Post-resuscitation myocardial microcirculatory dysfunction is ameliorated with eptifibatide.
BACKGROUND
The post-cardiac arrest syndrome includes a decline in myocardial microcirculation function. Inhibition of the platelet IIb/IIIa glycoprotein receptor has improved myocardial microvascular function post-percutaneous coronary intervention. Therefore, we evaluated such inhibition with eptifibatide for its effect on myocardial microcirculation function post-cardiac arrest and resuscitation.


METHODS
Four groups of swine were studied in a prospective, randomized, blinded, placebo-controlled protocol including; eptifibatide administered during CPR (Group 1, n=5), after resuscitation (Group 2, n=4), during and after resuscitation (Group 3, n=5), or placebo (Group 4, n=10). CPR was initiated following 12min of untreated VF. Those successfully resuscitated were studied during a 4-h post-resuscitation period. Coronary flow reserve, a measure of microcirculation function (in the absence of coronary obstruction), as well as parameters of left ventricular systolic and diastolic function, were measured pre-arrest and serially post-resuscitation.


RESULTS
Coronary flow reserve was preserved during the post-resuscitation period, indicating normal microcirculatory function in the eptifibatide-treated animals, but not in the placebo-treated group. However, LV function declined equally in both groups during the first 4h after cardiac arrest.


CONCLUSIONS
Inhibition of platelet IIb/IIIa glycoprotein receptors with eptifibatide post-resuscitation prevented myocardial microcirculation dysfunction. Left ventricular dysfunction post-resuscitation was not improved with eptifibatide, and perhaps transiently worse at 30min post-resuscitation. Post-cardiac arrest ventricular dysfunction may require a multi-modality treatment strategy for successful prevention or amelioration.
Kern
Karl B
KB
College of Medicine, Cardiac Catheterization Laboratories, Sarver Heart Center, University of Arizona, 1501 N. Campbell Avenue, Tucson, AZ 85724, USA. kernk@u.arizona.edu
Sasaoka
Taro
T
Higashi
Haruhiko
H
Hilwig
Ronald W
RW
Berg
Robert A
RA
Zuercher
Mathias
M
D000818:Animals; D016887:Cardiopulmonary Resuscitation / Q000379:methods*; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology*; D004195:Disease Models, Animal; D000077542:Eptifibatide; D005260:Female; D006323:Heart Arrest / Q000503:physiopathology / Q000628:therapy*; D008297:Male; D008833:Microcirculation / Q000187:drug effects*; D017202:Myocardial Ischemia / Q000188:drug therapy* / Q000503:physiopathology; D010455:Peptides / Q000494:pharmacology*; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors; D013552:Swine
D010455:Peptides; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D000077542:Eptifibatide