Key result
Acute onset atrial fibrillation was associated with higher concentrations of soluble thrombomodulin, von Willebrand factor, and fibrin D-dimer compared to healthy controls (all p < 0.05).
Why the study?
Does acute onset non-rheumatic atrial fibrillation create a prothrombotic state and endothelial dysfunction compared to healthy controls or chronic AF?
Observational (n=96)
Does acute onset non-rheumatic atrial fibrillation create a prothrombotic state and endothelial dysfunction compared to healthy controls or chronic AF?
p-value: p=< 0.05
Acute onset atrial fibrillation is associated with a prothrombotic state and endothelial dysfunction that persists for at least 30 days after cardioversion, highlighting the potential need for careful thromboembolic risk management even in short-duration AF.
Supports prothrombotic state in acute AF persisting 30 days post-cardioversion; hypothesis-generating for thromboembolic risk in short-duration episodes.
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, 3, 7, and 30 after cardioversion. Research indices were compared with those of 24 healthy participants, 24 patients with chronic AF, and 24 patients with 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 D-dimer concentrations (acute AF 2.35 (2.68) microg/ml; chronic AF 1.12 (0.65) microg/ml) than did healthy controls (5.9 (2.7) ng/ml, 86.7 (33.2) ng/ml, and 0.39 (0.28) microg/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) microg/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 von Willebrand 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.
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Francisco Marı́n (2004) conducted an observational in Acute onset non-rheumatic atrial fibrillation (n=96). Acute onset non-rheumatic atrial fibrillation vs. Healthy participants, chronic AF, and ischaemic heart disease was evaluated on Concentrations of soluble thrombomodulin, von Willebrand factor, and fibrin D-dimer (p=< 0.05). Acute onset atrial fibrillation was associated with higher concentrations of soluble thrombomodulin, von Willebrand factor, and fibrin D-dimer compared to healthy controls (all p < 0.05).
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