Additional very large-scale studies are warranted to provide conclusive evidence on the effects of the angiotensinogen gene and other genes within the renin-angiotensin system on risk of CHD.
Previous reports relating coronary artery disease and functional variants of the renin-angiotensin system have been contradictory in establishing the role of these polymorphisms in coronary artery disease (CAD) development.
Renin-angiotensin system genes are candidate genes in CHD and the deletion allele of the angiotensin converting enzyme (ACE) has been reported as deleterious.
Indeed, the development of hypertension as well as the progression of coronary artery disease and heart failure have two factors in common: (1) display distinct gender specific characteristics and (2) are enhanced by the renin-angiotensin system.
Polymorphisms within renin angiotensin system genes have been investigated as risk factors for coronary artery disease in different populations with contradicting results.
Genes encoding components of the renin-angiotensin system have been associated with elevated blood pressure (BP) and an increased risk of coronary artery disease.
Experimental and clinical data show that the renin-angiotensin system has important indications in coronary artery disease by influencing progressive ventricular dilatation, ventricular function, and outcome.
The renin-angiotensin system and angiotensin converting enzyme (ACE) are increasingly being implicated in the pathogenesis of coronary artery disease and its sequelae.
Genetic variations in the renin-angiotensin and kallikrein-kinin systems could prove to be significant pathophysiological mechanisms affecting coronary heart disease (CHD), particularly given the powerful vasoactivity of products such as angiotensin II and bradykinin.