AIM: To evaluate the serial changes of plasma secretory type II phospholipase A(2)(sPLA(2)), C-reactive protein (CRP) and cardiac injury markers in coronary artery disease (CAD) patients undergoing percutaneous coronary intervention (PCI) and their prognostic impacts. METHODS AND RESULTS: Plasma levels of sPLA(2), CRP, creatine kinase (CK), CK-MB and troponin-T were measured in 247 consecutive CAD patients receiving PCI procedure and 100 control subjects without CAD. In CAD group, serial blood samples were taken before coronary angiography, after coronary angiography, immediately after PCI, 24-h and 48-h after PCI. The sPLA(2)and CRP levels did not change after coronary angiography. The level of sPLA(2)significantly increased immediately after PCI. Creatine kinase and cardiac injury markers did not rise immediately after PCI, but elevated significantly at 24h after intervention. After a 2-year follow up, increased sPLA(2)(>450 ng/dl) after PCI, smoking and diabetes mellitus were the independent risk factors for subsequent coronary events (odds ratios 2.1, 2.3 and 3.1, respectively) in patients with CAD. CONCLUSION: The present study showed that PCI might cause immediate elevation of circulating levels of sPLA(2)following the mechanical disruption of coronary plaque, and the elevated level of sPLA(2)had significant prognostic impact.
AIM: To evaluate the serial changes of plasma secretory type II phospholipase A(2)(sPLA(2)), C-reactive protein (CRP) and cardiac injury markers in coronary artery disease (CAD) patients undergoing percutaneous coronary intervention (PCI) and their prognostic impacts. METHODS AND RESULTS: Plasma levels of sPLA(2), CRP, creatine kinase (CK), CK-MB and troponin-T were measured in 247 consecutive CAD patients receiving PCI procedure and 100 control subjects without CAD. In CAD group, serial blood samples were taken before coronary angiography, after coronary angiography, immediately after PCI, 24-h and 48-h after PCI. The sPLA(2)and CRP levels did not change after coronary angiography. The level of sPLA(2)significantly increased immediately after PCI. Creatine kinase and cardiac injury markers did not rise immediately after PCI, but elevated significantly at 24h after intervention. After a 2-year follow up, increased sPLA(2)(>450 ng/dl) after PCI, smoking and diabetes mellitus were the independent risk factors for subsequent coronary events (odds ratios 2.1, 2.3 and 3.1, respectively) in patients with CAD. CONCLUSION: The present study showed that PCI might cause immediate elevation of circulating levels of sPLA(2)following the mechanical disruption of coronary plaque, and the elevated level of sPLA(2)had significant prognostic impact.
Authors: Aleksandra A Korotaeva; Elena V Samoilova; Aleksander I Kaminny; Aleksandra A Pirkova; Therese J Resink; Paul Erne; Nina V Prokazova; Vsevolod A Tkachuk; Evgeny I Chazov Journal: Mol Cell Biochem Date: 2005-02 Impact factor: 3.396
Authors: Akintunde O Akinkuolie; Patrick R Lawler; Audrey Y Chu; Michael Caulfield; Jianying Mu; Bo Ding; Fredrik Nyberg; Robert J Glynn; Paul M Ridker; Eva Hurt-Camejo; Daniel I Chasman; Samia Mora Journal: Arterioscler Thromb Vasc Biol Date: 2019-06 Impact factor: 8.311
Authors: Michelle L O'Donoghue; Ziad Mallat; David A Morrow; Joelle Benessiano; Sarah Sloan; Torbjørn Omland; Scott D Solomon; Eugene Braunwald; Alain Tedgui; Marc S Sabatine Journal: Clin Chem Date: 2011-07-22 Impact factor: 8.327