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

Sung Jin Hong, Hyuk-Jae Chang, Sungha Park, Dae Ryong Kang, Sanghoon Shin, In Jeong Cho, ChiYoung Shim, Geu Ru Hong, Jong Won Ha, Namsik Chung

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Background A family history of premature coronary artery disease (CAD) is a well-known risk factor for cardiovascular events. Hypothesis Atorvastatin may improve endothelial dysfunction (ED) in the first-degree relatives (FDRs) of patients with premature CAD with ED. Methods 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. Results 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. Conclusions 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.

Original languageEnglish
Pages (from-to)480-485
Number of pages6
JournalClinical Cardiology
Volume36
Issue number8
DOIs
Publication statusPublished - 2013 Aug 1

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Cross-Over Studies
Coronary Artery Disease
Placebos
Hyperemia
Therapeutics
Atorvastatin Calcium
Hydroxymethylglutaryl-CoA Reductase Inhibitors
Primary Prevention
LDL Cholesterol
Cholesterol
Guidelines
Lipids
Education
Population

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

@article{1c31742dd62547348965cd88bb1b2836,
title = "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",
abstract = "Background A family history of premature coronary artery disease (CAD) is a well-known risk factor for cardiovascular events. Hypothesis Atorvastatin may improve endothelial dysfunction (ED) in the first-degree relatives (FDRs) of patients with premature CAD with ED. Methods 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. Results 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. Conclusions 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.",
author = "Hong, {Sung Jin} and Hyuk-Jae Chang and Sungha Park and Kang, {Dae Ryong} and Sanghoon Shin and Cho, {In Jeong} and ChiYoung Shim and Hong, {Geu Ru} and Ha, {Jong Won} and Namsik Chung",
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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. / Hong, Sung Jin; Chang, Hyuk-Jae; Park, Sungha; Kang, Dae Ryong; Shin, Sanghoon; Cho, In Jeong; Shim, ChiYoung; Hong, Geu Ru; Ha, Jong Won; Chung, Namsik.

In: Clinical Cardiology, Vol. 36, No. 8, 01.08.2013, p. 480-485.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Impact of atorvastatin treatment in first-degree relatives of patients with premature coronary artery disease with endothelial dysfunction

T2 - A double-blind, randomized, placebo-controlled crossover trial

AU - Hong, Sung Jin

AU - Chang, Hyuk-Jae

AU - Park, Sungha

AU - Kang, Dae Ryong

AU - Shin, Sanghoon

AU - Cho, In Jeong

AU - Shim, ChiYoung

AU - Hong, Geu Ru

AU - Ha, Jong Won

AU - Chung, Namsik

PY - 2013/8/1

Y1 - 2013/8/1

N2 - Background A family history of premature coronary artery disease (CAD) is a well-known risk factor for cardiovascular events. Hypothesis Atorvastatin may improve endothelial dysfunction (ED) in the first-degree relatives (FDRs) of patients with premature CAD with ED. Methods 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. Results 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. Conclusions 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.

AB - Background A family history of premature coronary artery disease (CAD) is a well-known risk factor for cardiovascular events. Hypothesis Atorvastatin may improve endothelial dysfunction (ED) in the first-degree relatives (FDRs) of patients with premature CAD with ED. Methods 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. Results 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. Conclusions 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.

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U2 - 10.1002/clc.22152

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