Remote ischemic preconditioning immediately before percutaneous coronary intervention does not impact myocardial necrosis, inflammatory response, and circulating endothelial progenitor cell counts: a single center randomized sham controlled trial

Catheter Cardiovasc Interv. 2013 May;81(6):930-6. doi: 10.1002/ccd.24443. Epub 2012 Nov 8.

Abstract

Aims: Percutaneous coronary intervention (PCI) is frequently accompanied by myocardial injury. The present study was performed to determine whether remote ischemic preconditioning (IP) induces cardioprotection during PCI.

Methods: We enrolled 95 patients requiring nonemergency PCI for stable disease or unstable angina into this prospective clinical trial. Patients were randomized to either remote IP (induced by three 3-min cycles of blood pressure cuff inflations to 200 mm Hg around the upper arm, followed by 3-min of reperfusion n = 47) or sham control (n = 48) immediately preceding PCI. The primary outcome measure was the frequency of post-PCI myonecrosis, defined as a peak postprocedural cTnT T ≥ 0.03 ng/dL. Secondary outcome measures were the change in plasma high-sensitivity C-reactive protein (hsCRP) levels following PCI and in endothelial progenitor cells (EPC) counts following IP.

Results: There was no difference in the primary endpoint of the frequency of PCI related myonecrosis which occurred in 22 (47%) and 19 (40%) patients in the remote IP and control groups, respectively, P = 0.42. There was significant increase in hsCRP post-PCI in both groups (P < 0.001), but there was no difference between the groups (median %change in hsCRP 46% vs. 54%, P = 0.73). There was no significant change in circulating early (CD34 -/CD133+/KDR+), intermediate (CD34+/CD133+/KDR+), or late (CD34+/CD133-/KDR+) EPC in the two groups immediately following IP. The composite rate of death, myocardial infarction, and target lesion revascularization at 1 year was 14.1% versus 13.7% (P = 0.90).

Conclusions: Our study indicates that remote IP immediately before PCI does not induce cardioprotection in low to moderate risk patients.

Trial registration: ClinicalTrials.gov NCT00588042.

Publication types

  • Randomized Controlled Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • AC133 Antigen
  • Aged
  • Angina, Stable / blood
  • Angina, Stable / pathology
  • Angina, Stable / therapy
  • Angina, Unstable / blood
  • Angina, Unstable / pathology
  • Angina, Unstable / therapy
  • Antigens, CD / blood
  • Antigens, CD34 / blood
  • Biomarkers / blood
  • C-Reactive Protein / metabolism
  • Cell Count
  • Chi-Square Distribution
  • Coronary Artery Disease / blood
  • Coronary Artery Disease / pathology
  • Coronary Artery Disease / therapy*
  • Endothelial Cells / metabolism
  • Endothelial Cells / pathology*
  • Female
  • Glycoproteins / blood
  • Humans
  • Inflammation / blood
  • Inflammation / etiology*
  • Inflammation Mediators / blood
  • Ischemic Preconditioning / methods*
  • Kaplan-Meier Estimate
  • Male
  • Middle Aged
  • Minnesota
  • Myocardium / metabolism
  • Myocardium / pathology*
  • Necrosis
  • Peptides / blood
  • Percutaneous Coronary Intervention / adverse effects*
  • Prospective Studies
  • Risk Factors
  • Stem Cells / metabolism
  • Stem Cells / pathology*
  • Time Factors
  • Treatment Outcome
  • Troponin T / blood
  • Upper Extremity / blood supply*
  • Vascular Endothelial Growth Factor Receptor-2 / blood

Substances

  • AC133 Antigen
  • Antigens, CD
  • Antigens, CD34
  • Biomarkers
  • Glycoproteins
  • Inflammation Mediators
  • PROM1 protein, human
  • Peptides
  • Troponin T
  • C-Reactive Protein
  • Vascular Endothelial Growth Factor Receptor-2

Associated data

  • ClinicalTrials.gov/NCT00588042