Author + information
- Received February 12, 2014
- Revision received March 25, 2014
- Accepted April 10, 2014
- Published online October 1, 2014.
- Rishi Puri, MB, BS∗,†,
- Steven E. Nissen, MD∗,
- Mingyuan Shao, MS†,
- Christie M. Ballantyne, MD‡,
- Phillip J. Barter, MB, BS, PhD§,
- M. John Chapman, PhD, DSc‖,
- Raimund Erbel, MD¶,
- Peter Libby, MD#,
- Joel S. Raichlen, MD∗∗,
- Kiyoko Uno, MD, PhD∗,
- Yu Kataoka, MD†† and
- Stephen J. Nicholls, MB, BS, PhD†,††∗ ()
- ∗Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio
- †C5Research, Cleveland Clinic, Cleveland, Ohio
- ‡Section of Cardiovascular Research, Baylor College of Medicine, and the Methodist DeBakey Heart and Vascular Center, Houston, Texas
- §Centre for Vascular Research, University of New South Wales, Sydney, Australia
- ‖INSERM Dyslipidaemia and Atherosclerosis Research Unit, Pitié-Salpetriere University Hospital, Paris, France
- ¶West German Heart Center, Essen, Germany
- #Cardiovascular Division, Brigham and Women’s Hospital, Boston, Massachusetts
- ∗∗AstraZeneca, Wilmington, Delaware
- ††South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia
- ↵∗Reprint requests and correspondence:
Dr. Stephen J. Nicholls, South Australian Health and Medical Research Institute, University of Adelaide, Level 9, 121 King William Street, Adelaide, SA, 5001 Australia.
Objectives The study sought to explore sex-related differences in coronary atheroma regression following high-intensity statin therapy.
Background Guidelines now recommend high-intensity statins in all individuals with atherosclerotic cardiovascular disease.
Methods SATURN (Study of Coronary Atheroma by Intravascular Ultrasound: Effect of Rosuvastatin Versus Atorvastatin) employed serial intravascular ultrasound measures of coronary atheroma volume in patients treated with rosuvastatin 40 mg or atorvastatin 80 mg for 24 months. The treatment groups did not differ significantly in change from baseline of percent atheroma volume (PAV) or total atheroma volume (TAV) on intravascular ultrasound, nor in safety or clinical outcomes.
Results Compared with men (n = 765), women (n = 274) were older (p < 0.001) and more likely to have hypertension (p < 0.001), diabetes (p = 0.002), and higher low-density lipoprotein cholesterol (LDL-C) (p = 0.01), high-density lipoprotein cholesterol (p < 0.001), and C-reactive protein (CRP) (p = 0.004) levels. At follow-up, women had higher high-density lipoprotein cholesterol (p < 0.001) and CRP (p < 0.001), but similar LDL-C (p = 0.46) levels compared with men. Compared with men, women had lower baseline PAV (34.0 ± 8.0% vs. 37.2 ± 8.2%, p < 0.001) and TAV (122.4 ± 55 mm3 vs. 151.9 ± 63 mm3, p < 0.001), yet demonstrated greater PAV regression (–1.52 ± 0.18% vs. –1.07 ± 0.10%, p = 0.03) and TAV regression (–8.27 ± 0.9 mm3 vs. –6.59 ± 0.50 mm3, p = 0.11) following treatment. Greater PAV regression in women versus men occurred with rosuvastatin (p = 0.004), those with diabetes (p = 0.01), stable coronary disease (p = 0.01), higher baseline LDL-C (p = 0.02), and higher CRP (p = 0.04) levels. On multivariable analysis, female sex was independently associated with PAV regression (p = 0.01), and a sex-treatment interaction was found (p = 0.036). For participants with on-treatment LDL-C levels <70 mg/dl, women achieved greater PAV regression (–1.81 ± 0.22% vs. –1.12 ± 0.13%, p = 0.007) and TAV regression (–10.1 ± 1.1 mm3 vs. –7.16 ± 0.65 mm3, p = 0.023) than men, whereas PAV and TAV regression did not differ by sex, with LDL-C levels ≥70 mg/dl.
Conclusions Women with coronary disease demonstrate greater coronary atheroma regression than men when empirically prescribed guideline-driven potent statin therapy. This benefit appears in the setting of lower on-treatment LDL-C levels. (CRESTOR Athero Imaging Head to Head IVUS Study [SATURN]; NCT000620542)
The SATURN (Study of Coronary Atheroma by Intravascular Ultrasound: Effect of Rosuvastatin Versus Atorvastatin) study was sponsored by AstraZeneca Pharmaceuticals. This abstract was presented on November 18, 2013, at the American Heart Association meeting in Dallas, Texas. Dr. Nissen has received research support to perform clinical trials through the Cleveland Clinic Coordinating Center for Clinical Research from Pfizer, AstraZeneca, Novartis, Roche, Daiichi-Sankyo, Takeda, Sanofi-Aventis, Resverlogix, and Eli Lilly; and is a consultant/advisor for many pharmaceutical companies but requires them to donate all honoraria or consulting fees directly to charity so that he receives neither income nor a tax deduction. Dr. Libby has served as an unpaid consultant for Novartis, Johnson & Johnson, Amgen, and Roche; has served in unpaid leadership roles for clinical trials sponsored by AstraZeneca, GlaxoSmithKline, Novartis, Pfizer, Pronova, and Sigma Tau; and has previously received royalties from Roche for the patent on CD40L in cardiovascular risk stratification. Dr. Ballantyne has received grant support from Abbott, Amarin, the American Heart Association, AstraZeneca, Bristol-Myers Squibb, Genentech, GlaxoSmithKline, Kowa, Merck, Novartis, Roche, Sanofi-Synthelabo, and Takeda; has received consulting fees and honoraria from Abbott, Adnexus, Amarin, Amylin, AstraZeneca, Bristol-Myers Squibb, Esperion, Genentech, GlaxoSmithKline, Idera, Kowa, Merck, the National Institutes of Health, Novartis, Omthera, Resverlogix, Roche, Sanofi-Synthelabo, and Takeda; has served as a consultant for Abbott, Aegerion, Amarin, Amgen, Arena, Cerenis, Esperion, Genetech, Genzyme, Kowa, Merck, Novartis, Pfizer, Resverlogix, Regeneron, Roche, and Sanofi-Synthelabo; has received lecture fees from Abbott, AstraZeneca, GlaxoSmithKline, and Merck; and has served on the Speakers’ Bureau for Abbott. Dr. Barter holds an advisory board position for AstraZeneca, Merck, Roche, CSL, Behring, and Pfizer; has received grant support from Merck; has received consulting fees from CSL Behring; and has received lecture fees from AstraZeneca, Kowa, Merck, Pfizer, and Roche. Dr. Chapman has received grant support from CSL, GlaxoSmithKline, Pfizer, Randox, and Merck; has received consulting fees from Merck and Pfizer; has received lecture fees from Genzyme, Merck, Lilly, Roche, and Kowa; and owns equity interests in Wiley. Dr. Erbel has received grant and travel support from the Heinz Nixdorf Foundation, German Research Foundation; and has received accommodations/meeting expenses from Biotronik, Sanofi-Aventis, and Novartis. Dr. Libby has performed uncompensated work on clinical trials for and has received business travel reimbursement from AstraZeneca. Dr. Raichlen is an employee of and owns stock in AstraZeneca. Dr. Nicholls has received speaking honoraria from AstraZeneca, Pfizer, Merck Schering-Plough, and Takeda; has received consulting fees from AstraZeneca, Pfizer, Merck Schering-Plough, Takeda, Roche, Novo Nordisk, LipoScience, and Anthera; and has received research support from AstraZeneca and Lipid Sciences. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received February 12, 2014.
- Revision received March 25, 2014.
- Accepted April 10, 2014.
- American College of Cardiology Foundation