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.