholesterol (HDL-C) and triglycerides in coronary heart disease (CHD) using multiple instrumental variables for Mendelian randomization. METHODS AND
RESULTS: We developed weighted allele scores based on single nucleotide polymorphisms (SNPs) with established associations with HDL-C, triglycerides, and low-density lipoprotein cholesterol (LDL-C). For each trait, we constructed two scores. The first was unrestricted, including all independent SNPs associated with the lipid trait identified from a prior meta-analysis (threshold P < 2 × 10(-6)); and the second a restricted score, filtered to remove any SNPs also associated with either of the other two lipid traits at P ≤ 0.01. Mendelian randomization meta-analyses were conducted in 17 studies including 62,199 participants and 12,099 CHD events. Both the unrestricted and restricted allele scores for LDL-C (42 and 19 SNPs, respectively) associated with CHD. For HDL-C, the unrestricted allele score (48 SNPs) was associated with CHD (OR: 0.53; 95% CI: 0.40, 0.70), per 1 mmol/L higher HDL-C, but neither the restricted allele score (19 SNPs; OR: 0.91; 95% CI: 0.42, 1.98) nor the unrestricted HDL-C allele score adjusted for triglycerides, LDL-C, or statin use (OR: 0.81; 95% CI: 0.44, 1.46) showed a robust association. For triglycerides, the unrestricted allele score (67 SNPs) and the restricted allele score (27 SNPs) were both associated with CHD (OR: 1.62; 95% CI: 1.24, 2.11 and 1.61; 95% CI: 1.00, 2.59, respectively) per 1-log unit increment. However, the unrestricted triglyceride score adjusted for HDL-C, LDL-C, and statin use gave an OR for CHD of 1.01 (95% CI: 0.59, 1.75).
CONCLUSION: The genetic findings support a causal effect of triglycerides on CHD risk, but a causal role for HDL-C, though possible, remains less certain.
© The Author 2014. Published by Oxford University Press on behalf of the European Society of Cardiology.

Entities:  

Keywords:  Aetiology; Epidemiology; Heart disease; Lipids; Mendelian randomization

Mesh:

Substances:

Year:  2014        PMID: 24474739      PMCID: PMC4344957          DOI: 10.1093/eurheartj/eht571

Source DB:  PubMed          Journal:  Eur Heart J        ISSN: 0195-668X            Impact factor:   29.983


  33 in total

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3.  Effect of acute myocardial infarction on cholesterol ratios.

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