(Circulation. 2001;103:346.)
© 2001 American Heart Association, Inc.
Editorials |
Do Interventions to Reduce Coronary Heart Disease Reduce the Incidence of Type 2 Diabetes? A Possible Role for Inflammatory Factors
From the Department of Medicine, Division of Clinical Epidemiology, University of Texas Health Science Center at San Antonio.
Correspondence to Steven M. Haffner, MD, Department of Medicine, 7703 Floyd Curl Drive–MSC 7873, San Antonio, TX 78229-3900. E-mail haffner@uthscsa.edu
Key Words: Editorials • diabetes • C-reactive protein • statins
Type 2 diabetes is as a major cause of coronary heart disease (CHD). In some studies, the rate of CHD in type 2 diabetic subjects approaches that observed in some subjects with prevalent CHD.1 Additionally, the case fatality rate of CHD is increased in type 2 diabetics.2 In one Finnish study, 50% of diabetic men who had a first coronary heart event died within a year of their initial presentation; 50% of these fatal cases died before they reached the hospital ("sudden death"). These subjects, by definition, could not benefit from a secondary prevention program.2 Clearly, preventing type 2 diabetes would be important in the reduction of CHD. The Diabetes Prevention Program3 is a large National Institutes of Health–funded trial to prevent diabetes in subjects with impaired glucose tolerance. The interventions being tested are metformin and intensive lifestyle changes. Recently, the Finnish Diabetes Prevention Program reported a 58% reduction in the incidence of type 2 diabetes in 523 subjects with impaired glucose tolerance (American Diabetes Association, personal communication, June 2000).
Approaches to reduce CHD have focused on the benefits
of lowering LDL cholesterol with HMG CoA reductase inhibitors
(statins)4 5 and
angiotensin-converting enzyme (ACE)
inhibitors.6 Recently, it was
suggested that ACE inhibitors may prevent
diabetes.6 7 In
this issue, Freeman et al8
suggest that, in the West of Scotland Coronary Prevention Study
(WOSCOPS), pravastatin reduced the incidence of diabetes by 30%. What
might explain this effect? One possibility, as the investigators
suggest, is that because the analysis was done post hoc and
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