LOW-DOSE DOBUTAMINE IN PATIENTS WITH ACUTE MYOCARDIAL-INFARCTION IDENTIFIES VIABLE BUT NOT CONTRACTILE MYOCARDIUM AND PREDICTS THE MAGNITUDE OF IMPROVEMENT IN WALL MOTION ABNORMALITIES IN RESPONSE TO CORONARY REVASCULARIZATION

被引:204
作者
BARILLA, F [1 ]
GHEORGHIADE, M [1 ]
ALAM, M [1 ]
KHAJA, F [1 ]
GOLDSTEIN, S [1 ]
机构
[1] HENRY FORD HOSP, INST HEART & VASC, DIV CARDIOVASC MED, 2799 W GRAND BLVD, DETROIT, MI 48202 USA
关键词
D O I
10.1016/0002-8703(91)90267-L
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
To assess the effects of coronary revascularization on viable but noncontractile myocardium, we examined 21 patients with a documented anterior acute myocardial infarction who had a significant improvement in wall motion abnormality evaluated by two-dimensional echocardiography in the infarct-related artery in response to low-dose dobutamine infusion. All patients had a significant residual stenosis in the infarct-related artery. In response to low-dose dobutamine, there was a marked improvement in contractility in the infarct-related area segments and this was reflected by a decrease in echocardiographic score index from 1.5 +/- 0.15 to 1.09 +/- 0.08 (p = 0.0001). Of these 21 patients, 13 underwent successful revascularization: 10 had percutaneous transluminal coronary angioplasty (PTCA) and three had coronary artery bypass grafts (CABG) (group I). Eight patients received medical therapy only (group II). At 40 +/- 15 days of follow-up, both groups had improvement in their segmental wall motion abnormalities. However, the improvement in group I was greater than that in group II, 1.1 +/- 0.13 and 1.35 +/- 0.1, respectively (p = 0.0002). We conclude that: (1) low-dose dobutamine infusion may identify viable but noncontractile myocardium in patients with acute myocardial infarction and (2) in these patients revascularization causes a greater improvement in left ventricular function over time when compared with a nonrevascularized group.
引用
收藏
页码:1522 / 1531
页数:10
相关论文
共 23 条
[1]  
[Anonymous], 1988, LANCET, V2, P349
[2]  
[Anonymous], 1986, LANCET, V1, P397
[3]   REVERSAL OF DYSFUNCTION IN POSTISCHEMIC STUNNED MYOCARDIUM BY EPINEPHRINE AND POSTEXTRASYSTOLIC POTENTIATION [J].
BECKER, LC ;
LEVINE, JH ;
DIPAULA, AF ;
GUARNIERI, T ;
AVERSANO, T .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1986, 7 (03) :580-589
[4]  
BISSETT JK, 1987, BRIT HEART J, V58, P460
[5]   MECHANISM OF MYOCARDIAL STUNNING [J].
BOLLI, R .
CIRCULATION, 1990, 82 (03) :723-738
[6]   BETA-ADRENERGIC STIMULATION REVERSES POSTISCHEMIC MYOCARDIAL DYSFUNCTION WITHOUT PRODUCING SUBSEQUENT FUNCTIONAL DETERIORATION [J].
BOLLI, R ;
ZHU, WX ;
MYERS, ML ;
HARTLEY, CJ ;
ROBERTS, R .
AMERICAN JOURNAL OF CARDIOLOGY, 1985, 56 (15) :964-968
[7]   THE STUNNED MYOCARDIUM - PROLONGED, POST-ISCHEMIC VENTRICULAR DYSFUNCTION [J].
BRAUNWALD, E ;
KLONER, RA .
CIRCULATION, 1982, 66 (06) :1146-1149
[8]  
BRAUNWALD E, 1987, CIRCULATION, V76, P2
[9]   REVERSIBLE ISCHEMIC LEFT-VENTRICULAR DYSFUNCTION - EVIDENCE FOR THE HIBERNATING MYOCARDIUM [J].
BRAUNWALD, E ;
RUTHERFORD, JD .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1986, 8 (06) :1467-1470
[10]   RESPONSE OF REPERFUSION-SALVAGED, STUNNED MYOCARDIUM TO INOTROPIC STIMULATION [J].
ELLIS, SG ;
WYNNE, J ;
BRAUNWALD, E ;
HENSCHKE, CI ;
SANDOR, T ;
KLONER, RA .
AMERICAN HEART JOURNAL, 1984, 107 (01) :13-19