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.
| Original language | English |
|---|---|
| Pages (from-to) | 31-34 |
| Number of pages | 4 |
| Journal | Heart and Metabolism |
| Issue number | 33 |
| Publication status | Published - 1 Dec 2006 |
Keywords
- Atrial fibrillation
- Cardiomyocyte function
- Contractile proteins
- Contractility