Abstract 2834: Post Resuscitation Myocardial Microcirculatory Dysfunction Is Ameliorated with Platelet Glycoprotein IIb/IIIa Inhibition
Background: Post resuscitation myocardial dysfunction is common after prolonged VF. In a swine model of prolonged VF followed by successful resuscitation, significant declines in LV function were accompanied by marked dysfunction of the myocardial microcirculation. Abnormalities in the myocardial microcirculation during and after PCI for ACS have been successfully treated with platelet glycoprotein IIb/IIIa inhibition. We hypothesized that post resuscitation platelet glycoprotein IIb/IIIa inhibitors would improve myocardial microcirculatory function.
Methods: Domestic swine (n=7; 25–30 kg) were electrically fibrillated and left untreated for 12 minutes. Aggressive ACLS was performed to restore spontaneous circulation. Controls received saline placebo treatment. Treatment group received a platelet glycoprotein IIb/IIIa inhibitor (Epitifibatide 180 mcg/kg bolus x2, then 2mcg/kg/min infusion) immediately after ROSC. Hemodynamics, left ventricular ejection fraction, cardiac output, and coronary flow reserve (CFR) [using standard techniques of intracoronary Doppler flow measurements before and after intracoronary administration of 48 mcg adenosine] were performed pre-arrest and post resuscitation at 30 min, 2, and 4 hours. Abnormal CFR indicates abnormal myocardial microcirculatory function since these swine had no coronary artery obstructive disease.
Results: Significant differences (p<0.05) in CFR were found between controls and Eptifibatide groups post resuscitation. Coronary flow reserve decreased nearly 50% in the control group post resuscitation indicating substantial microcirculatory dysfunction. The Epitifibatide treated group showed no decrease in CFR post resuscitation.
Conclusion: In this swine model of prolonged VF followed by successful resuscitation, significant declines in myocardial microcirculation function were ameliorated with administration of a platelet glycoprotein IIb/IIIa inhibitor.