SAN FRANCISCO – Atheromas regressed to similar degrees in patients with or without diabetes on high-intensity statin therapy for symptomatic coronary artery disease, a post hoc subgroup analysis of 1,039 patients found.
The primary endpoint, percent atheroma volume (PAV), decreased by a mean of 1.04% in 159 diabetic patients and by 1.21% in 880 nondiabetic patients compared with baseline – significant drops in both groups, Dr. Brian Stegman and his associates reported. PAV is the percentage of a single vessel’s volume occupied by atheroma.
The total atheroma volume (TAV), a secondary endpoint, decreased compared with baseline by 5.62 mm3 in the diabetic group and by 7.29 mm3 in the nondiabetic group, both of which also were significant changes, he said at the annual meeting of the American College of Cardiology.
Data came from the SATURN (Study of Coronary Atheroma by Intravascular Ultrasound: Effect of Rosuvastatin Versus Atorvastatin) trial, which compared intensive therapy with one of the two statin drugs in patients who underwent serial intravascular ultrasonography to assess disease regression. Patients were treated with either 40 mg/day rosuvastatin or 80 mg/day atorvastatin for 2 years. The two drug groups showed similar reductions in PAV, with a greater reduction in TAV using rosuvastatin (N. Engl. J. Med. 2011;365:2078-87).
Previous studies using have shown that aggressive reductions in LDL levels lead to significant regression in coronary atheromas as measured by intravascular ultrasound, but it has not been clear whether this is true in patients with diabetes as well as those without, said Dr. Stegman of the Cleveland Clinic Foundation.
The current analysis regrouped the SATURN cohort by diabetes status. High-intensity statin therapy produced substantial reductions in LDL in both groups, to a similar degree: a 52-mg/dL drop in diabetics and a 55-mg/dL decrease in nondiabetics. HDL levels increased by 3 mg/dL in diabetics and 5 mg/dL in nondiabetics, a significant difference between groups. Total cholesterol decreased 52 mg/dL in diabetics and 54 mg/dL in nondiabetics, and triglyceride levels decreased 13 mg/dL in diabetics and 12 mg/dL in nondiabetics, measures that were not significantly different between groups.
In both diabetics and nondiabetics, the lower the LDL on treatment, the greater the regression of atheroma, according to a linear regression model constructed by the investigators.
The changes in PAV and TAV in both groups showed that ”with high-intensity statin therapy, we saw equal regression of atheroma in diabetics compared with nondiabetics,” Dr. Stegman said. Lumen volumes were preserved over the 2-year period to a similar degree in both groups, as measured by change in lumen volume and external elastic membrane volume.
The findings differ from previous results in a pooled analysis of five trials involving intravascular ultrasound measurements of atherosclerosis progression in 2,237 patients, 416 of whom had diabetes, he noted. In that analysis, PAV increased by 0.05% in diabetics and by 0.6% in nondiabetics, compared with decreases of 1.21% and 1.04%, respectively, in the current analysis. The TAV decreased by 2.7 mm3 in diabetics and 0.6 mm3 in nondiabetics, much less than the 7.29-mm3and 5.62-mm3 decreases, respectively, in the current analysis (J. Am. Coll. Cardiol. 2008;52:255-62).
From http://www.internalmedicinenews.com
Effect of diabetes on progression of coronary atherosclerosis and arterial remodeling: a pooled analysis of 5 intravascular ultrasound trials.
Source
Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio 44195, USA. nichols1@ccf.org
Abstract
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 mm(3) vs. 189.4 +/- 7.1 mm(3), 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 mm(3) vs. 306.5 +/- 108.2 mm(3), p = 0.005) but no difference in external elastic membrane (494.9 +/- 166.9 mm(3) vs. 498.8 +/- 167.2 mm(3), 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 mm(3) vs. -2.7 +/- 2.4 mm(3), p = 0.03) was observed in diabetic patients on multivariate analysis. Smaller external elastic membrane (482.5 +/- 160.7 mm(3) vs. 519.9 +/- 166.9 mm(3), p = 0.03) and lumen (276.0 +/- 100.3 mm(3) vs. 310.1 +/- 105.6 mm(3), p = 0.001) volumes were observed in diabetic patients treated with insulin despite the presence of a similar TAV (206.5 +/- 88.6 mm(3) vs. 209.9 +/- 90.2 mm(3), 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.
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