title: A 60-s postconditioning protocol by percutaneous coronary intervention inhibits myocardial apoptosis in patients with acute myocardial infarction.
abstract: Different postconditioning (Postcon) methods have been demonstrated to protect heart from ischemia/reperfusion injury. The relationship between Postcon by percutaneous coronary intervention (PCI) and apoptosis is not clear. Our objective was to test whether Postcon by PCI in patients with acute myocardial infarction (AMI) reduces myocardial apoptosis. Seventy-five patients were randomly assigned to one of three groups before stenting. The Routine group (n = 26) received no Postcon intervention prior to the onset of reperfusion; Postcon-30s (n = 25) and Postcon-60s groups (n = 24) underwent three cycles of 30- or 60-s balloon deflation and 30- or 60-s inflation. Additionally, 34 normal controls (NC) were enrolled in the study. Plasma concentrations of soluble Fas/APO-1 ([sFas]) and Fas ligand ([sFasL]) were determined at baseline and 7 days after PCI via ELISA. The [sFas] and [sFasL] in AMI patients were significantly elevated at baseline as compared with NC (P < 0.01), and showed an upward trend in the Routine group, a slightly upward trend in Postcon-30s, and a downward trend in Postcon-60s at 7 days. Comparison among the three groups showed significant differences (P < 0.05, 3.8 vs. 4.6 vs. 5.1 ng ml(-1)). The [sFasL] in Postcon-60s was significantly decreased at 7 days (P < 0.05, 3.9 vs. 3.1 ng ml(-1)) compared with baseline, but not Postcon-30s and Routine. More importantly, Postcon-60s group had the lowest [sFasL], followed by Postcon-30s, which had a lower value than Routine at 7 days (P < 0.05, 3.1 vs.3.7 vs. 4.2 ng ml(-1)). Our results suggest that Postcon-60s was visibly better than Postcon-30s, which in turn was better than Routine for inhibition of the effects of myocardial apoptosis and reduction of reperfusion injury in patients with acute myocardial infarction.
authors.affiliation: Department of Medicine, Chao-Yang Hospital, Capital Medical University, Beijing, China.
authors.forename: Wen-Shu
authors.initials: WS
authors.lastname: Zhao
authors.forename: Lin
authors.initials: L
authors.lastname: Xu
authors.forename: Le-Feng
authors.initials: LF
authors.lastname: Wang
authors.forename: Li
authors.initials: L
authors.lastname: Zhang
authors.forename: Zhi-Yong
authors.initials: ZY
authors.lastname: Zhang
authors.forename: Yu
authors.initials: Y
authors.lastname: Liu
authors.forename: Xiu-Lan
authors.initials: XL
authors.lastname: Liu
authors.forename: Xin-Chun
authors.initials: XC
authors.lastname: Yang
authors.forename: Liang
authors.initials: L
authors.lastname: Cui
authors.forename: Lin
authors.initials: L
authors.lastname: Zhang
mesh_terms: D015906:Angioplasty, Balloon, Coronary / Q000379:methods*; D017209:Apoptosis; D016022:Case-Control Studies; D003402:Creatine Kinase / Q000097:blood; D053222:Fas Ligand Protein / Q000097:blood; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000473:pathology*; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000473:pathology*; D012995:Solubility; D013318:Stroke Volume; D013997:Time Factors; D019210:Troponin I / Q000097:blood; D019014:fas Receptor / Q000097:blood
chemical_list: C491901:FAS protein, human; D053222:Fas Ligand Protein; D019210:Troponin I; D019014:fas Receptor; D003402:Creatine Kinase