CAROTID-ARTERY INTIMA-MEDIA THICKNESS IN ELDERLY PATIENTS WITH NIDDM AND IN NONDIABETIC SUBJECTS

Background and Purpose The risk of atherosclerotic vascular disease is increased both in subjects with non-insulin-dependent diabetes mellit us (NIDDM) and in those with impaired glucose tolerance compared with nondiabetic subjects. Although classic cardiovascular risk factors are operative in subjects with NIDDM, other factors closely related to in sulin resistance syndrome such as diabetic dyslipidemia and hyperglyce mia itself may contribute to an excessive cardiovascular disease risk in subjects with NIDDM. The purpose of this study was to investigate t he carotid intimal-medial thicknesses (IMTs) and their determinants in elderly patients with NIDDM and in control subjects. Methods We inves tigated the common carotid and carotid bifurcation IMTs and their dete rminants in groups Of elderly patients (n = 84, age 67.2 +/- 0.6 years ) with NIDDM and in 119 con control subjects (21 with impaired and 98 with normal glucose tolerance; ages 67.5 +/- 1.0 and 65.1 +/- 0.6 year s, respectively). Results Common carotid and carotid bifurcation IMTs were greater in the NIDDM group than in control subjects (P < .05 to . 01). In NIDDM patients, the mean carotid IMT con elated with postgluco se 1-hour plasma insulin (r = .305, P = .01, adjusted for age and sex) , serum LDL triglyceride (r = .237, P < .05, and apolipoprotein B conc entrations (r = .263, P < .05). Fasting plasma immunoreactive insulin, proinsulin, or specific insulin levels were not significantly associa ted with carotid IMT. Both diabetic status (P < .05) and the presence of clinical macrovascular disease (P < .01) contributed independently to carotid IMT. Conclusions Carotid IMT was greater in NIDDM patients than in control subjects, The main determinants of IMT in NIDDM patien ts were related to both postglucose insulin levels and abnormal lipopr otein profiles characteristic of NIDDM and insulin resistance syndrome . Treatment of these factors is likely to reduce the atherosclerotic b urden in NIDDM.