Effect of Diabetes on Progression of Coronary Atherosclerosis and Arterial Remodeling: A Pooled Analysis of 5 Intravascular Ultrasound Trials Original Research Article

Objectives Our goal was to characterize coronary atherosclerosis progression and arterial remodeling in diabetic patients. Background The mechanisms that underlie adverse cardiovascular outcomes in diabetic patients have not been well characterized. Methods A systematic analysis was performed in 2,237 subjects in randomized controlled studies of atherosclerosis progression. The pattern of arterial remodeling, extent of coronary atherosclerosis, and disease progression was compared in subjects with and without diabetes. Results In association with more risk factors, diabetic patients demonstrated a greater percent atheroma volume (PAV) (40.2 ± 0.9% vs. 37.5 ± 0.8%, p < 0.0001) and total atheroma volume (TAV) (199.4 ± 7.9 mm3 vs. 189.4 ± 7.1 mm3, p = 0.03) on multivariate analysis. A stronger correlation was observed between PAV and glycated hemoglobin (r = 0.22, p = 0.0003) than fasting glucose (r = 0.09, p < 0.0001), although the difference just failed to meet statistical significance after controlling for study. Diabetic patients exhibited a smaller lumen (291.1 ± 104.8 mm3 vs. 306.5 ± 108.2 mm3, p = 0.005) but no difference in external elastic membrane (494.9 ± 166.9 mm3 vs. 498.8 ± 167.2 mm3, p = 0.61) volumes. More rapid progression of PAV (0.6 ± 0.4% vs. 0.05 ± 0.3%, p = 0.0001) and TAV (−0.6 ± 2.5 mm3 vs. −2.7 ± 2.4 mm3, p = 0.03) was observed in diabetic patients on multivariate analysis. Smaller external elastic membrane (482.5 ± 160.7 mm3 vs. 519.9 ± 166.9 mm3, p = 0.03) and lumen (276.0 ± 100.3 mm3 vs. 310.1 ± 105.6 mm3, p = 0.001) volumes were observed in diabetic patients treated with insulin despite the presence of a similar TAV (206.5 ± 88.6 mm3 vs. 209.9 ± 90.2 mm3, p = 0.84). Intensive low-density lipoprotein cholesterol lowering in patients improved the rate of plaque progression, but only to the level observed in nondiabetic patients with suboptimal lipid control. Conclusions Diabetes is accompanied by more extensive atherosclerosis and inadequate compensatory remodeling. Accelerated plaque progression, despite use of medical therapies, supports the need to develop new antiatherosclerotic strategies in diabetic patients.