Post-resuscitation myocardial microcirculatory dysfunction is ameliorated with eptifibatide

Karl B Kern, Taro Sasaoka, Haruhiko Higashi, Ronald W. Hilwig, Robert A. Berg, Mathias Zuercher

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

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 12. min 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 4. h after cardiac arrest. Conclusion: 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 30. min post-resuscitation. Post-cardiac arrest ventricular dysfunction may require a multi-modality treatment strategy for successful prevention or amelioration.

Original languageEnglish (US)
Pages (from-to)85-89
Number of pages5
JournalResuscitation
Volume82
Issue number1
DOIs
StatePublished - Jan 2011

Fingerprint

Resuscitation
Microcirculation
Heart Arrest
Integrin beta3
Placebos
Cardiopulmonary Resuscitation
Ventricular Dysfunction
eptifibatide
Left Ventricular Dysfunction
Percutaneous Coronary Intervention
Swine

Keywords

  • Cardiac arrest
  • Microcirculation
  • Post-resuscitation

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Emergency
  • Emergency Medicine

Cite this

Post-resuscitation myocardial microcirculatory dysfunction is ameliorated with eptifibatide. / Kern, Karl B; Sasaoka, Taro; Higashi, Haruhiko; Hilwig, Ronald W.; Berg, Robert A.; Zuercher, Mathias.

In: Resuscitation, Vol. 82, No. 1, 01.2011, p. 85-89.

Research output: Contribution to journalArticle

Kern, Karl B ; Sasaoka, Taro ; Higashi, Haruhiko ; Hilwig, Ronald W. ; Berg, Robert A. ; Zuercher, Mathias. / Post-resuscitation myocardial microcirculatory dysfunction is ameliorated with eptifibatide. In: Resuscitation. 2011 ; Vol. 82, No. 1. pp. 85-89.
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AB - 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 12. min 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 4. h after cardiac arrest. Conclusion: 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 30. min post-resuscitation. Post-cardiac arrest ventricular dysfunction may require a multi-modality treatment strategy for successful prevention or amelioration.

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