Quinapril (an ACE inhibitor) improves coronary endothelial dysfunction, according to the Brachial Artery Normalisation of Forearm Function (BANFF) crossover study published in the Journal of the American College of Cardiology (2000;35:60).
Dr Todd Anderson (University of Calgary, Alberta, US) and colleagues explain that endothelial dysfunction contributes to the morbidity of coronary disease and occurs early in the course of atherosclerosis in response to cardiovascular risk factors. Previous studies have suggested that bradykinin is the mediator responsible for the beneficial effects of ACE inhibition on endothelial function and atherosclerosis development.
The authors compared the effects of ACE inhibition (quinapril 20mg or enalapril 10mg daily), angiotensin II blockade (losartan 50mg daily) and calcium-channel blockade (amlodipine 5mg daily) on endothelium-dependent brachial artery flow-mediated vasodilatation, in patients with coronary artery disease. Eighty patients were randomised to one of four drug sequences, receiving three of the drugs, with a two-week washout period between treatments. Quinapril was the only drug in the trial found to improve the opening of vessels significantly. The researchers say that that the response appeared to be related to participants' ACE genotype. According to Dr Anderson et al, treatment with enalapril did not result in any significant change in the flow-mediated dilatation. This suggests that drugs with higher tissue affinity for ACE, such as quinapril, are likely to be more effective in restoring endothelial function than those with lower affinity, such as enalapril, they say. Some improvement was seen with losartan, although, in this study, it was not statistically significant. Dr Anderson and colleagues say that further dose-ranging and time-course studies are needed. The study was funded by Parke-Davis.