<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="6.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Antonia Trichopoulou</style></author><author><style face="normal" font="default" size="100%">Nikos Yiannakouris</style></author><author><style face="normal" font="default" size="100%">Christina Bamia</style></author><author><style face="normal" font="default" size="100%">Vassiliki Benetou</style></author><author><style face="normal" font="default" size="100%">Dimitrios Trichopoulos</style></author><author><style face="normal" font="default" size="100%">Jose M Ordovas</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Genetic predisposition, nongenetic risk factors, and coronary infarct</style></title><secondary-title><style face="normal" font="default" size="100%">Archives of Internal Medicine</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">diet</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Predisposition to Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Greece</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Hypertension</style></keyword><keyword><style  face="normal" font="default" size="100%">Lipoproteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Mediterranean</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Myocardial Infarction</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism</style></keyword><keyword><style  face="normal" font="default" size="100%">Risk Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Smoking</style></keyword><keyword><style  face="normal" font="default" size="100%">Treatment Refusal</style></keyword><keyword><style  face="normal" font="default" size="100%">{Case-Control} Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">{HDL</style></keyword><keyword><style  face="normal" font="default" size="100%">} Male</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2008</style></year><pub-dates><date><style  face="normal" font="default" size="100%">apr</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/18443266</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">8</style></number><volume><style face="normal" font="default" size="100%">168</style></volume><pages><style face="normal" font="default" size="100%">891–896</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">{{\textless}AbstractText} {Label=&quot;BACKGROUND&quot;} {NlmCategory=&quot;BACKGROUND&quot;{\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=&quot;METHODS&quot;} {NlmCategory=&quot;METHODS&quot;{\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=&quot;RESULTS&quot;} {NlmCategory=&quot;RESULTS&quot;{\textgreater}The} joint presence of a high {GPS} (&amp;gt; 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=&quot;CONCLUSIONS&quot;} {NlmCategory=&quot;CONCLUSIONS&quot;{\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}}</style></abstract><notes><style face="normal" font="default" size="100%">{PMID:} 18443266</style></notes></record></records></xml>