Delayed restoration of atrial function after conversion of atrial flutter by pacing or electrical cardioversion

Jordaens, Luc; Missault, Luc; Germonpré, Eric; Callens, Benedict; Adang, Luc; Vandenbogaerde, J; Clément, Denis

doi:10.1016/0002-9149(93)90711-k

Cited by 54 publications

(9 citation statements)

References 22 publications

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“…This idea is consistent with recent work that has shown that atrial flutter, which produces atrial rates of the order we studied, causes significant impairments in atrial contractile function. 26 The contractile impairments we observed most likely explain the significant atrial dilation observed by Morillo et al 16 in dogs subjected to 6 weeks of atrial pacing at 400 bpm. Short-term AF (15 minutes) has been shown by Leistad et al 15 to reduce atrial contractility, a phenomenon antagonized by verapamil infusion.…”

Section: Pathogenesis Of Atrial Contractile Dysfunctionmentioning

confidence: 62%

Cellular Mechanisms of Atrial Contractile Dysfunction Caused by Sustained Atrial Tachycardia

et al. 1998

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Background-Transient atrial contractile dysfunction ("atrial stunning") follows conversion of atrial fibrillation (AF) to sinus rhythm and has significant clinical implications; however, the underlying mechanisms are poorly understood. We investigated the hypothesis that rapid atrial activation (as during AF) impairs cellular contractility and affects cellular Ca 2ϩ handling. Methods and Results-Edge detection and indo 1 fluorescence techniques were used to measure unloaded cell shortening and intracellular Ca 2ϩ transients in atrial myocytes from control (Ctl) dogs and dogs subjected to atrial pacing at 400 bpm for 7 (P7) or 42 (P42) days. Atrial tachycardia reduced fractional cell shortening (0.

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Section: Pathogenesis Of Atrial Contractile Dysfunctionmentioning

confidence: 62%

Cellular Mechanisms of Atrial Contractile Dysfunction Caused by Sustained Atrial Tachycardia

et al. 1998

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“…Second, associated abnormalities are often present that favor thromboembolic complications such as valvular disease, hypertension, and heart failure. Third, as shown by Jordaens et al, 31 delayed restoration of atrial function occurs after conversion of AFl by pacing or electrical shock. It is therefore advisable to anticoagulate the AFl patient unless the duration of the arrhythmia is Ͻ48 hours or lone AFl with preserved left ventricular function is present, in which case aspirin could be given, as noted above.…”

Section: Anticoagulant Therapy?mentioning

confidence: 84%

Contemporary Management of Atrial Flutter

Wellens

2002

Circulation

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“…In atrial flutter, the risk of thromboembolism seems related to the same mechanism as in atrial fibrillation. A delay of several days before restoration of the atrial function has been described after cardioversion [51] . The stunning effect has also been noted after cardioversion in patients with atrial flutter [52] ; however, the impairment in flow in the left atrial appendage is not so pronounced as in atrial fibrillation [53] which might suggest a lower thromboembolic risk compared to cardioversion of atrial fibrillation.…”

Section: Atrial Fluttermentioning

confidence: 99%

Transoesophageal echocardiography-guided cardioversion of atrial fibrillation or flutter. Selection of a low-risk group for immediate cardioversion

Roijer

Eskilsson

Olsson

2000

European Heart Journal

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Aims Despite exclusion of left atrial thrombi by transoesophageal echocardiography, cardioversion-related thromboembolism has been reported in atrial fibrillation or flutter. To define a low-risk group for cardioversion without previous anticoagulation, patients were selected for immediate cardioversion if there were no thrombi, no echo spontaneous contrast and the outflow velocity of the left atrial appendage was greater than 0·25 m . s 1 on transoesophageal echocardiography. Methods and ResultsTwo hundred and forty-two consecutive patients referred for cardioversion of atrial fibrillation or flutter with a duration of more than 2 days and no anticoagulation therapy were examined with transoesophageal echocardiography. After the transoesophageal echocardiography examination, patients who were eligible for immediate cardioversion were anticoagulated with low molecular weight heparin (dalteparin) subcutaneously, together with warfarin prior to cardioversion. Dalteparin treatment was continued until the patient had reached therapeutic prothrombin values.Based on the transoesophageal echocardiographic findings the patients were divided into two groups: immediate cardioversion, group A, with a mean age of 62 13 years (n=162); or conventional warfarin treatment before cardioversion, group B, with a mean age of 67 10 years (P<0·05) (n=80). In group A, lone atrial fibrillation or flutter was more common (53%; 95% CI: 45-61) compared to group B (34%; 95% CI: 23-44, P<0·05), while heart disease was more common in group B (45%; 95% CI: 34-56) compared to group A (31%; 95% CI: 24-39, P<0·05). Echocardiography revealed thrombi in 5% (95% CI: 2·6-8) of the patients, left atrial size was larger, fractional shortening lower, and a higher proportion had impaired left ventricular function in group B. No thromboembolic event occurred at or after cardioversion in any of the patients; however, before planned cardioversion one transitory ischaemic attack, one lethal stroke and one cardiac death occurred in three of the patients with thrombi despite warfarin therapy. One-month follow-up maintenance of sinus rhythm was 75% in group A compared to 45% in group B (P<0·01).Conclusion After using our transoesophageal echocardiographic exclusion criteria (no thrombi, no spontaneous echo contrast and left atrial appendage outflow velocity d0·25 m . s 1 ) cardioversion can safely be performed in 2/3 of patients with atrial fibrillation or flutter without previous anticoagulation therapy. These patients maintained sinus rhythm significantly better after 1 month compared to patients with prolonged warfarin therapy before cardioversion.

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Delayed restoration of atrial function after conversion of atrial flutter by pacing or electrical cardioversion

Cited by 54 publications

References 22 publications

Cellular Mechanisms of Atrial Contractile Dysfunction Caused by Sustained Atrial Tachycardia

Cellular Mechanisms of Atrial Contractile Dysfunction Caused by Sustained Atrial Tachycardia

Contemporary Management of Atrial Flutter

Transoesophageal echocardiography-guided cardioversion of atrial fibrillation or flutter. Selection of a low-risk group for immediate cardioversion

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