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Higher rates to reduce irregularity: the use of overdrive pacing in atrial fibrillation.

For a long time, it was a matter of debate whether fast rate or ventricular irregularity during atrial fibrillation (AF) was primarily responsible for the perception of palpitations, development of cardiomyopathy, and system emboli from the fibrillating atria. Recent studies have shown that ventricular irregularity associated with AF and manifested by random QRS intervals that constitute the diagnostic clue in scalar electrocardiography, can elicit symptoms and cardiomyopathy regardless of the rate. Reduction of ventricular irregularity in AF patients in addition to control of fast ventricular rates, therefore, appears sensible to reduce symptoms and minimize the risk of cardiomyopathy. The underlying mechanisms of ventricular irregularity are uncertain and include concealed conduction within the atrioventricular (AV) node secondary to decremental conduction or electrical modulation of AV nodal propagation or pacemaker activity in the AV node. If rate control is preferred to rhythm control, suppression of AV conduction with pharmacologic treatment and ablation of the AV junction are nowadays the established methods according to guidelines. However, the side effects and non-compliance associated with drug treatment or pacemaker dependency after ablation with potentially unfavourable effects of long-term right ventricular apical pacing often undermine the effectiveness of these therapies. These disadvantages urge the search for other therapeutic modalities for a safe and easy reduction of ventricular irregularity in AF. In 1983, Wittkampf and De Jongste showed that continuous pacing in the right ventricle reduced the irregularity of QRS intervals during AF; faster pacing rates produced even more regularity by elimination of a large proportion of longer QRS intervals observed during slower ventricular rates. This phenomenon of rate stabilization is attributed to suppression or delay in AV nodal conduction by retrograde penetration of ventricular stimuli. This concept was incorporated in rate smoothing pacing algorithms that indeed significantly reduced variability of successive QRS intervals in AF patients. Unfortunately, the application of this algorithm was associated with a concomitant increase in mean heart rate by 21–29%. This drawback limited the widespread use of rate smoothing algorithms in paced patients with paroxysmal or permanent AF. In 1997, we tested a new rate smoothing programme delivered by the former Vitatron company, that uses a dynamic average of successive sensed or paced heart rates as a reference point. The pacing rate followed the average heart rate and started pacing when the average ventricular rate dropped by 2.5 bpm. In addition, the algorithm prevented the occurrence of sudden bradyor tachyarrhythmia by pacing at a decelerating or accelerating rate at 2 bpm. In the acute pacing study, we observed that variability of the RR intervals could be reduced by 73% while the heart rate during pacing did not increase significantly (2%) compared with the preceding period without pacing. In the unpublished randomized, single-blinded cross-over trial of patients with permanent (n 1⁄4 91) and paroxysmal AF (n 1⁄4 93), we observed a significant reduction in the variance of RR intervals in both patients categories. However, quality of life, measured with instruments specific for pacemaker patients, did not change significantly with ventricular rate smoothing. A preference for rate smoothing pacing was observed in patients with paroxysmal AF. These dissatisfying findings prevented further clinical exploration. Treatment and specifically prevention of AF with atrial pacing was also investigated in the mid-90s. Assuming that atrial overdrive of the atria would suppress triggering atrial premature beats, short2long intervals and atrial pauses, thereby diminishing potentially arrhythmogenic increased dispersion of atrial refractoriness, oneor two-site atrial pacing has been extensively studied. The results of many studies are very conflicting because of differences in overdrive pacing algorithms, profiles of included AF patients, calculation of AF burden based on the number of mode switches, and other methodological differences including control groups and duration of follow-up. For example, Carlson et al. showed the