Song-Zhao Zhang1, Ya-Ping Jin, Guang-Ming Qin, Jun-Hong Wang. 1. Department of Clinical Laboratory Medicine, the Second Affiliated Hospital of Zhejiang University, No. 88 Jiefang Road, Hangzhou 310009, P.R. China. zsongz@hotmail.com
Abstract
BACKGROUND: Platelet-monocyte aggregates (PMA) and C-reactive protein (CRP) are increased in unstable coronary disease. The interrelation of PMA with platelet activation, systemic inflammation, and their association with markers of myocardial injury has not been studied extensively. HYPOTHESIS: The study was undertaken to evaluate the association of CRP, PMA, and cardiac troponin I (cTnI) in patients admitted with non-ST elevation acute coronary syndromes (NSTE-ACS). METHODS: In all, 69 consecutive patients with NSTE-ACS, 58 patients with stable angina pectoris (SAP), and 46 control patients without coronary artery disease were selected; PMA, sP-selectin, sCD40L inter leukin, (IL)-6, CRP, and cTnI concentrations were measured in these patients at the time of admission. Patients with NSTE-ACS were classified into two groups: those with troponin normal (cTnI < 0.06 ng/ml) and those with troponin elevation (cTnI > or = 0.06 ng/ml). Their risk for clinical in-hospital cardiac events (death and nonfatal myocardial infarction) was analyzed. RESULTS: Compared with SAP and control, patients with NSTE-ACS exhibited higher levels of PMA, sP-selectin, sCD40L, IL-6, and CRP. All these parameters were found to be higher (p < 0.001 ) in patients with troponin elevation than in those with normal troponin. There was a significant relationship between PMA and CRP (r =0.628, p < 0.001) and cTnI (r = 0.557, p < 0.001) in patients with NSTE-ACS. Logistic analysis further demonstrated that the presence of elevated PMA, CRP, and cTnI levels each confers and increases risk of future cardiac events. CONCLUSIONS: Levels of PMA and CRP were significantly increased in patients with NSTE-ACS, especially in those with troponin elevation. This increase is strongly related to the risk of in-hospital cardiac events. A panel of PMA, CRP, and cTnI may provide important information additional to current laboratory data for the treatment of NSTE-ACS. Copyright (c) 2007 Wiley Periodicals, Inc.
BACKGROUND: Platelet-monocyte aggregates (PMA) and C-reactive protein (CRP) are increased in unstable coronary disease. The interrelation of PMA with platelet activation, systemic inflammation, and their association with markers of myocardial injury has not been studied extensively. HYPOTHESIS: The study was undertaken to evaluate the association of CRP, PMA, and cardiac troponin I (cTnI) in patients admitted with non-ST elevation acute coronary syndromes (NSTE-ACS). METHODS: In all, 69 consecutive patients with NSTE-ACS, 58 patients with stable angina pectoris (SAP), and 46 control patients without coronary artery disease were selected; PMA, sP-selectin, sCD40L inter leukin, (IL)-6, CRP, and cTnI concentrations were measured in these patients at the time of admission. Patients with NSTE-ACS were classified into two groups: those with troponin normal (cTnI < 0.06 ng/ml) and those with troponin elevation (cTnI > or = 0.06 ng/ml). Their risk for clinical in-hospital cardiac events (death and nonfatal myocardial infarction) was analyzed. RESULTS: Compared with SAP and control, patients with NSTE-ACS exhibited higher levels of PMA, sP-selectin, sCD40L, IL-6, and CRP. All these parameters were found to be higher (p < 0.001 ) in patients with troponin elevation than in those with normal troponin. There was a significant relationship between PMA and CRP (r =0.628, p < 0.001) and cTnI (r = 0.557, p < 0.001) in patients with NSTE-ACS. Logistic analysis further demonstrated that the presence of elevated PMA, CRP, and cTnI levels each confers and increases risk of future cardiac events. CONCLUSIONS: Levels of PMA and CRP were significantly increased in patients with NSTE-ACS, especially in those with troponin elevation. This increase is strongly related to the risk of in-hospital cardiac events. A panel of PMA, CRP, and cTnI may provide important information additional to current laboratory data for the treatment of NSTE-ACS. Copyright (c) 2007 Wiley Periodicals, Inc.
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