This work was supported by the National Research Foundation of Korea grant funded by the Korea government (MEST; no. 2012027176) and by the Chong Kun Dang Pharmaceutical Corp., Seoul, Korea. ClinicalTrials.gov: NCT00917527. The authors have no other funding, financial relationships, or conflicts of interest to disclose.
Impact of Atorvastatin Treatment in First-Degree Relatives of Patients With Premature Coronary Artery Disease With Endothelial Dysfunction: A Double-Blind, Randomized, Placebo-Controlled Crossover Trial
Article first published online: 10 JUN 2013
© 2013 Wiley Periodicals, Inc.
Volume 36, Issue 8, pages 480–485, August 2013
How to Cite
Hong, S.-J., Chang, H.-J., Park, S., Kang, D. R., Shin, S., Cho, I.-J., Shim, C. Y., Hong, G.-R., Ha, J.-W. and Chung, N. (2013), Impact of Atorvastatin Treatment in First-Degree Relatives of Patients With Premature Coronary Artery Disease With Endothelial Dysfunction: A Double-Blind, Randomized, Placebo-Controlled Crossover Trial. Clin Cardiol, 36: 480–485. doi: 10.1002/clc.22152
- Issue published online: 12 AUG 2013
- Article first published online: 10 JUN 2013
- Manuscript Revised: 6 MAY 2013
- Manuscript Received: 25 MAR 2013
A family history of premature coronary artery disease (CAD) is a well-known risk factor for cardiovascular events.
Atorvastatin may improve endothelial dysfunction (ED) in the first-degree relatives (FDRs) of patients with premature CAD with ED.
Thirty-five FDRs (median age, 52 years [interquartile range (IQR), 46–57 years], 21 male) of patients with premature CAD with ED were recruited in a prospective trial with a crossover double-blind design: 6 weeks of treatment with atorvastatin 40 mg/day followed by placebo, or vice versa. After each treatment, the digital pulse wave amplitude was determined by EndoPAT to obtain the reactive hyperemia index (RHI), a measure for endothelial function. The primary outcome was the difference of RHI between atorvastatin and placebo treatment.
Low-density lipoprotein cholesterol was lower after atorvastatin compared with placebo treatment (124 [102–145] mg/dL vs 67 [50–73] mg/dL, P < 0.001). However, RHI was not different after atorvastatin compared with placebo treatment (1.9 [1.5–2.4] vs 1.9 [1.6–2.2], P = 0.902). Also, the augmentation index was similar after each treatment. These results were observed both in subjects who had indications for statin treatment (31%) and those who did not (69%) according to National Cholesterol Education Program Adult Treatment Panel III guidelines.
Despite improvement in the lipid profile, atorvastatin failed to improve ED in the FDRs of patients with premature CAD with ED. Although we identified those with ED in FDRs of patients with premature CAD as a high-risk group for future cardiovascular events, atorvastatin treatment may not be a beneficial primary prevention strategy for this population.