Brian Stegman1, Rishi Puri2, Leslie Cho1, Mingyuan Shao3, Christie M Ballantyne4, Phillip J Barter5, M John Chapman6, Raimund Erbel7, Peter Libby8, Joel S Raichlen9, Kiyoko Uno1, Yu Kataoka10, Steven E Nissen2, Stephen J Nicholls11. 1. Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH. 2. Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH C5Research, Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH. 3. C5Research, Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH. 4. Section of Cardiovascular Research, Baylor College of Medicine, and the Methodist DeBakey Heart and Vascular Center, Houston, TX. 5. Centre for Vascular Research, University of New South Wales, Sydney, Australia. 6. INSERM Dyslipidaemia and Atherosclerosis Research Unit, Pitié-Salpètrière University Hospital, Paris, France. 7. West German Heart Center, Essen, Germany. 8. Cardiovascular Division, Brigham and Women's Hospital, Boston, MA. 9. AstraZeneca, Wilmington, DE. 10. South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia. 11. South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia stephen.nicholls@sahmri.com.
Abstract
OBJECTIVE: Although statins can induce coronary atheroma regression, this benefit has yet to be demonstrated in diabetic individuals. We tested the hypothesis that high-intensity statin therapy may promote coronary atheroma regression in patients with diabetes. RESEARCH DESIGN AND METHODS: The Study of Coronary Atheroma by Intravascular Ultrasound: Effect of Rosuvastatin Versus Atorvastatin (SATURN) used serial intravascular ultrasound measures of coronary atheroma volume in patients treated withrosuvastatin 40 mg or atorvastatin80 mg for 24 months. This analysis compared changes in biochemistry and coronary percent atheroma volume (PAV) in patients with (n = 159) and without (n = 880) diabetes. RESULTS: At baseline, patients with diabetes had lower LDL cholesterol (LDL-C) and HDL cholesterol (HDL-C) levels but higher triglyceride and CRP levels compared with patients without diabetes. At follow-up, diabetic patients had lower levels of LDL-C (61.0 ± 20.5 vs. 66.4 ± 22.9 mg/dL, P = 0.01) and HDL-C (46.3 ± 10.6 vs. 49.9 ± 12.0 mg/dL, P < 0.001) but higher levels of triglycerides (127.6 [98.8, 163.0] vs. 113.0 mg/dL [87.6, 151.9], P = 0.001) and CRP (1.4 [0.7, 3.3] vs. 1.0 [0.5, 2.1] mg/L, P = 0.001). Both patients with and without diabetes demonstrated regression of coronary atheroma as measured by change in PAV (-0.83 ± 0.13 vs. -1.15 ± 0.13%, P = 0.08). PAV regression was less in diabetic compared with nondiabetic patients when on-treatment LDL-C levels were >70 mg/dL (-0.31 ± 0.23 vs. -1.01 ± 0.21%, P = 0.03) but similar when LDL-C levels were ≤70 mg/dL (-1.09 ± 0.16 vs. -1.24 ± 0.16%, P = 0.50). CONCLUSIONS:High-intensity statin therapy alters the progressive nature of diabetic coronary atherosclerosis, yielding regression of disease in diabetic and nondiabetic patients.
RCT Entities:
OBJECTIVE: Although statins can induce coronary atheroma regression, this benefit has yet to be demonstrated in diabetic individuals. We tested the hypothesis that high-intensity statin therapy may promote coronary atheroma regression in patients with diabetes. RESEARCH DESIGN AND METHODS: The Study of Coronary Atheroma by Intravascular Ultrasound: Effect of Rosuvastatin Versus Atorvastatin (SATURN) used serial intravascular ultrasound measures of coronary atheroma volume in patients treated with rosuvastatin 40 mg or atorvastatin 80 mg for 24 months. This analysis compared changes in biochemistry and coronary percent atheroma volume (PAV) in patients with (n = 159) and without (n = 880) diabetes. RESULTS: At baseline, patients with diabetes had lower LDL cholesterol (LDL-C) and HDL cholesterol (HDL-C) levels but higher triglyceride and CRP levels compared with patients without diabetes. At follow-up, diabeticpatients had lower levels of LDL-C (61.0 ± 20.5 vs. 66.4 ± 22.9 mg/dL, P = 0.01) and HDL-C (46.3 ± 10.6 vs. 49.9 ± 12.0 mg/dL, P < 0.001) but higher levels of triglycerides (127.6 [98.8, 163.0] vs. 113.0 mg/dL [87.6, 151.9], P = 0.001) and CRP (1.4 [0.7, 3.3] vs. 1.0 [0.5, 2.1] mg/L, P = 0.001). Both patients with and without diabetes demonstrated regression of coronary atheroma as measured by change in PAV (-0.83 ± 0.13 vs. -1.15 ± 0.13%, P = 0.08). PAV regression was less in diabetic compared with nondiabeticpatients when on-treatment LDL-C levels were >70 mg/dL (-0.31 ± 0.23 vs. -1.01 ± 0.21%, P = 0.03) but similar when LDL-C levels were ≤70 mg/dL (-1.09 ± 0.16 vs. -1.24 ± 0.16%, P = 0.50). CONCLUSIONS: High-intensity statin therapy alters the progressive nature of diabetic coronary atherosclerosis, yielding regression of disease in diabetic and nondiabeticpatients.
Authors: Adrian Quan; Yi Pan; Krishna K Singh; John Polemidiotis; Hwee Teoh; Howard Leong-Poi; Subodh Verma Journal: Mol Cell Biochem Date: 2017-03-16 Impact factor: 3.396