title: Progression of coronary artery calcium and occurrence of myocardial infarction in patients with and without diabetes mellitus.
abstract: Progression of coronary artery calcium, a marker of atherosclerosis, can be slowed with statins, and continued progression of calcium is associated with an increased risk of myocardial infarction. However, it is not known whether statins are effective in slowing calcium progression in diabetes mellitus. In a retrospective study, we examined 1153 nondiabetic and 157 diabetic subjects who underwent sequential electron beam tomography scans at a minimum 1-year interval to assess progression of coronary calcium. A yearly score increase >15% was considered evidence of true progression. The use of statins and occurrence of myocardial infarction were recorded. There was no difference in baseline calcium score between diabetic and nondiabetic patients. Diabetic patients with no coronary calcium on the baseline scans developed it more often than nondiabetic subjects (42% versus 25%; P=0.046) during follow-up. Calcium progression was 33% greater in diabetic patients than nondiabetic subjects (P<0.001) if no statin therapy was provided and 17.7% greater when statins were used (P<0.001). Among the 49 subjects who experienced a myocardial infarction, the calcium score increased on average 20% more in diabetic than nondiabetic patients (P<0.001). In logistic models, diabetes mellitus and systemic hypertension were the best predictors of calcium progression (odds ratio, 3.1 and 1.9, respectively), whereas baseline calcium score percentile and statin therapy were the best predictors of infarction. These findings support the notion that diabetes mellitus causes accelerated atherosclerosis, even in the presence of statin therapy, and provide evidence that coronary calcium monitoring is an effective method to assess treatment efficacy.
authors.affiliation: Tulane University School of Medicine, 1430 Tulane Ave, SL-48, New Orleans, LA 70112, USA. praggi@tulane.edu
authors.forename: Paolo
authors.initials: P
authors.lastname: Raggi
authors.forename: Bruce
authors.initials: B
authors.lastname: Cooil
authors.forename: Carlo
authors.initials: C
authors.lastname: Ratti
authors.forename: Tracy Q
authors.initials: TQ
authors.lastname: Callister
authors.forename: Matthew
authors.initials: M
authors.lastname: Budoff
mesh_terms: D000328:Adult; D000368:Aged; D002118:Calcium / Q000378:metabolism*; D016022:Case-Control Studies; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000378:metabolism; D003331:Coronary Vessels / Q000378:metabolism*; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000000981:diagnostic imaging / Q000378:metabolism*; D003925:Diabetic Angiopathies / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000378:metabolism; D018450:Disease Progression; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D006973:Hypertension / Q000150:complications; D015994:Incidence; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000453:epidemiology* / Q000209:etiology / Q000378:metabolism; D011237:Predictive Value of Tests; D012189:Retrospective Studies; D013997:Time Factors; D014057:Tomography, X-Ray Computed
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D002118:Calcium