We appreciate the interest of Ostberg and Hurel (1) in our article (2) and the opportunity to clarify the point raised.
As we described in conclusions in our article, intima-media thickness (IMT) may have become thicker after coronary artery bypass grafting (CABG), because one cannot establish temporal sequence with cross-sectional data. We measured IMT of 15 patients before the CABG procedure (mean IMT ± SD 1.44 ± 0.14 mm) and IMT of 5 patients within 3–6 months after CABG (1.56 ± 0.07 mm). IMT was not significantly different between these two groups (P = 0.62). Even if we had excluded the latter 5 patients’ measured IMT after CABG, IMT would have been still significantly greater in the 15 CABG patients’ measured IMT before CABG than in the controls drawn from the diabetic patients (1.44 ± 0.14 vs. 1.07 ± 0.07 mm, P < 0.05). And there is no conclusive proof that CABG itself has an effect on the change in IMT. Therefore, we did not consider that our result was confounded strongly by the CABG procedure itself. Yet, we need further studies, because the number of patients with CABG was relatively small, and we did not compare IMT before and after CABG among the same patients.
Next, we state the correlation with the number of involved coronary vessels between two groups with and without CABG. The non-CABG group (n = 20) was divided into 9 patients with two-vessel disease and 11 patients with three-vessel disease. The CABG group (n = 20) included 4 patients with two-vessel disease and 16 patients with three-vessel disease. The CABG group had more severe disease than the non-CABG group, but the correlation was not significantly different (χ2 = 2.849, P = 0.09). In addition, we show the correlation between the severity of coronary artery disease (CAD) and IMT. In the group with two-vessel disease, the IMT was 1.08 ± 0.08 mm, and in the group with three-vessel disease, it was 1.36 ± 0.10 mm (P = 0.07). IMT was not significantly associated with the number of involved vessels, but had a tendency to associate with the number of total vessels. Moreover, as shown in Tables 2 and 3, IMT was independently associated with CAD by logistic regression analysis using all other independent variables. Thus, we consider that IMT could be used as a predictor of severity of CAD assessed by the number of involved vessels in diabetic patients.
With regard to the clinical characteristics, as shown in results, CAD patients had a significantly higher prevalence of hypertension and uric acid level and a lower HDL cholesterol level than the control diabetic patients. Both the Framingham Study (3,4) and Multiple Risk Factor Intervention Trial (MRFIT) (5), as referred to by Drs. Ostberg and Hurel, are studies to assess CAD mortality with and without diabetes, but the subjects of our study are all diabetic patients. Thus, we cannot compare these large studies with our study in the same way. Yet, it is well known that hyperlipidemia and hypertension are strong and independent predictors of CAD in diabetic patients (5–10). Similarly, our patients with CAD had more cardiovascular risk factors than those without CAD. On one hand, among only CAD patients, including the patients with and without CABG, as shown in Table 4, factors such as hypertension, hyperlipidemia, and hyperuricemia did not differ between the two groups. The reason was not obvious. But, as many of the patients without CABG already had hypertension and hyperlipidemia, there might not have been a significant difference between the two groups with and without CABG. However, the IMT was significantly greater in patients with CABG than in those without CABG. These results indicate that IMT is one important indicator of severe CAD that was needed for CABG.
Currently, only 32 of 48 patients with abnormal exercise electrocardiogram testing proceeded to angiography. Some patients received an angiography after the period, but we estimated only 32 patients who had CAD by angiography from February 1998 to January 1999. Furthermore, we agree with Drs. Ostberg and Hurel that we should also state that the control subjects were drawn from the diabetic patients within results as well as within research design and methods. To clarify the meanings, the sentence in results should be replaced as follows: Carotid IMT was significantly greater in the CAD patients than in the controls drawn from the diabetic patients.
We believe that IMT is a predictor of severity of CAD in diabetic patients, but further investigation in a large population is necessary.
References
Address correspondence to Naomi Mitsuhashi, Department of Medicine, Metabolism, and Endocrinology, Juntendo University, 2-1-1 Hongo, Bunkyo-k, Tokyo, Japan 113-8421. E-mail: [email protected].
