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March 1, 1973Journal of Clinical Investigation291 citationsOpen Access

Reduction of Experimental Myocardial Infarct Size by Corticosteroid Administration

PLPeter LibbyPMPeter R. MarokoCBColin M. Bloor

Structured PICO

Does hydrocortisone administration reduce myocardial infarct size and ischemic injury in a canine model of acute coronary occlusion?

P
Population
28 mongrel dogs of both sexes weighing 18 to 27 kg undergoing experimental acute coronary occlusion.
I
Intervention
Hydrocortisone hemisuccinate 50 mg/kg IV bolus administered either 30 minutes or 6 hours after coronary occlusion, with a supplementary dose of 25 mg/kg IV 12 hours after occlusion.
C
Comparator
Control group undergoing coronary occlusion without hydrocortisone treatment.
O
Outcome
Extent and severity of acute myocardial ischemic injury (average ST segment elevation and number of sites with ST > 2 mV) at 30 and 60 minutes, and myocardial necrosis (myocardial creatine phosphokinase activity [CPK] and histologic appearance) at 24 hours.surrogate

Pharmacological doses of hydrocortisone prevent myocardial cells from progressing to ischemic necrosis in a canine model, even when initiated up to 6 hours after coronary occlusion.

Limitations

  • Model is not suitable for study of the hemodynamic effects of such changes due to small hemodynamic alterations produced by mid-LAD occlusion in dogs.

Abstract

The influence of the administration of pharmacologic doses of hydrocortisone on the extent and severity of acute myocardial ischemic injury and on subsequent necrosis after acute coronary occlusion was investigated in 28 dogs. In order to study acute myocardial injury, repeated epicardial electrocardiograms were recorded from 10 to 15 sites on the anterior surface of the left ventricle. Average ST segment elevation (ST) and the number of sites in which ST segment elevation exceeded 2 mV (NST), indices of the magnitude and extent of myocardial injury, respectively, were analyzed at 30 and 60 min after coronary occlusion. In the control group ST and NST did not change significantly in this time interval while in the treated group, which received 50 mg/kg hydrocortisone just after the 30 min recording, ST fell from 3.5+/-0.8 to 1.1+/-0.4 mV (P 2 mV) in the control group showed histologic changes compatible with early myocardial infarction in 96% of specimens, while this occurred only in 61% and 63% of specimens, respectively, in the treated groups, showing that over one third of the sites were protected from undergoing necrosis due to the intervening hydrocortisone treatment. Thus pharmacological doses of hydrocortisone prevent myocardial cells from progressing to ischemic necrosis even when administration is initiated 6 h after coronary occlusion.

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Cite This Study

Libby et al. (1973) studied this question.

synapsesocial.com/papers/6a1551a75347fbb1739f95dahttps://doi.org/10.1172/jci107221
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