ENALAPRIL IN THE PREVENTION OF RESTENOSIS FOLLOWING INTRACORONARY INTERVENTION IN A SWINE MODEL

被引:19
作者
CHURCHILL, DA [1 ]
SIEGEL, CO [1 ]
MINOR, ST [1 ]
WEST, MS [1 ]
RAIZNER, AE [1 ]
机构
[1] BAYLOR COLL MED,DEPT MED,CARDIOL SECT,HOUSTON,TX 77030
关键词
PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY; INTRACORONARY STENT; RESTENOSIS MODEL;
D O I
10.1097/00019501-199305000-00010
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Restenosis following percutaneous transluminal coronary angioplasty continues to be a major limitation of the procedure. To test whether an angiotensin-converting enzyme inhibitor may reduce restenosis, this study utilized an atherosclerotic, stented, Hanford miniature swine model of restenosis. Methods: Each animal first was started on an atherogenic diet and had balloon abrasion of the left anterior descending and right coronary arteries. Four months later, balloon-mounted coil stents were placed into the abraded coronary arteries of each animal. Twenty-four animals then were randomly assigned to one of two groups: enalapril, and control. The enalapril group received 50 mg orally twice daily starting 1 week before intracoronary stenting. Results: Follow-up 2 months later revealed angiographic stenosis in the control group of 30% +/- 13%/25% +/- 10% (left anterior descending/right coronary artery) versus 37% +/- 9%/20% +/- 11% in the enalapril group (P = not significant). The change in minimal lumen diameter from immediately after stenting to follow-up was not significantly different between control and enalapril groups. Area stenosis and maximal intimal thickness obtained by morphometric analysis were also compared, and the mean percentage area stenosis for the control group was 39 +/- 12%/31% +/- 16% and for enalapril 36% +/- 14%/35% +/- 19%. The maximal intimal thickness in the control group was 573 mum +/- 204 mum/605 mum +/- 266 mum and in the enalapril group 530 mum +/- 220 mum/424 mum +/- 237 mum. There was no statistical difference. Conclusions: Enalapril fails to reduce restenosis in this animal model.
引用
收藏
页码:461 / 467
页数:7
相关论文
共 24 条
[1]  
BELL L, 1990, AM J PATHOL, V137, P7
[2]   ANGIOTENSIN-II-STIMULATED PROTEIN-SYNTHESIS IN CULTURED VASCULAR SMOOTH-MUSCLE CELLS [J].
BERK, BC ;
VEKSHTEIN, V ;
GORDON, HM ;
TSUDA, T .
HYPERTENSION, 1989, 13 (04) :305-314
[3]   EFFECT OF ENALAPRIL ON AORTIC SMOOTH-MUSCLE CELL POLYPLOIDY IN THE SPONTANEOUSLY HYPERTENSIVE RAT [J].
BLACK, MJ ;
ADAMS, MA ;
BOBIK, A ;
CAMPBELL, JH ;
CAMPBELL, GR .
JOURNAL OF HYPERTENSION, 1989, 7 (12) :997-1003
[4]   ANGIOTENSIN-CONVERTING ENZYME - VASCULAR ENDOTHELIAL LOCALIZATION [J].
CALDWELL, PRB ;
SEEGAL, BC ;
HSU, KC ;
DAS, M ;
SOFFER, RL .
SCIENCE, 1976, 191 (4231) :1050-1051
[5]   EFFECTS OF ANGIOTENSIN-II AND VASOPRESSIN ON HUMAN SMOOTH-MUSCLE CELLS-INVITRO [J].
CAMPBELLBOSWELL, M ;
ROBERTSON, AL .
EXPERIMENTAL AND MOLECULAR PATHOLOGY, 1981, 35 (02) :265-276
[6]   LOCALIZATION OF ANGIOTENSINOGEN MESSENGER-RNA IN RAT AORTA [J].
CASSIS, LA ;
LYNCH, KR ;
PEACH, MJ .
CIRCULATION RESEARCH, 1988, 62 (06) :1259-1262
[7]   DIFFERENTIATION OF ANGIOTENSIN-CONVERTING ENZYME (ACE) INHIBITORS BY THEIR SELECTIVE-INHIBITION OF ACE IN PHYSIOLOGICALLY IMPORTANT TARGET ORGANS [J].
CUSHMAN, DW ;
WANG, FL ;
FUNG, WC ;
HARVEY, CM ;
DEFORREST, JM .
AMERICAN JOURNAL OF HYPERTENSION, 1989, 2 (04) :294-306
[8]   TRANSLUMINAL TREATMENT OF ARTERIOSCLEROTIC OBSTRUCTION - DESCRIPTION OF NEW TECHNIC + PRELIMINARY REPORT OF ITS APPLICATION [J].
DOTTER, CT ;
JUDKINS, MP .
CIRCULATION, 1964, 30 (05) :654-&
[9]  
FALLON RR, 1982, LIFE SCI, V30, P99
[10]   ANGIOTENSIN-II INDUCES HYPERTROPHY, NOT HYPERPLASIA, OF CULTURED RAT AORTIC SMOOTH-MUSCLE CELLS [J].
GEISTERFER, AAT ;
PEACH, MJ ;
OWENS, GK .
CIRCULATION RESEARCH, 1988, 62 (04) :749-756