Atrial fibrillation (AF) is the most common cardiac arrhythmia, associated with a five- to six-fold increase in the incidence of stroke due almost exclusively to embolization of thrombus formed in the left atrial appendage. Whereas epidemiological data links AF to increased mortality, recent clinical trials show no improvement in outcomes with strategies designed to maintain sinus rhythm. One possible explanation for this "AF paradox" is that AF is a manifestation of an underlying disease process that is not addressed by current treatment strategies. Several lines of evidence suggest that oxidant stress may contribute to the atrial remodeling and the hypercoagulable state associated with AF. These alterations involve an increase in reactive oxygen species and a concomitant decrease in the bioavailability of nitric oxide. Recently, we observed this situation in the left atrial appendage. Increased oxidant stress may be central to the perpetuation of AF, and failure to address this underlying pathology may explain the lack of efficacy seen in clinical trials.
|Original language||English (US)|
|Number of pages||6|
|Journal||Cardiovascular Reviews and Reports|
|State||Published - Oct 1 2003|