Effects of Combined Treatment with Angiotensin II Type 1 Receptor Blocker and Statin on Stent Restenosis

被引:20
作者
Yoshikawa, Masaki [1 ,2 ]
Nakamura, Kazufumi [1 ]
Nagase, Satoshi [1 ]
Sakuragi, Satoru [1 ]
Kusano, Kengo F. [1 ]
Matsubara, Hiromi [3 ]
Ohe, Tohru [1 ]
机构
[1] Okayama Univ, Grad Sch Dent & Pharmaceut Sci, Dept Cardiovasc Med, Okayama 7008558, Japan
[2] Onomichi Municipal Hosp, Dept Cardiovasc Med, Onomichi, Japan
[3] Natl Okayama Med Ctr, Div Cardiol, Okayama, Japan
关键词
ARB; statin; combined treatment; stent restenosis; LOW-DENSITY-LIPOPROTEIN; SMOOTH-MUSCLE-CELLS; INHIBITS PROLIFERATION; OXIDATIVE STRESS; ATHEROSCLEROSIS; FLUVASTATIN; VALSARTAN; ATHEROGENESIS; INVOLVEMENT; EXPRESSION;
D O I
10.1097/FJC.0b013e318199f30b
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Angiotensin II type 1 receptor blocker (ARB) or statin has been reported to be effective in preventing stent restenosis, but little is known about the combined effect on stent restenosis. The objective of this study was to determine the effect of combination therapy with ARB and statin on restenosis rate after coronary stenting and on proliferation and migration of and reactive oxygen species (ROS) production by human coronary artery smooth muscle cells (SMCs) in vitro. Clinical data were collected from 330 consecutive patients who underwent coronary stewing for de novo lesions. Six months after stenting, quantitative coronary angiography was performed. Combined therapy with the ARB and statin significantly inhibited stent restenosis (P < 0.05) compared with the effect of the ARB or statin alone. In an in vitro study, platelet-derived growth factor (PDGF) induced proliferation was significantly inhibited by combined treatment with CV11974, an ARB, an simvastatin (P < 0.01), but the inhibitory effect was not significantly greater than that of simvastatin alone. Migration of human coronary artery SMCs was significantly inhibited by the ARB + statin compared with the effect of the ARB or statin alone (P < 0.01). PDGF-induced production of ROS was also inhibited significantly by the ARB + statin compared with the effect of the ARB or statin alone (P < 0.01). These results indicate that inhibitory effects of combined therapy on PDGF-induced migration of and ROS production by SMCs play an important role in reduction of restenosis rate. Combined treatment with ARB and statin after stenting is useful for preventing stent restenosis.
引用
收藏
页码:179 / U2
页数:8
相关论文
共 33 条
[1]  
ABEDI H, 1995, CARDIOVASC RES, V30, P544, DOI 10.1016/0008-6363(95)00092-5
[2]   3-hydroxy-3-methylglutaryl coenzyme a (HMG-CoA) reductase inhibitors (statins), atherosclerosis and coronary syndromes [J].
Blum, A ;
Simsolo, C ;
Hasin, Y .
ATHEROSCLEROSIS, 2004, 175 (01) :1-5
[3]   Executive summary of the Third Report of the National Cholesterol Education Program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III) [J].
Cleeman, JI ;
Grundy, SM ;
Becker, D ;
Clark, LT ;
Cooper, RS ;
Denke, MA ;
Howard, WJ ;
Hunninghake, DB ;
Illingworth, DR ;
Luepker, RV ;
McBride, P ;
McKenney, JM ;
Pasternak, RC ;
Stone, NJ ;
Van Horn, L ;
Brewer, HB ;
Ernst, ND ;
Gordon, D ;
Levy, D ;
Rifkind, B ;
Rossouw, JE ;
Savage, P ;
Haffner, SM ;
Orloff, DG ;
Proschan, MA ;
Schwartz, JS ;
Sempos, CT ;
Shero, ST ;
Murray, EZ .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2001, 285 (19) :2486-2497
[4]   Impact of a combined treatment of angiotensin II type 1 receptor blockade and 3-hydroxy-3-methyl-glutaryl-CoA-reductase inhibition on secretory phospholipase A2-type IIA and low density lipoprotein oxidation in patients with coronary artery disease [J].
Divchev, Dimitar ;
Grothusen, Christina ;
Luchtefeld, Maren ;
Thoenes, Martin ;
Onono, Frederick ;
Koch, Rainer ;
Drexler, Helmut ;
Schieffer, Bernhard .
EUROPEAN HEART JOURNAL, 2008, 29 (16) :1956-1965
[5]   Carvedilol inhibits proliferation of cultured pulmonary artery smooth muscle cells of patients with idiopathic pulmonary arterial hypertension [J].
Fujio, H ;
Nakamura, K ;
Matsubara, H ;
Kusano, KF ;
Miyaji, K ;
Nagase, S ;
Ikeda, T ;
Ogawa, A ;
Ohta-Ogo, K ;
Miura, D ;
Miura, A ;
Miyazaki, M ;
Date, H ;
Ohe, T .
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 2006, 47 (02) :250-255
[6]   Comparison of cardiovascular events in patients with angiographically documented coronary narrowing with combined renin-angiotensin system inhibitor plus statin versus renin-angiotensin system inhibitor alone versus statin alone (from the Japanese Coronary Artery Disease Study) [J].
Fujita, Masatoshi ;
Yamazaki, Tsutomu ;
Hayashi, Dobun ;
Kohro, Takahide ;
Okada, Yoshihiro ;
Nagai, Ryozo .
AMERICAN JOURNAL OF CARDIOLOGY, 2007, 100 (12) :1750-1753
[7]  
Harrison DG, 1997, CLIN CARDIOL, V20, P11
[8]   The p53-activated gene, PAG608, requires a zinc finger domain for nuclear localization and oxidative stress-induced [J].
Higashi, Y ;
Asanuma, M ;
Miyazaki, I ;
Haque, ME ;
Fujita, N ;
Tanaka, K ;
Ogawa, N .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (44) :42224-42232
[9]   Fluvastatin enhances the inhibitory effects of a selective angiotensin II type 1 receptor blocker, valsartan, on vascular neointimal formation [J].
Horiuchi, M ;
Cui, TX ;
Li, Z ;
Li, JM ;
Nakagami, H ;
Iwai, M .
CIRCULATION, 2003, 107 (01) :106-112
[10]   Valsartan therapy has additive anti-oxidative effect to that of fluvastatin therapy against low-density lipoprotein oxidation: Studies in hypercholesterolernic and hypertensive patients [J].
Hussein, O ;
Shneider, J ;
Rosenblat, M ;
Aviram, M .
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 2002, 40 (01) :28-34