Atrial fibrillation pathophysiology: Difference between revisions
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== | ==Overview== | ||
The primary pathologic change observed in patients with atrial fibrillation is progressive fibrosis of the atria. This fibrosis is primarily due to atrial dilatation, however genetic causes and inflammation may also play a role in some individuals. | |||
==Dilation of the Atria== | |||
Dilatation of the atria can be due to almost any structural abnormality of the heart that can cause a rise in the intra-cardiac pressures. This includes: | |||
*[[Hypertension]], most likely the most common cause of atrial dilation in the current era | |||
*[[Valvular heart disease]] (such as [[mitral stenosis]], [[mitral regurgitation]], and [[tricuspid regurgitation]]) | |||
*[[Congestive heart failure]] | |||
*[[Coronary Artery Bypass Graft Surgery]] | |||
Any inflammatory state that affects the heart can cause fibrosis of the atria. This is typically due to sarcoidosis but may also be due to autoimmune disorders that create autoantibodies against myosin heavy chains. Mutation of the ''[[lamin]] AC'' gene is also associated with fibrosis of the atria that can lead to atrial fibrillation. | |||
Once dilatation of the atria has occurred, this begins a chain of events that leads to the activation of the [[renin-angiotensin system|renin aldosterone angiotensin system]] (RAAS) and subsequent increase in matrix metaloproteinases and disintegrin, which leads to atrial remodeling and fibrosis, with loss of atrial muscle mass. | Once dilatation of the atria has occurred, this begins a chain of events that leads to the activation of the [[renin-angiotensin system|renin aldosterone angiotensin system]] (RAAS) and subsequent increase in matrix metaloproteinases and disintegrin, which leads to atrial remodeling and fibrosis, with loss of atrial muscle mass. | ||
Revision as of 01:15, 16 October 2011
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
The primary pathologic change observed in patients with atrial fibrillation is progressive fibrosis of the atria. This fibrosis is primarily due to atrial dilatation, however genetic causes and inflammation may also play a role in some individuals.
Dilation of the Atria
Dilatation of the atria can be due to almost any structural abnormality of the heart that can cause a rise in the intra-cardiac pressures. This includes:
- Hypertension, most likely the most common cause of atrial dilation in the current era
- Valvular heart disease (such as mitral stenosis, mitral regurgitation, and tricuspid regurgitation)
- Congestive heart failure
- Coronary Artery Bypass Graft Surgery
Any inflammatory state that affects the heart can cause fibrosis of the atria. This is typically due to sarcoidosis but may also be due to autoimmune disorders that create autoantibodies against myosin heavy chains. Mutation of the lamin AC gene is also associated with fibrosis of the atria that can lead to atrial fibrillation.
Once dilatation of the atria has occurred, this begins a chain of events that leads to the activation of the renin aldosterone angiotensin system (RAAS) and subsequent increase in matrix metaloproteinases and disintegrin, which leads to atrial remodeling and fibrosis, with loss of atrial muscle mass.
This process is not immediate, and experimental studies have revealed patchy atrial fibrosis may precede the occurrence of atrial fibrillation and may progress with prolonged durations of atrial fibrillation.
Fibrosis is not limited to the muscle mass of the atria, and may occur in the sinus node (SA node) and atrioventricular node (AV node), correlating with sick sinus syndrome. Prolonged episodes of atrial fibrillation have been shown to correlate with prolongation of the sinus node recovery time,[1] [2] [3] suggesting that dysfunction of the SA node is progressive with prolonged episodes of atrial fibrillation.
References
- ↑ Fuster V, Rydén LE, Cannom DS, Crijns HJ, Curtis AB, Ellenbogen KA, Halperin JL, Le Heuzey JY, Kay GN, Lowe JE, Olsson SB, Prystowsky EN, Tamargo JL, Wann S, Smith SC, Jacobs AK, Adams CD, Anderson JL, Antman EM, Halperin JL, Hunt SA, Nishimura R, Ornato JP, Page RL, Riegel B, Priori SG, Blanc JJ, Budaj A, Camm AJ, Dean V, Deckers JW, Despres C, Dickstein K, Lekakis J, McGregor K, Metra M, Morais J, Osterspey A, Tamargo JL, Zamorano JL (2006). "ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society". Circulation. 114 (7): e257–354. doi:10.1161/CIRCULATIONAHA.106.177292. PMID 16908781. Unknown parameter
|month=ignored (help) - ↑ Elvan A, Wylie K, Zipes DP (1996). "Pacing-induced chronic atrial fibrillation impairs sinus node function in dogs. Electrophysiological remodeling". Circulation. 94 (11): 2953–60. PMID 8941126. Unknown parameter
|month=ignored (help) - ↑ Manios EG, Kanoupakis EM, Mavrakis HE, Kallergis EM, Dermitzaki DN, Vardas PE (2001). "Sinus pacemaker function after cardioversion of chronic atrial fibrillation: is sinus node remodeling related with recurrence?". Journal of Cardiovascular Electrophysiology. 12 (7): 800–6. PMID 11469431. Unknown parameter
|month=ignored (help)