Effect of coronary risk factors on arterial compensatory enlargement in Japanese middle-aged patients with de novo single-vessel disease - An intravascular ultrasound study

被引:4
作者
Isoda, K [1 ]
Arakawa, K [1 ]
Kamezawa, Y [1 ]
Nishizawa, KY [1 ]
Nishikawa, KI [1 ]
Shibuya, T [1 ]
Ohsuzu, F [1 ]
Nakamura, H [1 ]
机构
[1] Natl Def Med Coll, Dept Internal Med 1, Tokorozawa, Saitama 3590042, Japan
关键词
atherosclerosis; compensatory enlargement; coronary risk factors;
D O I
10.1002/clc.4960240605
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Compensatory enlargement (CE) of atherosclerotic human arteries has been reported; however, the pat tern of arterial remodeling in response to plaque formation is not unique. Hypothesis: The study was undertaken to determine the extent of coronary artery compensatory enlargement at stenotic lesions and to correlate the arterial compensatory enlargement with risk factors. Methods: We studied 62 patients with stable angina and de novo single-vessel disease using intravascular ultrasound and obtained good images in 42 patients (68%). The vessel cross-sectional area (VA), lumen cross-sectional area (LA), and plaque cross-sectional area (PA) were measured at the lesion site and at proximal and distal reference sites. Positive CE was defined as increase in VA of lesion site > 10% compared with that of proximal reference site (CE group, n = 15); shrinkage was defined as reduction in VA of lesion site > 10% compared with that of proximal reference site (S group, n = 14); inadequate CE was defined as intermediate between CE and S (IE group, n = 13). All subjects had coronary risk factors measured before this study. Results: There was no difference in VA, LA, or PA among the three groups at the proximal and distal reference sites, nor in LA at the lesion site; however, VA and PA were significantly smaller in the S group than in the other groups (p < 0.01). Of coronary risk factors, increased systolic blood pressure (SBP), increased diastolic blood pressure (DBP), and decreased high-density lipoprotein cholesterol (HDL-c) levels had the strongest association with shrinkage (p < 0.05). Conclusion: Hypertension and decreased HDL level may contribute to the shrinkage response in middle-aged patients with stable angina.
引用
收藏
页码:443 / 450
页数:8
相关论文
共 27 条
[1]   STRUCTURAL AND HEMODYNAMIC-RESPONSES OF PERIPHERAL ARTERIES OF MACAQUE MONKEYS TO ATHEROGENIC DIET [J].
ARMSTRONG, ML ;
HEISTAD, DD ;
MARCUS, ML ;
MEGAN, MB ;
PIEGORS, DJ .
ARTERIOSCLEROSIS, 1985, 5 (04) :336-346
[2]  
BOND MG, 1981, ARTERY, V9, P21
[3]   OSTEOCALCIN INDUCES CHEMOTAXIS, SECRETION OF MATRIX PROTEINS, AND CALCIUM-MEDIATED INTRACELLULAR SIGNALING IN HUMAN OSTEOCLAST-LIKE CELLS [J].
CHENU, C ;
COLUCCI, S ;
GRANO, M ;
ZIGRINO, P ;
BARATTOLO, R ;
ZAMBONIN, G ;
BALDINI, N ;
VERGNAUD, P ;
DELMAS, PD ;
ZALLONE, AZ .
JOURNAL OF CELL BIOLOGY, 1994, 127 (04) :1149-1158
[4]   ANTIATHEROGENIC EFFECT OF CAPTOPRIL IN THE WATANABE HERITABLE HYPERLIPIDEMIC RABBIT [J].
CHOBANIAN, AV ;
HAUDENSCHILD, CC ;
NICKERSON, C ;
DRAGO, R .
HYPERTENSION, 1990, 15 (03) :327-331
[5]   ENDOTHELIAL DYSFUNCTION AND SUBENDOTHELIAL MONOCYTE MACROPHAGES IN HYPERTENSION - EFFECT OF ANGIOTENSIN CONVERTING ENZYME-INHIBITION [J].
CLOZEL, M ;
KUHN, H ;
HEFTI, F ;
BAUMGARTNER, HR .
HYPERTENSION, 1991, 18 (02) :132-141
[6]   HIGH-DENSITY-LIPOPROTEINS INHIBIT CYTOKINE-INDUCED EXPRESSION OF ENDOTHELIAL-CELL ADHESION MOLECULES [J].
COCKERILL, GW ;
RYE, KA ;
GAMBLE, JR ;
VADAS, MA ;
BARTER, PJ .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1995, 15 (11) :1987-1994
[7]  
Ehara S, 1998, CIRCULATION, V98, P765
[8]  
GENG YJ, 1995, AM J PATHOL, V147, P251
[9]   COMPENSATORY ENLARGEMENT OF HUMAN ATHEROSCLEROTIC CORONARY-ARTERIES [J].
GLAGOV, S ;
WEISENBERG, E ;
ZARINS, CK ;
STANKUNAVICIUS, R ;
KOLETTIS, GJ .
NEW ENGLAND JOURNAL OF MEDICINE, 1987, 316 (22) :1371-1375
[10]   Cholesterol-lowering treatment is associated with improvement in coronary vascular remodeling and endothelial function in patients with normal or mildly diseased coronary arteries [J].
Hamasaki, S ;
Higano, ST ;
Al Suwaidi, J ;
Nishimura, RA ;
Miyauchi, K ;
Holmes, DR ;
Lerman, A .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2000, 20 (03) :737-743