PLASMA ANGIOTENSIN-CONVERTING ENZYME-ACTIVITY AND CAROTID WALL THICKENING

Background Mechanisms underlying the previously reported association b etween a deletion polymorphism in the gene encoding for angiotensin-co nverting enzyme (ACE) and the risk of myocardial infarction in low-ris k subjects are unclear. The purpose of this case-control study was to examine the relation of plasma ACE activity to intimal-medial thicknes s of the carotid wall measured ultrasonographically in an apparently h ealthy population. Methods and Results We determined plasma ACE activi ty in 80 pairs of subjects without any history of ischemic heart disea se or any treatment of hypertension and diabetes. Cases and control su bjects were defined on the basis of intimal-medial thickness measured in the common carotid arteries by B-mode ultrasound and were matched f or sex, sonographer, and the presence of atheromatous plaques. Subject s were selected from a sample of 434 men and 602 women between 60 and 69 years old participating in an ongoing study on vascular aging (EVA) . Subjects with intimal-medial thickening (cases) showed a slight but not significant increase in plasma ACE activity in comparison with con trol subjects (P<.16). However, after exclusion of subjects receiving lipid-lowering drugs, the mean plasma ACE activity became significantl y higher in cases than in control subjects (29.9+/-7.7 U/L versus 27.5 +/-8.0 U/L; n=54 pairs, P<.03). The mean case-control difference in pl asma ACE activity was further increased when analysis was restricted t o pairs without carotid atheromatous plaques (n=42 pairs). After adjus tment for body mass index, smoking, and systolic blood pressure, the o dds ratio for having carotid wall thickening based on 1 SD difference in log ACE was 2.29 (95% confidence interval, 1.16 to 4.52; P<.02). Co nclusions The results of the study suggest that chronic exposure to hi gh levels of plasma ACE could be involved in structural changes of the arterial wall.