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.
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.
Authors: V Fuster; L E Rydén; R W Asinger; D S Cannom; H J Crijns; R L Frye; J L Halperin; G N Kay; W W Klein; S Lévy; R L McNamara; E N Prystowsky; L S Wann; D G Wyse Journal: Eur Heart J Date: 2001-10 Impact factor: 29.983
Authors: I W Black; D Fatkin; K B Sagar; B K Khandheria; D Y Leung; J M Galloway; M P Feneley; W F Walsh; R A Grimm; C Stollberger Journal: Circulation Date: 1994-06 Impact factor: 29.690
Authors: Andreas Goette; Jonathan M Kalman; Luis Aguinaga; Joseph Akar; Jose Angel Cabrera; Shih Ann Chen; Sumeet S Chugh; Domenico Corradi; Andre D'Avila; Dobromir Dobrev; Guilherme Fenelon; Mario Gonzalez; Stephane N Hatem; Robert Helm; Gerhard Hindricks; Siew Yen Ho; Brian Hoit; Jose Jalife; Young-Hoon Kim; Gregory Y H Lip; Chang-Sheng Ma; Gregory M Marcus; Katherine Murray; Akihiko Nogami; Prashanthan Sanders; William Uribe; David R Van Wagoner; Stanley Nattel Journal: Heart Rhythm Date: 2016-06-10 Impact factor: 6.343
Authors: Renate B Schnabel; Martin G Larson; Jennifer F Yamamoto; Lisa M Sullivan; Michael J Pencina; James B Meigs; Geoffrey H Tofler; Jacob Selhub; Paul F Jacques; Philip A Wolf; Jared W Magnani; Patrick T Ellinor; Thomas J Wang; Daniel Levy; Ramachandran S Vasan; Emelia J Benjamin Journal: Circulation Date: 2010-01-04 Impact factor: 29.690