GROWTH-PROMOTING EFFECTS OF
ANGIOTENSIN:
Angiotensin, a vasoconstrictive
peptide, is now known to be an agent of vascular and cardiac growth and may directly influence the pathophysiology of
coronary artery disease and
ventricular remodeling. Vascular growth occurs when
angiotensin activates autocrine and paracrine
growth factors, including
fibroblast growth factor,
transforming growth factor beta-1 and
platelet-derived growth factor, and is modulated by endothelium-derived
vasodilators and
growth inhibitors.
ANGIOTENSIN AND
CARDIOVASCULAR DISEASE: The presence of
angiotensin converting enzyme (ACE) and
angiotensin II has been demonstrated in vascular tissue, and these local substances are causally involved in the development of vascular lesions. Similarly,
angiotensin can stimulate cardiac myocyte growth and matrix modulation. Cardiac tissue ACE is implicated in
ventricular remodeling in the course of progressive
heart failure. A genetic variant of the ACE gene has been reported to be associated with increased risks of cardiovascular pathology.
ACE INHIBITOR THERAPY: To date, studies of
ACE inhibitor treatment in human patients have not demonstrated any prevention of restenosis after angioplasty. However, recent clinical trials in postmyocardial
infarction reported that
ACE inhibitor therapy reduces recurrent
myocardial infarction and prevents cardiac enlargement. Long-term prospective trials are currently being conducted to examine the effects of
ACE inhibitor therapy on coronary ischemic events and
coronary atherosclerosis, as evaluated by angiography or intravascular ultrasound, and the relationship between coronary events and ACE gene polymorphism.