Cellular changes in atrial fibrillation

Jolanda Van Der Velden, Nadiya A. Narolska, Ger J.M. Stienen

Research output: Contribution to journalReview articleAcademicpeer-review

Abstract

Chronic atrial fibrillation represents one of the main risk factors for the occurrence of thromboembolic events. At present it is clear that thrombus formation is triggered, not only by irregular rhythm, but also by reduced intrinsic atrial contractility. Apart from the thromboembolic risk, reduced atrial contractility might contribute to reduced cardiac output in patients with ventricular heart disease. Hence, the clinical importance of atrial dysfunction induced by atrial fibrillation prompts research into the underlying mechanisms involved in reduced atrial contractility that may serve to develop new therapeutic strategies. This review addresses both structural and functional cellular alterations involved in contractile dysfunction associated with chronic atrial fibrillation.

LanguageEnglish
Pages31-34
Number of pages4
JournalHeart and Metabolism
Issue number33
Publication statusPublished - 1 Dec 2006

Cite this

Van Der Velden, J., Narolska, N. A., & Stienen, G. J. M. (2006). Cellular changes in atrial fibrillation. Heart and Metabolism, (33), 31-34.
Van Der Velden, Jolanda ; Narolska, Nadiya A. ; Stienen, Ger J.M. / Cellular changes in atrial fibrillation. In: Heart and Metabolism. 2006 ; No. 33. pp. 31-34.
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Van Der Velden, J, Narolska, NA & Stienen, GJM 2006, 'Cellular changes in atrial fibrillation', Heart and Metabolism, no. 33, pp. 31-34.

Cellular changes in atrial fibrillation. / Van Der Velden, Jolanda; Narolska, Nadiya A.; Stienen, Ger J.M.

In: Heart and Metabolism, No. 33, 01.12.2006, p. 31-34.

Research output: Contribution to journalReview articleAcademicpeer-review

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T1 - Cellular changes in atrial fibrillation

AU - Van Der Velden, Jolanda

AU - Narolska, Nadiya A.

AU - Stienen, Ger J.M.

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N2 - Chronic atrial fibrillation represents one of the main risk factors for the occurrence of thromboembolic events. At present it is clear that thrombus formation is triggered, not only by irregular rhythm, but also by reduced intrinsic atrial contractility. Apart from the thromboembolic risk, reduced atrial contractility might contribute to reduced cardiac output in patients with ventricular heart disease. Hence, the clinical importance of atrial dysfunction induced by atrial fibrillation prompts research into the underlying mechanisms involved in reduced atrial contractility that may serve to develop new therapeutic strategies. This review addresses both structural and functional cellular alterations involved in contractile dysfunction associated with chronic atrial fibrillation.

AB - Chronic atrial fibrillation represents one of the main risk factors for the occurrence of thromboembolic events. At present it is clear that thrombus formation is triggered, not only by irregular rhythm, but also by reduced intrinsic atrial contractility. Apart from the thromboembolic risk, reduced atrial contractility might contribute to reduced cardiac output in patients with ventricular heart disease. Hence, the clinical importance of atrial dysfunction induced by atrial fibrillation prompts research into the underlying mechanisms involved in reduced atrial contractility that may serve to develop new therapeutic strategies. This review addresses both structural and functional cellular alterations involved in contractile dysfunction associated with chronic atrial fibrillation.

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KW - Cardiomyocyte function

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Van Der Velden J, Narolska NA, Stienen GJM. Cellular changes in atrial fibrillation. Heart and Metabolism. 2006 Dec 1;(33):31-34.