Genetic predisposition, nongenetic risk factors, and coronary infarct

{{\textless}AbstractText} {Label="BACKGROUND"} {NlmCategory="BACKGROUND"{\textgreater}Using} a genetic predisposition score {(GPS),} additively integrating the associations of 11 polymorphisms with coronary heart disease {(CHD),} we examined the consequences of the joint presence of a high {GPS} and nongenetic {CHD} risk {factors.{\textless}/AbstractText{\textgreater}} {{\textless}AbstractText} {Label="METHODS"} {NlmCategory="METHODS"{\textgreater}Within} the European Prospective Investigation Into Cancer and Nutrition, 202 case patients with medically confirmed incident coronary infarct and 197 control subjects were identified in Greece. Each polymorphism contributed 1 unit (high-risk homozygous), one-half unit (heterozygous), or no units (low-risk homozygous) to the {GPS.} Odds ratios of coronary infarction for those at high risk because of genetic predisposition and simultaneous presence of an established {CHD} risk factor were estimated, compared with subjects at low risk, for both {GPS} and each {CHD} risk {factor.{\textless}/AbstractText{\textgreater}} {{\textless}AbstractText} {Label="RESULTS"} {NlmCategory="RESULTS"{\textgreater}The} joint presence of a high {GPS} (> or =3.5) and each studied {CHD} risk factor was in all instances associated with a significantly increased risk of coronary infarction. The odds ratio (95% confidence interval) was 2.62 (1.14-6.02) for ever smoking, 2.88 (1.33-6.24) for hypertension, 3.50 (1.67-7.33) for low high-density lipoprotein {(HDL)} level, 3.05 (1.53-6.08) for high {non-HDL} level, and 3.66 (1.75-7.65) for poor adherence to the Mediterranean diet. The odds ratios were always lower and nonsignificant when the {GPS} was low. There was suggestive evidence for interaction of a high {GPS} with hypertension {(P} = .05) and {non-HDL} cholesterol level {(P} = {.13).{\textless}/AbstractText{\textgreater}} {{\textless}AbstractText} {Label="CONCLUSIONS"} {NlmCategory="CONCLUSIONS"{\textgreater}Genetic} predisposition may interact with hypertension and, perhaps, also with the level of {non-HDL} cholesterol, in the causation of {CHD.} Genetic predisposition and the other studied exposures seem to have converging effects. Thus, the {GPS} may identify individuals who could realize disproportional benefits by controlling their hypertension and, possibly, their {non-HDL} cholesterol {level.{\textless}/AbstractText{\textgreater}}