Angiotensin converting enzyme and angiotensin II type 1 receptor gene polymorphisms and risk of ischaemic heart disease

Objective: Polymorphisms in several genes of the renin-angiotensin system h ave been implicated as risk factors for myocardial infarction and ischaemic heart disease. In particular, it has been suggested that the angiotensin c onverting enzyme insertion/deletion (TID) polymorphism and the angiotensin Ii type I receptor A(1166)C polymorphisms might act synergistically to incr ease the risk of myocardial infarction. The aim of this study was to invest igate associations between the angiotensin converting enzyme IID polymorphi sm and angiotensin II type I receptor polymorphisms and ischaemic heart dis ease. Methods: We screened 331 white European patients who were recruited f or routine angiographic investigation of chest pain, and 287 healthy white European controls for the angiotensin converting enzyme TID and angiotensin II type I receptor A(1166)C polymorphisms, and related the genotype freque ncies to angiotensin converting enzyme levels and the clinical phenotypes o f atheroma and history of myocardial infarction. Results: Angiotensin conve rting enzyme levels were related to IID polymorphism but not to angiotensin II type 1 receptor polymorphism genotypes. IID polymorphism and angiotensi n TI type 1 receptor genotypes did not relate individually to risk of myoca rdial infarction or atheroma in univariate or multivariate analysis. Howeve r, evidence of a synergistic relationship between the AC/II and CC/DD genot ypes and coronary stenosis in the major arteries was found. No evidence of any relationship between these polymorphisms and history of myocardial infa rction by World Health organisation (WHO) criteria was detected. Conclusion : These findings suggest that there is a weak relationship between the angi otensin converting enzyme IID and angiotensin II type 1 receptor A(1166)C p olymorphisms and coronary atheroma, but no evidence of a relationship with history of myocardial infarction. (C) 1999 Elsevier Science B.V. All rights reserved.