Objective: To investigate whether new onset acute atrial fibrillation (AF) of< 48 hours’duration creates a prothrombotic state in the absence of anticoagulation and to assess the evolution in research indices afte...Objective: To investigate whether new onset acute atrial fibrillation (AF) of< 48 hours’duration creates a prothrombotic state in the absence of anticoagulation and to assess the evolution in research indices after spontaneous or pharmacological cardioversion. Methods: 24 patients were recruited with first onset acute non-rheumatic AF, in whom sinus rhythm was restored within 48 hours of arrhythmia onset, without anticoagulant treatment. Atrial mechanical function was assessed by transmitral inflow. Soluble thrombomodulin and von Willebrand factor concentrations (both as indices of endothelial damage or dysfunction) and fibrin D-dimer concentrations(as an index of thrombogenesis) were measured. Blood samples were drawn and echocardiographic studies were performed at days 1, 2, 7, and 30 after cardioversion. Research indices were compared with those of 24 healthy participants, 24 patientswith chronicAF, and 24 patientswith ischaemic heart disease in sinus rhythm. Results: Patients with AF had higher concentrations of soluble thrombomodulin(acute AF 12.1 (4.1) ng/ml; chronic AF 11.8(4.6) ng/ml), von Willebrand factor(acute AF 137.2(36.9)ng/ml; chronic AF 133.1(25.0)ng/ml), and fibrin Ddimer concentrations(acute AF 2.35(2.68)μg/ml; chronic AF 1.12(0.65)μg/ml) than did healthy controls (5.9(2.7)ng/ml, 86.7(33.2)ng/ml, and 0.39(0.28)μg/ml, respectively) and patients with ischaemic heart disease(7.4 (3.7)ng/ml,110.0(29.0)ng/ml, and 0.99(0.73)μg/ml, respectively)(all p < 0.05). Day 30 concentrations of fibrin D-dimer were higher in patients with acute AF than in patients with chronic AF(p=0.038) but sTM and vonWillebrand factor concentrations were not different (both not significant). There were no significant changes in research indices or echocardiographic parameters after cardioversion (all p >0.05). Conclusions: There was evidence among patients with acute onset AF of endothelial damage or dysfunction and increased thrombogenesis, which persisted up to 30 days after cardioversion.展开更多
The aim of this study was to evaluate the pharmacogenetic role of the factor XIII(FXIII)valine 34 leucine(Val34Leu)polymorphism in the fibrinolytic therapy of acute myocardial infarction(MI). Fibrinolytic therapy is a...The aim of this study was to evaluate the pharmacogenetic role of the factor XIII(FXIII)valine 34 leucine(Val34Leu)polymorphism in the fibrinolytic therapy of acute myocardial infarction(MI). Fibrinolytic therapy is an established treatment for acute MI, but up to 40%of treated patients do not achieve optimal tissue reperfusion. The FXIII Val34Leu polymorphism is one of the most relevant functional polymorphisms described in the haemostatic system. The common Leu34 allele associates with an increased FXIII-transglutaminase activity, which results in an increased and faster rate of fibrin stabilization. We genotyped this polymorphism in 293 consecutive MI patients(62±12 years; 231 males)from two different European populations. All patients were treated with standard doses of fibrinolytic drugs. Noninvasive assessment of the efficacy of coronary fibrinolysis was evaluated by serial electrocardiograms and creatine kinase time-activity curves. The clinical outcome was also re-evaluated at 24 h(death, reinfarction, or urgent revascularization). Multivariate analysis showed that Leu34 carriers displayed a significantly less efficient fibrinolysis than carriers of Val/Val genotype(p=0.021; odds ratio [OR] 1.90, 95%confidence interval [CI] 1.10 to 3.28). At 24 h, Leu34 allele carriers had the worst outcome(p=0.006; OR 2.14, 95%CI 1.25 to 3.68). Interestingly, the combination of the Leu34 allele and nonsmoking status increased the risk of non-reperfusion criteria(p=0.003, OR 3.77), and worse outcomes at 24 h(p=0.001, OR 4.55). In a large cohort of nonselected and consecutive acute MI patients from two different European populations, we show clinical evidence that the presence of the Leu34 allele reduces the efficacy of fibrinolytic therapy.展开更多
Interleukin-6 levels, but not prothrombin fragment 1+2, correlates with a point-based score for stroke risk in atrial fibrillation, even after oral anticogulation.
文摘Objective: To investigate whether new onset acute atrial fibrillation (AF) of< 48 hours’duration creates a prothrombotic state in the absence of anticoagulation and to assess the evolution in research indices after spontaneous or pharmacological cardioversion. Methods: 24 patients were recruited with first onset acute non-rheumatic AF, in whom sinus rhythm was restored within 48 hours of arrhythmia onset, without anticoagulant treatment. Atrial mechanical function was assessed by transmitral inflow. Soluble thrombomodulin and von Willebrand factor concentrations (both as indices of endothelial damage or dysfunction) and fibrin D-dimer concentrations(as an index of thrombogenesis) were measured. Blood samples were drawn and echocardiographic studies were performed at days 1, 2, 7, and 30 after cardioversion. Research indices were compared with those of 24 healthy participants, 24 patientswith chronicAF, and 24 patientswith ischaemic heart disease in sinus rhythm. Results: Patients with AF had higher concentrations of soluble thrombomodulin(acute AF 12.1 (4.1) ng/ml; chronic AF 11.8(4.6) ng/ml), von Willebrand factor(acute AF 137.2(36.9)ng/ml; chronic AF 133.1(25.0)ng/ml), and fibrin Ddimer concentrations(acute AF 2.35(2.68)μg/ml; chronic AF 1.12(0.65)μg/ml) than did healthy controls (5.9(2.7)ng/ml, 86.7(33.2)ng/ml, and 0.39(0.28)μg/ml, respectively) and patients with ischaemic heart disease(7.4 (3.7)ng/ml,110.0(29.0)ng/ml, and 0.99(0.73)μg/ml, respectively)(all p < 0.05). Day 30 concentrations of fibrin D-dimer were higher in patients with acute AF than in patients with chronic AF(p=0.038) but sTM and vonWillebrand factor concentrations were not different (both not significant). There were no significant changes in research indices or echocardiographic parameters after cardioversion (all p >0.05). Conclusions: There was evidence among patients with acute onset AF of endothelial damage or dysfunction and increased thrombogenesis, which persisted up to 30 days after cardioversion.
文摘The aim of this study was to evaluate the pharmacogenetic role of the factor XIII(FXIII)valine 34 leucine(Val34Leu)polymorphism in the fibrinolytic therapy of acute myocardial infarction(MI). Fibrinolytic therapy is an established treatment for acute MI, but up to 40%of treated patients do not achieve optimal tissue reperfusion. The FXIII Val34Leu polymorphism is one of the most relevant functional polymorphisms described in the haemostatic system. The common Leu34 allele associates with an increased FXIII-transglutaminase activity, which results in an increased and faster rate of fibrin stabilization. We genotyped this polymorphism in 293 consecutive MI patients(62±12 years; 231 males)from two different European populations. All patients were treated with standard doses of fibrinolytic drugs. Noninvasive assessment of the efficacy of coronary fibrinolysis was evaluated by serial electrocardiograms and creatine kinase time-activity curves. The clinical outcome was also re-evaluated at 24 h(death, reinfarction, or urgent revascularization). Multivariate analysis showed that Leu34 carriers displayed a significantly less efficient fibrinolysis than carriers of Val/Val genotype(p=0.021; odds ratio [OR] 1.90, 95%confidence interval [CI] 1.10 to 3.28). At 24 h, Leu34 allele carriers had the worst outcome(p=0.006; OR 2.14, 95%CI 1.25 to 3.68). Interestingly, the combination of the Leu34 allele and nonsmoking status increased the risk of non-reperfusion criteria(p=0.003, OR 3.77), and worse outcomes at 24 h(p=0.001, OR 4.55). In a large cohort of nonselected and consecutive acute MI patients from two different European populations, we show clinical evidence that the presence of the Leu34 allele reduces the efficacy of fibrinolytic therapy.
文摘Interleukin-6 levels, but not prothrombin fragment 1+2, correlates with a point-based score for stroke risk in atrial fibrillation, even after oral anticogulation.
