Pathophysiology and prevention of atrial fibrillation.

Atrial fibrillation (AF) is a ubiquitous yet diverse cardiac arrhythmia whose incidence increases with age; with most forms of cardiac and some pulmonary diseases; and with a number of metabolic, toxic, endocrine, or genetic abnormalities.1,2 Classification of clinical AF subtypes can be achieved on the basis of the ease by which episodes of the arrhythmia terminate as follows3: “Paroxysmal” AF refers to episodes that generally stop spontaneously after no more than a few days. “Persistent” AF occurs less frequently than paroxysmal AF and, rather than self-terminating, requires cardioversion to restore sinus rhythm. “Permanent” AF cannot be converted to sinus rhythm. These terms apply strictly to chronic AF, because a single episode of the arrhythmia cannot be fully categorized. Although there are some mixed patterns, they generally derive from physician impatience for early cardioversion or from pragmatic clinical considerations (eg, to avoid thrombus formation or hemodynamic decompensation). Patients initially presenting with paroxysmal AF often progress to longer, non–self-terminating bouts. An exception may be paroxysmal AF during intense vagotonia. Moreover, AF initially responsive to pharmacological or electrical cardioversion tends to become resistant and cannot then be converted to sinus rhythm. To some extent, the failure of the physician to suggest or the patient to accept further cardioversion attempts may lead to diagnosis of “permanent” AF. Thus, the “point of no return” may be determined by true pathophysiological abnormalities or may merely be an artifact of clinical pragmatism. Effective prevention is essential in managing this arrhythmia whose occurrence is widespread, progression is relentless, and morbidity and mortality are significant. To focus on means for prevention necessitates considering both clinical risk factors and pathophysiology.