OBJECTIVE: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is among the multiple cardiovascular biomarkers that have been associated with increased cardiovascular disease. Lp-PLA2 appears, however, to be relatively unique in its high specificity for vascular inflammation as opposed to systemic inflammation, its low biologic variability, and its direct role in the causal pathway of plaque inflammation. Nevertheless, the relation between LP-PLA2 and isolated coronary artery ectasia (CAE) has not been investigated yet. The aim of our study was to assess this relation. METHODS: Twenty-five patients with isolated CAE without stenosis and 25 control subjects with angiographically normal coronary arteries were included in this study. Lp-PLA2 mass was determined in serum by a dual monoclonal antibody immunoassay. RESULTS: Patients with isolated CAE had significantly higher level of Lp-PLA2 compared to the control subjects with angiographically normal coronary arteries (284 ± 102 ng/ml in ectasia and 199 ± 62 ng/ml in control group, respectively, p 0.001). Also we detected a significant positive correlation between the presence of CAE and Lp-PLA2 (r = 0.452, p 0.001). CONCLUSION: We have demonstrated for the first time increased Lp-PLA2 level in patients with isolated CAE, suggesting that Lp-PLA2 may be involved in the pathogenesis of CAE.
OBJECTIVE:Lipoprotein-associated phospholipase A2 (Lp-PLA2) is among the multiple cardiovascular biomarkers that have been associated with increased cardiovascular disease. Lp-PLA2 appears, however, to be relatively unique in its high specificity for vascular inflammation as opposed to systemic inflammation, its low biologic variability, and its direct role in the causal pathway of plaque inflammation. Nevertheless, the relation between LP-PLA2 and isolated coronary artery ectasia (CAE) has not been investigated yet. The aim of our study was to assess this relation. METHODS: Twenty-five patients with isolated CAE without stenosis and 25 control subjects with angiographically normal coronary arteries were included in this study. Lp-PLA2 mass was determined in serum by a dual monoclonal antibody immunoassay. RESULTS:Patients with isolated CAE had significantly higher level of Lp-PLA2 compared to the control subjects with angiographically normal coronary arteries (284 ± 102 ng/ml in ectasia and 199 ± 62 ng/ml in control group, respectively, p 0.001). Also we detected a significant positive correlation between the presence of CAE and Lp-PLA2 (r = 0.452, p 0.001). CONCLUSION: We have demonstrated for the first time increased Lp-PLA2 level in patients with isolated CAE, suggesting that Lp-PLA2 may be involved in the pathogenesis of CAE.
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