کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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6003511 | 1183017 | 2011 | 4 صفحه PDF | دانلود رایگان |

IntroductionInflammation, endothelial dysfunction and metabolic pathways provide possible links between the inflammatory and hypofibrinolytic states in atrial fibrillation. Our aim was to explore the role of mass concentrations of PAI-1 and tPA, activities of PAI-1 and tPA as predictors of recurrence of atrial fibrillation adjusted for CRP.Materials and methodsThe study included 129 patients with persistent atrial fibrillation. Laboratory analyses were performed including PAI-1 activity, PAI-1 mass, tPA activity, tPA mass and CRP in baseline. Patients were then randomized to atorvastatin (40Â mg, two tablets once daily) or placebo, initiated at least 14Â days before the elective cardioversion. Further samples and follow-up were made at day 2 and 30Â days after cardioversion.ResultsIn univariate logistic regression no fibrinolytic variable was significantly correlated with rhythm in day 30. In multivariate analysis lower PAI-1 mass was significantly associated with sinus rhythm in all models including fibrinolytic variables, CRP, metabolic components, age, hypertension and smoking. After adding treatment allocation to the fully adjusted model, PAI-1 mass remained significantly associated with sinus rhythm both at day 2 and 30 (OR 0.98; 95% CI 0.95-1.00).ConclusionsNo fibrinolytic component alone was found to be a predictor of recurrence of atrial fibrillation. In multivariate models lower PAI-1 mass was associated with sinus rhythm even after adjusting for CRP, markers of the metabolic syndrome and treatment with atorvastatin. Our findings suggest a patophysiological link between AF and PAI-1 mass but the relation to inflammation remains unclear.
Journal: Thrombosis Research - Volume 127, Issue 3, March 2011, Pages 189-192