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Titolo:
CARDIOPROTECTION BY ACE-INHIBITORS IN ACUTE MYOCARDIAL-ISCHEMIA AND INFARCTION
Autore:
PRZYKLENK K; KLONER RA;
Indirizzi:
HOSP GOOD SAMARITAN,INST HEART,616 S WITMER ST LOS ANGELES CA 90017 UNIV SO CALIF LOS ANGELES CA 90089
Titolo Testata:
Basic research in cardiology
, volume: 88, anno: 1993, supplemento:, 1
pagine: 139 - 154
SICI:
0300-8428(1993)88:<139:CBAIAM>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
CONVERTING ENZYME-INHIBITORS; RENIN-ANGIOTENSIN SYSTEM; STUNNED MYOCARDIUM; THROMBOLYTIC THERAPY; CONTRACTILE FUNCTION; CORONARY-OCCLUSION; REPERFUSION INJURY; CAPTOPRIL; SIZE; ENALAPRIL;
Keywords:
CORONARY ARTERY OCCLUSION; CORONARY ARTERY REPERFUSION; MYOCARDIAL INFARCT SIZE; CREATINE KINASE; MYOCARDIAL CONTRACTILE FUNCTION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
61
Recensione:
Indirizzi per estratti:
Citazione:
K. Przyklenk e R.A. Kloner, "CARDIOPROTECTION BY ACE-INHIBITORS IN ACUTE MYOCARDIAL-ISCHEMIA AND INFARCTION", Basic research in cardiology, 88, 1993, pp. 139-154

Abstract

Coronary artery occlusion results in the acute activation of the renin-angiotensin system and production of angiotensin II, a potent vasoconstrictor and positive inotropic agent. This has raised the possibility that angiotensin converting enzyme (ACE) inhibitors might be ''cardioprotective'' (that is, might attenuate myocardial injury, dysfunctionand necrosis) in the setting of acute ischemia and infarction. Captopril, enalapril and ramipril have, in fact, been reported to acutely limit myocardial injury and necrosis in models of permanent coronary artery occlusion. The mechanisms responsible for this cardioprotection are complex, but include favorable alterations in myocardial oxygen supply/demand, and, in some instances, inhibition of bradykinin metabolismand/or increased prostaglandin synthesis. Other studies, however, have failed to document a reduction in infarct size with ACE inhibitor treatment. Results obtained in models of coronary occlusion/reperfusion have also been mixed. In models of brief transient ischemia not associated with necrosis, captopril and zofenopril have consistently been found to attenuate postischemic contractile dysfunction of the viable but ''stunned'' myocardium during the early hours following relief of ischemia. In contrast, there is no consensus on the effects of enalaprilon the stunned myocardium: both positive and negative results have been obtained. Similar disparity has been reported in models of more prolonged ischemia/reperfusion resulting in subendocardial necrosis: somestudies have reported myocardial salvage, while others have provided disturbing evidence of apparent exacerbation of myocardial necrosis with captopril and enalapril therapy. Thus, after a decade of investigative effort, the question of whether ACE inhibitors are ''cardioprotective'' in the setting of acute myocardial ischemia and infarction remains unresolved. Nonetheless, clinical protocols are in progress to assess the effects of early ACE inhibitor treatment in patients with acutemyocardial infarction.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/09/20 alle ore 21:26:24