Abstract
In the 1970s, pharmacological therapy interrupting the renin-angiotensin system was considered beneficial for patients with high-renin hypertension. Angiotensin-converting enzyme (ACE) inhibitors proved to be effective not only in patients with high renin and elevated blood pressure, but also in many hypertensive patients with normal levels of plasma renin activity. ACE inhibitors are used in a wide range of chronic illnesses such as atherosclerosis, hypertension, myocardial infarction, heart failure, diabetic complications, and stroke. To date, more than ninety controlled clinical trials evaluating the beneficial effects of 14 different ACE inhibitors were conducted. Moreover, data from experimental studies showed that ACE inhibitors can attenuate the development of atherosclerosis, oxidative stress, and vascular inflammation in a wide range of species indicating that ACE inhibition also favourably affects the vasculature. More than fifteen years ago, the bi-sulfydryl ACE-inhibitor zofenopril has shown an excellent clinical safety and efficacy in patients with hypertension and in those with myocardial infarction. More recently, this compound exhibited a potent antioxidant and antiatherosclerotic effect indicating a clinical useful vasoprotective action.
Highlights
The Angiotensin-converting enzyme (ACE) inhibitor captopril has a sulfydryl group to coordinate to the active site zinc ion, enalaprilat has a carboxylate group, and fosinopril has a phosphate group; zofenopril has 2 sulfydryl groups.[2,3]
We still do not know whether some parameters, such as genetic determinants, for example such of endothelial nitric oxide synthase in affording atheroprotective effect,[46] or markers of inflammation not investigated in the Heart Outcomes Prevention Evaluation (HOPE) study, can help to identify patients in whom ACE inhibitors would produce a more marked benefit than that found in the total trial population
Improvement in endothelial function with quinapril was limited to coronary patients with the insertion allele (DI or II) of the ACE gene;[47] and, enalapril improved endothelial function primarily in patients with the deletion allele (DI or DD genotypes).[48]
Summary
The rate of recurrent infarction did not differ between groups; a systematic overview of these trials reported a significant reduction in recurrent infarction with ACE inhibition.[24] Another detailed meta-analysis of trials of ACE inhibitors after AMI found that ACE inhibitor therapy lowered the risk of sudden cardiac death significantly (odds RATIO = 0.80; [CI]: 0.70 to 0.92).[25] Taken together, these clinical data can be interpreted that ACE inhibitors lower the risk of coronary events attributed to plaque instability and/or rupture.[2,17,18,19] In the Prevention of Atherosclerosis with Ramipril-2 (PART-2) study,[26] patients with carotid atherosclerosis were assigned to receive ramipril or placebo.
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