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Common Variants in Candidate Genes and Premature MI Risk

This study has been completed.
National Heart, Lung, and Blood Institute (NHLBI)
Information provided by:
University of Washington Identifier:
First received: May 25, 2000
Last updated: February 8, 2016
Last verified: January 2005
To examine the impact of an interaction between common genetic susceptibility markers and environmental exposures on risk for early onset myocardial infarction in cases with myocardial infarction and matching controls.

Cardiovascular Diseases Heart Diseases Myocardial Infarction

Study Type: Observational

Further study details as provided by University of Washington:

Study Start Date: July 1998
Estimated Study Completion Date: August 2002
Detailed Description:


Inherited factors play a role in the pathogenesis of myocardial infarction (MI), and there is growing interest in identifying common genetic susceptibility markers that interact with common environmental exposures to contribute to the occurrence of myocardial infarction (MI) in the population.


The study had a case-control design. The preliminary data addressed the contribution of common genetic and environmental factors to the risk of MI among women under 45 years of age. Those data showed that common polymorphisms in genes coding for two clotting factors, coagulation Factor V and coagulation Factor II, were risk factors for MI only among cigarette smokers in this sample. These relationships, and others observed, provided strong evidence of gene-environment interactions between thrombotic and atherosclerotic factors in early-onset MI. One intent was to determine whether the risk of early-onset MI was related to interactions between environmental factors (e.g., cigarette smoking, exercise, alcohol consumption) and common polymorphisms in genes coding for thrombotic factors (coagulation Factor V, coagulation Factor II, plasminogen activator inhibitor-1, and beta-fibrinogen) and atherosclerotic factors (the adhesion molecule E-selectin and metalloproteinase stromelysin-1; the lipid metabolism enzymes paraoxinase, lipoprotein lipase, cholesterol ester transfer protein; and the apolipoproteins apolipoprotein E and apolipoprotein B). Additionally, there were plans to determine whether the risk of early-onset MI was related to interactions between plasma lipoprotein(a) levels (which were largely genetically determined) and environmental risk factors and/or polymorphisms in the candidate genes. Interactions among candidate polymorphisms were also assessed.

Newly-diagnosed cases of MI and controls will be interviewed in person to assess medical and behavioral characteristics related to MI risk. A venous blood sample will be obtained and processed into aliquots of plasma and white cells. DNA extracted from the white cells will be tested using the polymerase chain reaction (PCR), PCR/restriction fragment length polymorphisms (RFLP), and oligonucleotide ligation assays to determine the genotypes of interest. Plasma will be tested for lipid, lipoprotein, and homocysteine concentrations. Analyses will address both the overall association between the genotypes and MI risk, along with posited gene-environment and gene-gene interactions.


Ages Eligible for Study:   18 Years to 59 Years   (Adult)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No
No eligibility criteria
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Please refer to this study by its identifier: NCT00005488

Sponsors and Collaborators
University of Washington
National Heart, Lung, and Blood Institute (NHLBI)
OverallOfficial: Stephen Schwartz University of Washington
  More Information Identifier: NCT00005488     History of Changes
Other Study ID Numbers: 5004
R01HL056931 ( U.S. NIH Grant/Contract )
Study First Received: May 25, 2000
Last Updated: February 8, 2016

Additional relevant MeSH terms:
Cardiovascular Diseases
Heart Diseases
Myocardial Infarction
Pathologic Processes
Myocardial Ischemia
Vascular Diseases processed this record on September 19, 2017