Positive Effect of Ischemic Postconditioning During Acute Myocardial Infarction


The purpose of this study is to determine whether brief periods of ischemia performed just at the time of reperfusion -postconditioning- can reduce coronary endothelial dysfunction and infarct size in humans

Study Type

  • Study Type: Interventional
  • Study Design
    • Allocation: Randomized
    • Intervention Model: Parallel Assignment
    • Primary Purpose: Treatment
    • Masking: Single (Outcomes Assessor)
  • Study Primary Completion Date: July 2010

Detailed Description

Desobstruction of the culprit artery after acute myocardial infarction allows to reduce the consequences of prolonged ischemia. However, it is now clearly established that reperfusion induces by itself severe myocardial injuries. Postconditioning has been described as an adaptive response triggered by a brief ischemia applied after a prolonged coronary occlusion. Several teams have reported that ischemia/reperfusion cycles allow to reduce infarct size in experimental models.

Different pathophysiological processes have been proposed to explain the beneficial effect of postconditioning. It has been reported that postconditioning reduces the inflammatory response, and activates cardioprotective signaling pathways (Akt, eNOS, p70S6K). In addition, an improvement of the endothelial function has been reported.

This controlled trial aim to study the potential beneficial effect of postconditioning in patients with acute myocardial infarction. Forty six patients will be included in the study and the culprit artery will be reoccluded three times for 1 minutes after desobstruction in one of the both groups after randomization of the patients.

The evaluation will be focused on the comparison of the coronary reserve after intracoronary adenosine injection. In addition, additional parameters will be used to study the effect of postconditioning on post-ischemic endothelial dysfunction: frequencies of low reflow and slow reflow situation, myocardial blush and regression of ST elevation. The effect of postconditioning on the left ventricular systolic function will be studied by Doppler tissue imaging and RMN.


  • Procedure: postconditioning
    • patients were treated by repeated cycles of cycles of reperfusion/ischemia at the end of the procedure within the first minute after reperfusion
  • Procedure: Control group
    • Percutaneous coronary interventions were performed following international guidelines. No additional intervention was performed in the control group.

Arms, Groups and Cohorts

  • Placebo Comparator: – Control
  • Experimental: -postconditioning group

Clinical Trial Outcome Measures

Primary Measures

  • coronary reserve after intracoronary adenosine injection
    • Time Frame: Immediately after the postconditioning procedure

Secondary Measures

  • frequencies of low reflow and slow reflow situation
    • Time Frame: after postconditioning
  • regression of ST elevation
    • Time Frame: 1h and 24h after postconditioning
  • left ventricular systolic function by Doppler tissue imaging (DAY 1 and 6)
    • Time Frame: day 1 and 6
  • left ventricular systolic function by RMN
    • Time Frame: day 8-12
  • myocardial blush
    • Time Frame: after postconditioning

Participating in This Clinical Trial

Inclusion Criteria

  • Acute myocardial infarction (<6 hours)
  • Occlusion of a major coronary vessel

Exclusion Criteria

  • History of previous myocardial infarction
  • History of Coronary Artery Bypass Grafting
  • Need for Coronary Artery Bypass Grafting
  • Stenosis not eligible for angioplasty
  • Limited ischemic area
  • Cardiogenic shock
  • Interventricular septum rupture
  • Mitral regurgitation>2
  • Ventricular tachycardia
  • Atrioventricular block class II and III

Gender Eligibility: All

Minimum Age: 18 Years

Maximum Age: N/A

Are Healthy Volunteers Accepted: No

Investigator Details

  • Lead Sponsor
    • French Cardiology Society
  • Provider of Information About this Clinical Study
    • Sponsor
  • Overall Official(s)
    • Philippe Le Corvoisier, MD, Principal Investigator, Henri Mondor University Hospital

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