Clinical Investigations: Interventional CardiologyA1166C polymorphism of the angiotensin II type 1 receptor gene and risk of adverse events after coronary catheter interventions☆
Section snippets
Methods
This study was designed to investigate genetic traits as putative risk factors of CAD and of adverse events complicating coronary catheter interventions. This study, with a multiple end point, enrolled 1000 consecutive patients with CAD admitted for elective or emergency angiography at the Charité University Medical Center between October 1995 and January 1997. An additional 1000 patients also admitted to this hospital served as controls. They were matched by age (± 3 years), sex, and time of
Study group characteristics
Table I lists baseline characteristics of cases and controls.Empty Cell Cases (n = 1000) Controls (n = 1000) P value Age (y)* 60.6 60.5 (55.1, 67.1) (54.5, 66.5) .48 Female (%) 24.1 24.1 History (%) Diabetes 22.8 11.4 <.001 Smoking 44.0 35.2 <.001 Hypertension 55.2 35.9 <.001 Hypercholesterolemia 52.7 30.3 <.001 Age of manifestation <40 years 6.8 Angina (%) Stable 66.5 Unstable 14.4 Myocardial infarction (%) 66.9 Acute 9.1 History of 57.8 Severity of CAD (%) 1-Vessel 29.7 2-Vessel 36.5 3-Vessel 33.8 *Values
Discussion
An increasing number of genetic studies on the association of polymorphisms of the RAS and CAD have been published during recent years. Instead of shedding light on the role of the RAS in development of chronic or acute manifestation of CAD, however, contributions to the literature remain contradictory. Nakauchi et al4 on the one hand, suggested that the A1166C polymorphism in Japanese patients was related to severity of coronary stenosis. The Coronary Disease and Angiotensin-Converting Enzyme
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A1166C genetic variation of the angiotensin II type I receptor gene and susceptibility to coronary heart disease: Collaborative of 53 studies with 20,435 cases and 23,674 controls
2010, AtherosclerosisCitation Excerpt :Since then, considerable effort has been poured on exploring the relationships between the AGTR1 polymorphisms and CHD. However, a number of studies yielded apparently conflicting and inconsistent results [6–60]. These disparate findings may partly due to improper study design and insufficient power in most of such studies (which have not involved more than a few hundred disease cases), and are too few to assess reliably any genetic effects that might be realistically expected (such as per-allele odds ratio (OR) increases of about 10–20%).
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2007, American Journal of Epidemiology
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Reprint requests: Karl Stangl, MD, Medizinische Klinik und Poliklinik mit Schwerpunkt Kardiologie, Angiologie und Pneumologie, Campus Mitte, Charité, Schumannstr. 20/21, D–10117 Berlin, Germany. E-mail: [email protected]