Angiotensinogen T174M and M235T gene polymorphisms are associated with the extent of coronary atherosclerosis

• Published in: Atherosclerosis Vol. 145; no. 2; pp. 309 - 314
• Main Authors: Gardemann, Andreas, Stricker, Jürgen, Humme, Jörg, Nguyen, Quoc D, Katz, Norbert, Philipp, Monika, Tillmanns, Harald, Hehrlein, Friedrich Wilhelm, Haberbosch, Werner
• Format: Journal Article Conference Proceeding
• Language: English
• Published: Amsterdam Elsevier Ireland Ltd 01.08.1999; Elsevier
• Subjects: Alleles; Angiotensinogen - blood; Angiotensinogen - genetics; Angiotensinogen gene; Apolipoprotein A-I - blood; Apolipoproteins B - blood; Biological and medical sciences; Cardiology. Vascular system; Cardiovascular disease; Codon; Coronary Angiography; Coronary Artery Disease - blood; Coronary Artery Disease - diagnostic imaging; Coronary Artery Disease - genetics; Coronary heart disease; Gene Frequency; Genetic Markers; Genotype; Gensini score; Heart; Humans; Linkage Disequilibrium; Male; Medical sciences; Middle Aged; Myocardial infarction; Polymorphism, Genetic; Renin-angiotensin-aldosteron system; Risk Factors; Severity of Illness Index; Myocardial infarction; Angiotensinogen gene; Cardiovascular disease; Gensini score; Renin-angiotensin-aldosteron system; Risk factors; Human; Gene; Infarct; Pathogenesis; Angiotensinogen; Myocardium; Coronary heart disease; Myocardial disease; Genetic determinism; Polymorphism
• ISSN: 0021-9150; 1879-1484
• DOI: 10.1016/S0021-9150(99)00082-9

Background: The relations of the angiotensinogen (AGT) T174M and M235T gene polymorphisms to the risk of coronary heart disease (CHD) have been investigated in only a few studies with conflicting results. Results: Therefore, we analysed the relationship of the AGT gene polymorphisms to the presence and extent of CHD in 2250 male Caucasians whose coronary anatomy was defined by means of coronary angiography. The relative frequencies of the T and M alleles of the T174M and of the M235T gene variation did not significantly differ between patients without or with single-, double- or triple-vessel disease and between subjects without or with myocardial infarction (MI). In contrast the mean CHD score–defined by Gensini–was higher within MM homozygotes of the T174M gene variation than within TT genotypes; TM subjects had intermediate values. In M235T genotypes, mean CHD scores were similar in the total sample and in older individuals (≥62 years), whereas in younger individuals (<62 years) a higher CHD score was found within AGT 235 T allele carriers than within MM homozygotes. In younger individuals with high apoAI plasma levels, the mean CHD score was clearly higher within TT homozygotes of the M235T gene variation than within MM genotypes; MT subjects had intermediate values. An interaction between both angiotensinogen gene polymorphisms on the extent of CHD or on the risk of non-fatal MI were not observed when the M allele of AGT T174M was combined either with the T allele or the TT genotype of M235T. Conclusions: The present study strengthens the hypothesis of an association of both angiotensinogen gene polymorphisms with the extent of coronary heart disease.