Abstract

A concomitant condition found in many patients with atrial fibrillation (AF) commonly requires bradycardia pacing. Comparing AAI to VVI pacing, atrial pacing appears to have an apparent protective effect on the subsequent development of AF. By addressing the proposed mechanisms responsible for AF (long-short cycles, increased temporal dispersion of refractoriness, frequent atrial ectopic beats), overdrive appears to be a promising technique to postpone or even prevent entirely the development of chronic AF while reducing the incidence of paroxysmal AF. These observations led to the development of a pacing algorithm (Dynamic Atrial Overdrive-DAO) designed to provide a high percentage of atrial pacing just above the patient’s own intrinsic atrial rate. The algorithm is a dynamic stimulation technique to suppress AF effectively, overdrives the atrium just enough to prevent the intrinsic rhythm from emerging while maintaining both normal diurnal variation and rate response. Dynamic Atrial Overdrive is a unique pacemaker algorithm designed specifically for suppression of paroxysmal AF arising from either an absolute or relative bradycardia. By maintaining an atrial stimulation rate just above the intrinsic rate, the goal is to control both the atrial rate and rhythm, reducing the incidence of ectopic beats which might be a trigger, long-short cycles, or the dispersion of refractoriness from initiating AF. In addition, because the algorithm routinely searches for intrinsic atrial activity and adjusts the stimulation rate accordingly, it avoids sustained periods of rapid stimulation that may not be required. At the same time, it preserves the normal circadian rate variation in association with normal sinus function or in the presence of sinus node dysfunction if the sleep rate feature is also enabled. I N T R O D U C T I O N Atrial fibrillation (AF), the most common significant cardiac arrhythmia, affects an estimated 4 million people around the world. Its rapid and uncoordinated atrial rhythm compromises hemodynamics, decreases cardiac output, predisposes to ventricular arrhythmias, and sets the stage for thromboembolic complications. Contributing mechanisms are presumed to be the occurrence of long-short cycles, an increased temporal dispersion of refractoriness, and atrial ectopic activity. The incidence increases with age, affecting 4% of those over 60, and up to 15% of those over 70. Although it can RevIew St. Jude Medical CRMD, Sylmar, CA,

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