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BACKGROUND In five chronically instrumented conscious dogs, we studied the effects of rapid pacing on sustained electrically induced atrial fibrillation. METHODS AND RESULTS Twenty-three unipolar atrial electrograms were recorded simultaneously from the bundle of Bachmann and the lateral wall of the right and left atria. During sustained atrial fibrillation, the surface electrocardiogram showed continuous irregularities of the baseline without P or F waves as well as an irregular ventricular rhythm with narrow QRS complexes. The atrial electrograms showed rapid irregular activity with a median cycle length of 85 +/- 8 msec and a range (P5-95) of 33 +/- 18 msec. Overdrive pacing of atrial fibrillation was performed using symmetric biphasic rectangular stimuli (2-msec duration, sixfold that of threshold) applied to a pair of stimulating electrodes at the left atrial appendage. Stimulation was started at pacing intervals of about 10 msec longer than the local median fibrillation interval and subsequently shortened in steps of 1 msec. At a critical pacing interval slightly shorter than the median fibrillation interval, the atrium around the pacing site was suddenly captured by the electrical stimuli. The area of local capture had a diameter of 6.1 +/- 1.6 cm. The time window of capture was 12 +/- 4 msec. CONCLUSIONS These observations show that during electrically induced atrial fibrillation in chronically instrumented conscious dogs, a short excitable gap is present, permitting regional control of the fibrillatory process by rapid pacing.

Background —After upper-limit-of-vulnerability (ULV) shocks of the same strength and coupling interval (CI) during the T wave, (1) the epicardial activation pattern (EAP) for the first postshock cycle is indistinguishable between shocks that do (VF) and do not (NoVF) induce ventricular fibrillation (VF) and (2) ≥3 cycles in rapid succession always occur during VF but not during NoVF episodes. To study the role of these rapid cycles, rapid pacing was performed after a shock stronger than the ULV that by itself did not induce rapid cycles and VF. Methods and Results —A 504-electrode sock was sutured to the heart in 6 pigs to map EAPs. The S2 shock strength and S1-S2 CI at the ULV were determined by T-wave scanning with an up/down protocol. Ten shocks 50 to 100 V above the ULV (aULV) were delivered at the same S1-S2 CI to confirm that VF was not induced. Then, the postshock interval after aULV shocks was scanned with an S3 pacing stimulus from the LV apex until the shortest S2-S3 CI that captured was reached. This was repeated for S4, S5, etc, until VF was induced. To induce VF, 3 pacing stimuli (S3-S5) with progressively shorter CIs were required; S3 or S3, S4 never induced VF. After cycle S5, which induced VF, 2 EAP types occurred: focal (74%) and reentrant (26%). Conclusions —At least 3 cycles with short CIs are necessary for VF induction after aULV shocks. Cycles S3-S4 may create the substrate for cycle S5 to initiate VF.

Background The critical-point and upper-limit-of-vulnerability (ULV) hypotheses predict that the ULV dose-response curve should be steeper and to the right of the defibrillation (DF) curve. Yet, some recent experimental data contradict this prediction. Two studies are presented that test two explanations for the contradiction: (1) Testing at a single point in the T wave underestimates the ULV dose-response curve and (2) ULV testing at normal heart rates does not mimic the mechanical or electrical state of the heart in ventricular fibrillation (VF). Methods and Results A nonthoracotomy lead system with a biphasic waveform was used throughout. In eight dogs, the dose-response curve widths (a measure of steepness) were compared between DF data and ULV data gathered at the peak (ULV PK ), middownslope (ULV DWN ), midupslope (ULV UP ), and all times (scanning or ULV SCN ) in the T wave. In another eight dogs, ULV data (ULV RAP ) were gathered by scanning the T wave after 15 rapidly paced beats (166- to 198-ms pacing interval). The rapid pacing interval was chosen to more closely mimic the hemodynamics and activation rate of early VF. ULV data (ULV STD ) at normal heart rates were gathered for all animals. In the first study, scanning significantly reduced the ULV curve width (ULV SCN , 63.5±29.7 V; ULV PK , 81.9±45.2 V; ULV DWN , 116±36.5 V; DF, 105±22.0 V; P 80 SCN , 410±62.6 V; ULV 80 PK , 266±35.3 V; ULV 80 DWN , 355±80.4 V; DF 80 , 427±60.9 V; P RAP curve was shifted dramatically to the right, the average ULV 50 RAP being greater than the average DF 90 . Furthermore, 92% of the ULV RAP VF inductions occurred between 10 ms before and 50 ms after the peak of the T wave, suggesting that scanning of the entire T wave may not be necessary. Conclusions With a single rapidly paced ULV sequence with limited T-wave scanning, it may be possible to estimate highly effective defibrillation doses with few VF episodes and high-voltage stimuli.

Using temporary atrial wire electrodes placed at selected atrial sites, rapid atrial pacing at rates of up to 368 beats/min was used to study atrial excitability and conduction in seven patients who underwent open heart surgery. The threshold for atrial pacing was found to be an exponential function of pacing rate (r = 0.55, p less than 0.01), increasing threefold when the fastest pacing rates were compared with the slowest pacing rates (p less than 0.005). Atrial conduction times (measured from pacing to recording sites), prolonged during rapid atrial pacing both for studies conducted before institution of cardiopulmonary bypass (p less than 0.005) and for those done 7 days postoperatively (p less than 0.05). However, prolongation of conduction times always depended on achievement of a critically rapid pacing rate. During rapid atrial pacing, we observed a high incidence of alternans of the atrial electrogram (17 of 42 studies). Thus, human atrial excitability, conduction and electrogram morphology are not constant during pacing at rapid rates. Rather, at rapid pacing rates, there is depression of atrial excitability, prolongation of atrial conduction times and alternation in electrogram morphology. These findings have clinical relevance and theoretical implications for the understanding and treatment of rapid atrial rhythms.