BACKGROUND: The aim of the present study was to assess the effects of angiotensin II receptor blocker (ARB) on coronary plaque progression in patients with acute myocardial infarction (AMI) who received an angiotensin-converting enzyme inhibitor (ACEI). METHODS AND RESULTS: After local ethics committee approval and obtaining of informed consent, 116 patients with AMI were randomly assigned to receive a combination of valsartan and captopril or captopril alone. Non-culprit intermediate coronary atherosclerosis was assessed on intravascular ultrasound. The primary and secondary endpoints were the nominal change in percent atheroma volume (PAV) and percent change in lumen volume (%ΔLV), respectively. The combination group had a significantly lower systolic blood pressure (117 vs. 125 mmHg; P=0.02) and a lower plasma aldosterone level (56 vs. 75 pg/ml; P=0.02) at follow-up. The nominal change in PAV was slightly lower in the combination group than in the ACEI group (-1.9 vs. -0.68%, P=0.06). %ΔLV was -0.3% in the ACEI group and was 4.3% in the combination group (P=0.03). Logistic regression analysis showed that additional ARB therapy was independently associated with LV enlargement (odds ratio, 2.144; 95% confidence interval: 1.818-5.618; P=0.03). CONCLUSIONS: In this study of patients with AMI, additionalARB therapy had minimal impact on the progression of coronary atherosclerosis as compared with an ACEI alone. The combination of these 2 drugs, however, induces coronary artery enlargement.
RCT Entities:
BACKGROUND: The aim of the present study was to assess the effects of angiotensin II receptor blocker (ARB) on coronary plaque progression in patients with acute myocardial infarction (AMI) who received an angiotensin-converting enzyme inhibitor (ACEI). METHODS AND RESULTS: After local ethics committee approval and obtaining of informed consent, 116 patients with AMI were randomly assigned to receive a combination of valsartan and captopril or captopril alone. Non-culprit intermediate coronary atherosclerosis was assessed on intravascular ultrasound. The primary and secondary endpoints were the nominal change in percent atheroma volume (PAV) and percent change in lumen volume (%ΔLV), respectively. The combination group had a significantly lower systolic blood pressure (117 vs. 125 mmHg; P=0.02) and a lower plasma aldosterone level (56 vs. 75 pg/ml; P=0.02) at follow-up. The nominal change in PAV was slightly lower in the combination group than in the ACEI group (-1.9 vs. -0.68%, P=0.06). %ΔLV was -0.3% in the ACEI group and was 4.3% in the combination group (P=0.03). Logistic regression analysis showed that additional ARB therapy was independently associated with LV enlargement (odds ratio, 2.144; 95% confidence interval: 1.818-5.618; P=0.03). CONCLUSIONS: In this study of patients with AMI, additional ARB therapy had minimal impact on the progression of coronary atherosclerosis as compared with an ACEI alone. The combination of these 2 drugs, however, induces coronary artery enlargement.