Pathophysiology

Atrial fibrillation is thought to be caused by atrial fibrosis, and lost of atrial muscle mass.  This fibrosis would occur as result of aging, chamber dilatation, inflammatory processes, and genetic causes.  Dilatation of the atria can be due to any structural abnormalities of the heart that cause a rise in the intra-cardiac pressures.  This includes valvular heart disease (such as mitral stenosis, mitral and tricuspid regurgitation), hypertension, and congestive heart failure.  Inflammatory processes such as sarcoidosis, and other autoimmune disorders will also result in similar cardiac remodeling.  Finally, mutation of the lamin AC gene has also been associated with fibrosis of the atria and seen in familial cases.

Dilatation of the atria activates several molecular pathways, including the renin-aldosterone-angiotensin system (RAAS).  Angiotensin II is upregulated in response to stretch leading to increase in matrix metaloproteinases and disintegrin, which leads to atrial remodeling and fibrosis, with loss of atrial muscle mass.  The use of an angiotensin-converting enzyme inhibitor (ACE inhibitor) is then an effective mean to lower atrial pressure, and wall stress.  Fibrosis is not limited to the muscle mass of the atria, and may occur in the sinoatrial node (SA) node and atrioventricular node (AV node), often leading to sick sinus syndrome (SSS).  Prolonged episodes of atrial fibrillation have been shown to correlate with prolongation of the sinus node recovery time, suggesting that dysfunction of the SA node is progressive with prolonged episodes of atrial fibrillation.  Both arrhythmias are commonly seen together.  Atrial remodeling, change in electrical refractoriness, and disturb contractile function make cardioversion unlikely to succeed. 

In atrial fibrillation, the regular impulses produced by the sinus node to provide rhythmic contraction of the heart are overwhelmed by the rapid randomly generated electrical discharges produced by larger areas of triggering atrial tissue.  Those focuses are often localized to the pulmonary veins involving re-entrant conduction pathway.  Ablation of the triggering focuses becomes an interesting management option to restore sinus rhythm (Picture 1).
Atrial fibrillation is different than flutter in which there is the presence of a more organized electrical circuit.  The activation is usually within the right atrium and produces characteristic saw-toothed p-waves on the electrocardiogram (ECG) (Picture 2).


 Picture 1. Atrial FibrillationPicture 1. Atrial Fibrillation

 Picture 2. Atrial Flutter
Picture 2. Atrial Flutter

 

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