Cerebral thromboembolization after cardioversion of atrial fibrillation in patients without transesophageal echocardiographic findings of left atrial thrombus

Salka, Samer; Saeian, Kooroush; Sagar, Kiran B.

doi:10.1016/0002-8703(93)90430-h

Cited by 17 publications

(2 citation statements)

References 9 publications

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“…Despite the absence of left atrial appendage thrombi on precardioversion TEE, stroke has been described among patients who did not receive anticoagulation at the time of TEE or continued anticoagulation during the peri-cardioversion period through a full month after cardioversion. [251][252][253][254] These adverse events may have occurred because the sensitivity of TEE for small atrial appendage thrombus is not 100%, development of new thrombus because of transient atrial dysfunction during the postcardioversion period, or other mechanisms.…”

Section: Conventional Vs Tee-guided Cardioversionmentioning

confidence: 99%

Antithrombotic Therapy in Atrial Fibrillation

Singer

Albers

Dalen

et al. 2008

Chest

648

139

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Section: Conventional Vs Tee-guided Cardioversionmentioning

confidence: 99%

Antithrombotic Therapy in Atrial Fibrillation

Singer

Albers

Dalen

et al. 2008

Chest

648

139

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“…An alternative approach would be to perform transoesophageal echocardiography and progress to immediate cardioversion without anticoagulation if no thrombi are present 34. This would minimise the duration of atrial fibrillation before cardioversion and increase the likelihood of success 35.…”

Section: Imaging Left Atrial Appendage Thrombusmentioning

confidence: 99%

Left atrial appendage: structure, function, and role in thromboembolism

Al-Saady

Obel

Camm

1999

Heart

553

361

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The left atrial appendage (LAA) is derived from the left wall of the primary atrium, which forms during the fourth week of embryonic development. It has developmental, ultrastructural, and physiological characteristics distinct from the left atrium proper. The LAA lies within the confines of the pericardium in close relation to the free wall of the left ventricle and thus its emptying and filling may be significantly aVected by left ventricular function. The physiological properties and anatomical relations of the LAA render it ideally suited to function as a decompression chamber during left ventricular systole and during other periods when left atrial pressure is high. These properties include the position of the LAA high in the body of the left atrium; the increased distensibility of the LAA compared with the left atrium proper; the high concentration of atrial natriuretic factor (ANF) granules contained within the LAA; and the neuronal configuration of the LAA. Thrombus has a predilection to form in the LAA in patients with atrial fibrillation, mitral valve disease, and other conditions. The pathogenesis has not been fully elucidated; however, relative stasis which occurs in the appendage owing to its shape and the trabeculations within it is thought to play a major role. Obliteration or amputation of the LAA may help to reduce the risk of thromboembolism, but this may result in undesirable physiological sequelae such as reduced atrial compliance and a reduced capacity for ANF secretion in response to pressure and volume overload.

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Resource Utilization in Atrial Fibrillation

Wahi

Klein

1999

Developments in Cardiovascular Medicine

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Cerebral thromboembolization after cardioversion of atrial fibrillation in patients without transesophageal echocardiographic findings of left atrial thrombus

Cited by 17 publications

References 9 publications

Antithrombotic Therapy in Atrial Fibrillation

Antithrombotic Therapy in Atrial Fibrillation

Left atrial appendage: structure, function, and role in thromboembolism

Resource Utilization in Atrial Fibrillation

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