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The primary pathologic change seen in atrial fibrillation is the progressive fibrosis of the atria (1,2).

  • fibrosis is primarily due to atrial dilation, however genetic causes and inflammation may have a cause in some individuals
    • dilation of the atria can be due to almost any structural abnormality of the heart that can cause a rise in the intra-cardiac pressures
      • atrial fibrillation is classically caused by hypertension, heart failure, myocardial infarction, mitral stenosis, thyrotoxicosis and alcohol, previously unrecognized risk factors, such as obesity, metabolic syndrome, diastolic dysfunction, sleep apnoea, psychological stress, and tall stature, have emerged
      • genetic predisposition to AF or specific genetically predetermined forms of the arrhythmia have also been described
      • any inflammatory state that affects the heart can cause fibrosis of the atria e.g. sarcoidosis

      • enlargement of the left atrium results in turbulence and stasis of blood which in turn predisposes to thrombus formation, especially in the atrial appendage
        • thrombus may embolize to any part of the peripheral circulation
        • embolization may result in a transient ischaemic attack or stroke, or infarction of a major viscus, e.g. gut.
        • embolization from thrombi in the right atrium may result in pulmonary emboli
        • atrial dilation 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

    • 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)
        • suggests that dysfunction of the SA node is progressive with prolonged episodes of atrial fibrillation

Exact electrophysiological mechanisms of initiation and maintenance of AF remain controversial

  • AF appears to be a micro re-entrant arrhythmia with multiple wavelets and daughter wavelets randomly colliding with each other
  • factors such as persistent tachycardia, valvular diseases, myocardial ischaemia, systemic hypertension and diastolic dysfunction lead to excessive pressure or volume overload on the left atrium which responds with various time-dependent adaptive processes
  • structural, functional, electrical and metabolic consequences eventually lead to permanent remodelling and dilatation
    • these responses include atrophy or hypertrophy of atrial myocardial fibres, age-related degenerative changes with increase in fibrous tissue and senile amyloidosis and are associated with genesis of atrial ectopics, paroxysmal AF or atrial tachycardia (AT), which eventually results in chronic AF or atrial flutter (AFL)
    • majority of AF originates from the left atrium
      • there is evidence that 'sleeves' of atrial tissue extend into the pulmonary veins are frequently involved in the initiation of atrial arrhythmias (the basis of pulmonary vein isolation procedure for termination of AF)
      • AFL represents a more organized form of re-entrant circuit and unlike AF, generally arises predominantly from the right atrium
        • there is a close interrelationship between AF and AFL
          • AF of variable duration generally precedes the onset of AFL. On the other hand, fast AFL can degenerate into fibrillatory conduction and maintain AF


Last reviewed 05/2021