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constitute 78% of this patient population20. In a recent study, this sex difference
was further investigated, showing that the proportion of males was greater 1 among sporadic LAF. Sporadic LAF is also more common in men than in women21.
The natural history of LAF has not been well studied. However, accumulated
data suggest that it is associated with a low-risk of progression to permanent AF,
mortality, congestive heart failure, and stroke/transient ischaemic attack20, 22.
The clinical course of LAF also suggests that many of these patients have a
paroxysmal form of the arrhythmia, with an estimated risk of progression to
permanent AF of 29% over 30 years 20. Patton and coworkers confirmed the
prevalence of a paroxysmal form of LAF (94% of patients) with a lower progression
rate (7.8%), but this was evaluated on the basis of a shorter follow-up period23.
The course of LAF may be influenced by several factors such as left atrial volume.
Indeed, Osranek and coworkers24 demonstrated that patients with LAF and
increased left atrial volume at diagnosis or later during the follow-up experienced
more adverse events, such as cerebral infarction, myocardial infarction and
congestive heart failure. Furthermore, increasing age and the development
of hypertension may increase the risk of cerebrovascular events20. Finally, approximately 44% of patients with an initial diagnosis of LAF may represent
occult cases of arterial hypertension. In these patients, hypertension may affect
AF recurrence and treatment outcomes25.
Pathophysiology
The onset and the maintenance of AF require an event (trigger) that initiates the arrhythmia and the presence of a predisposing substrate and genetic factors that perpetuate it.Additional factors may also cooperate as modulators in facilitating initiation or continuation of AF.
AF behaves as a progressive disease in which the arrhythmia itself may induce further structural changes and a worsening in the underlying diseases, thus creating a vicious cycle (“AF begets AF”) that does nothing except it does make the myocardial architecture distortion worse, and very often leads to paroxysmal AF becoming persistent or permanent26, 27. Structural remodelling only seems to be reversible during the first phases of the arrhythmic disorder, but its extent is crucial because it may reach a threshold beyond which sinus rhythm can no longer be restored26. In addition, AF can be maintained by re-entry and/or rapid focal ectopic firing28.
The mechanism maintaining AF is often called the driver. The irregular atrial
Introduction
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