We read with interest the article by Mitsuhashi et al. (1) concerning the role of carotid artery intima-media thickness (IMT) measurements in the detection of coronary artery disease (CAD) in Japanese type 2 diabetic patients. The article suggested that carotid IMT was significantly greater in diabetic patients with CAD (1.27 ± 0.07 mm) than in those without CAD (termed “control subjects”) (1.03 ± 0.04 mm, P < 0.05). In the subgroup with CAD, IMT was significantly greater in those who had undergone coronary artery bypass grafting (CABG) than in the non-CABG group (1.47 ± 0.11 vs. 1.07 ± 0.07 mm, P < 0.05). Although statistical differences in IMT between the CABG and non-CABG subgroups of CAD patients and between control subjects and the total CAD group were emphasized, no test statistic was given for the comparison of control subjects with non-CABG subjects, where the difference would appear to be nonsignificant (1.03 ± 0.04 vs. 1.07 ± 0.07 mm).
We question the validity of the authors’ conclusions that early atherosclerosis in the carotid artery suggests a high probability of coronary involvement in Japanese patients with type 2 diabetes, and that an increased IMT in diabetic patients should prompt further screening for CAD to prevent progression of CAD.
First, there is the issue of possible confounding by the CABG procedure itself, which the authors do concede in their conclusion. Second, there is no evidence of a gradient of IMT between the CAD non-CABG group and those post-CABG, nor is there any correlation with number of vessels involved or any mention of correlation with severity of exercise electrocardiogram (ECG) results. It appears that the authors have demonstrated that in post-CABG patients, the IMT measurement offers the self-evident conclusion that they have CAD. A clinically relevant marker that can predict progression and perhaps be used as a screening tool, not one that merely confirms a clinically manifest condition, is needed.
This study has shown a statistical difference in serum HDL concentration, uric acid, and hypertension between the control and CAD groups, which is consistent with other large studies such as the Framingham Heart Study and the Multiple Risk Factor Intervention Trial (2–4), but no statistical difference between the non-CABG and post-CABG groups. Furthermore, only 32 of 48 subjects with abnormal exercise ECG testing proceeded to angiography. One wonders whether exclusion of 25% of subjects apparently eligible for angiography in this group may have led to an underestimation of the efficacy of IMT.
Finally, the abstract states that “carotid IMT was significantly greater in the diabetic patients than in the control subjects, ” which implies that the control subjects were not diabetic. This is later clarified in research design and methods, which states that the control subjects were “drawn from the diabetic patients.”
Our conclusion is that, while this study has undoubtedly shown a statistical difference in IMT between type 2 diabetic patients with and without CABG, an increased IMT was only shown in those who had already undergone treatment for CAD. Therefore, it has not shown IMT to be a good marker to prompt further screening for CAD or treatment to prevent progression of CAD in type 2 diabetic patients.
References
Address correspondence to Steven J. Hurel, PHD, FRCP, Department of Diabetes and Endocrinology, UCLH, Cleveland Street, London, England W1T 3AA, U.K. E-mail: [email protected].
