There is also a clear interaction between RAS predisposing genes and some biochemical/environmental risk factors in CAD onset, demonstrating a significant enhancement of classical markers particularly by ACE I/D and ACE11860.
Cigarette smoking increases the synthesis of angiotensin-1 converting enzyme (ACE) and induces oxidative modifications of the apolipoprotein E (apo E).Thus we explored the gene-environment interactions between APOE gene epsilon and ACE gene insertion/deletion polymorphisms and cigarette smoking in coronary artery disease (CAD) patients.
The ACE I/D polymorphism influences individual differences in severity of coronary artery disease and the D allele promotes generation of numerous and critical atherosclerotic lesions.
The existence of the angiotensin converting enzyme (ACE) gene polymorphisms has been known, and deletion (D) of the allele has been associated with coronary artery disease.
Our data suggest that genetic variation at the ACE is a genetic factor related with the susceptibility to coronary artery disease in the Mexican Mestizo population.
The angiotensin-converting enzyme gene insertion/deletion polymorphism and effects of quinapril and atorvastatin on haemostatic parameters in patients with coronary artery disease.
The contribution of the angiotensin-converting enzyme (ACE) genotype to the development of coronary artery disease and restenosis after coronary stenting was investigated in 67 Japanese patients in whom 103 lesions in which stents had been successfully implanted were assessed by quantitative coronary angiography, before, immediately after coronary stenting, and during follow-up.