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

被引:62
作者
Prasad, Abhiram [1 ,2 ]
Goessl, Mario [1 ,2 ]
Hoyt, John [1 ,2 ]
Lennon, Ryan J. [3 ]
Polk, Lynn [1 ,2 ]
Simari, Robert [1 ,2 ]
Holmes, David R., Jr. [1 ,2 ]
Rihal, Charanjit S. [1 ,2 ]
Lerman, Amir [1 ,2 ]
机构
[1] Mayo Clin & Mayo Fdn, Div Cardiovasc Dis, Rochester, MN 55905 USA
[2] Mayo Clin & Mayo Fdn, Dept Internal Med, Rochester, MN 55905 USA
[3] Mayo Clin & Mayo Fdn, Div Biomed Stat & Informat, Rochester, MN 55905 USA
关键词
REPERFUSION; PROTECTION; CARDIOPROTECTION; DYSFUNCTION; MECHANISMS; INFARCTION; INJURY; STENT;
D O I
10.1002/ccd.24443
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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. (c) 2012 Wiley Periodicals, Inc.
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收藏
页码:930 / 936
页数:7
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