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Titolo:
LIMITATION OF INFARCT EXPANSION AND VENTRICULAR REMODELING BY LATE REPERFUSION - STUDY OF TIME-COURSE AND MECHANISM IN A RAT MODEL
Autore:
BOYLE MP; WEISMAN HF;
Indirizzi:
CENTOCOR INC,200 GREAT VALLEY PKWY MALVERN PA 19355 JOHNS HOPKINS MED INST BALTIMORE MD 00000
Titolo Testata:
Circulation
fascicolo: 6, volume: 88, anno: 1993,
pagine: 2872 - 2883
SICI:
0009-7322(1993)88:6<2872:LOIEAV>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACUTE MYOCARDIAL-INFARCTION; 12-MONTH FOLLOW-UP; INTRACORONARY STREPTOKINASE; THROMBOLYTIC THERAPY; CORONARY REPERFUSION; IMPROVED SURVIVAL; NECROSIS; TRIAL; REDUCTION; SALVAGE;
Keywords:
MYOCARDIAL INFARCTION; THROMBOLYSIS; VENTRICLES; REPERFUSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
33
Recensione:
Indirizzi per estratti:
Citazione:
M.P. Boyle e H.F. Weisman, "LIMITATION OF INFARCT EXPANSION AND VENTRICULAR REMODELING BY LATE REPERFUSION - STUDY OF TIME-COURSE AND MECHANISM IN A RAT MODEL", Circulation, 88(6), 1993, pp. 2872-2883

Abstract

Background. Reperfusion of acutely infarcted myocardium may be beneficial in limiting infarct expansion and ventricular remodeling even if established after the time that salvage of ischemic myocardium is possible. Methods and Results. To examine the permanency, time course, andmechanism of this effect of late reperfusion, 200 rats were randomized into one of four groups: (1) infarction with reperfusion after 1 to 2 hours, (2) infarction with reperfusion after 6 to 8 hours, (3) infarction without reperfusion, and (4) sham operation. Surviving rats werekilled at either 7 days, when infarct expansion has plateaued, or 21 days, when infarct healing is complete. In both 7- and 21-day analyses, late reperfusion did not reduce infarct size or degree of transmuralnecrosis but significantly limited infarct expansion, as measured by an index based on infarct endocardial segment lengthening and infarct wall thinning (expansion index at 7 days: no reperfusion, 2.73+/-0.25,n=13; reperfusion after 1 to 2 hours, 1.56+/-0.13, n=23, P<.001; reperfusion after 6 to 8 hours, 1.78+/-0.15, n=16, P=.002; at 21 days: no reperfusion, 3.45+/-0.39, n=13; reperfusion after 1 to 2 hours, 2.21+/-0.24, n=15, P=.01; reperfusion after 6 to 8 hours, 2.02+/-0.20, n=9, P=.01). Reperfusion after 6 to 8 hours was equally effective in limiting expansion as reperfusion after 1 to 2 hours. Late reperfusion also significantly reduced ventricular remodeling at 21 days, as measured by an index based on left ventricular cavity dilatation and noninfarcted myocardial hypertrophy (remodeling index at 21 days: no reperfusion,2.67+/-0.15, n=13; reperfusion after 1 to 2 hours, 2.20+/-0.15, n=15,P=.035; reperfusion after 6 to 8 hours, 2.12+/-0.10, n=9, P=.012). Histological examination revealed that reperfusion accelerated the clearance of residual dead myofibrils, suggesting an increase in the rate of healing, and increased the degree of myocytolysis but did not changethe final degree of infarct healing, tissue density, or viable subepicardial cells. Conclusions. Late reperfusion causes a permanent reduction in postinfarction expansion that is present even after complete infarct healing. The time after coronary occlusion in which reperfusion is of benefit in reducing subsequent expansion and remodeling is substantially longer than previously established. The mechanism by which late reperfusion limits expansion may involve changing the rate of healing and the nature of myocardial necrosis but does not involve preserving subepicardial cells.

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Documento generato il 05/12/20 alle ore 09:28:51