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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: AC133 Antigen, Aged, Angina, Stable, Angina, Unstable, Antigens, CD, Antigens, CD34, Biomarkers, C-Reactive Protein, Cell Count, Chi-Square Distribution, Coronary Artery Disease, Endothelial Cells, Female, Glycoproteins, Humans, Inflammation, Inflammation Mediators, Ischemic Preconditioning, Kaplan-Meier Estimate, Male, Middle Aged, Minnesota, Myocardium, Necrosis, Peptides, Percutaneous Coronary Intervention, Prospective Studies, Risk Factors, Stem Cells, Time Factors, Treatment Outcome, Troponin T, Upper Extremity, Vascular Endothelial Growth Factor Receptor-2.
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Does remote ischemic preconditioning immediately before percutaneous coronary intervention impact myocardial necrosis , inflammatory response , and circulating endothelial progenitor cell counts : a single center randomized sham controlled trial? Context: 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. 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. 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).
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Our study indicates that remote IP immediately before PCI does not induce cardioprotection in low to moderate risk patients. Final Decision: no