Introduction: Antitachycardia pacing (ATP) effectively treats monomorphic ventricular tachycardia (VT). The VT may cease immediately upon ATP completion (type‐1 break), or it may persist or change to another tachyarrhythmia for one or more beats before termination (type‐2 break). We investigated the prevalence and characteristics of type‐2 breaks in ICD patients. Methods and Results: We analyzed VT episodes with stored electrograms that had at least one ATP therapy delivered in PainFREE R x trial, a multicenter trial with 220 coronary artery disease patients. Further subanalysis was performed by classifying the VT as slow or fast based on the cycle length (CL); slow VT: CL > 320 ms, fast VT: 240 ≤ CL ≤ 320 ms. To assess the effect of ATP on VT, comparison was performed of pre‐ATP and post‐ATP CL variability, average CL, and morphology. A total of 514 episodes (264 slow VT and 250 fast VT) were analyzed. The burst ATP terminated 457 (89%; 239 slow VT and 218 fast VT) of 514 episodes. Forty five (10%) episodes in 18 (32%) patients had type‐2 breaks. The mean number of beats during type‐2 breaks was 5.4 ± 3.1 (median 4). The mean time for episode termination measured from the end of ATP to return of first sinus/paced beat was 2.9 ± 1.2 seconds (median 2.6). The VT CL variability increased by 150% after ATP delivery. The ATP affected either VT CL or morphology, or both of 36 (80%) type‐2 breaks (9% accelerated, 47% decelerated, 22% changed in morphology only). Among the 9 (20%) episodes that remained unchanged in morphology and CL, four episodes (9%) were unaffected by ATP. Conclusion: Approximately 10% of VT episodes that were successfully terminated with burst ATP therapy had type‐2 breaks. Type‐2 breaks are associated with an increase in CL variability. Approximately 9% of all type‐2 episodes may be spontaneously terminating nonsustained VT given that ATP did not affect these episodes in any way. (J Cardiovasc Electrophysiol, Vol. 14, pp. 1156‐1162, November 2003)
Successful antitachycardia pacing (ATP) terminates ventricular tachycardia (VT) up to 250 bpm without the need for painful shocks in implantable cardioverter-defibrillator (ICD) patients. Fast VT (FVT) >200 bpm is often treated by shock because of safety concerns, however. This prospective, randomized, multicenter trial compares the safety and utility of empirical ATP with shocks for FVT in a broad ICD population.We randomized 634 ICD patients to 2 arms-standardized empirical ATP (n=313) or shock (n=321)-for initial therapy of spontaneous FVT. ICDs were programmed to detect FVT when 18 of 24 intervals were 188 to 250 bpm and 0 of the last 8 intervals were >250 bpm. Initial FVT therapy was ATP (8 pulses, 88% of FVT cycle length) or shock at 10 J above the defibrillation threshold. Syncope and arrhythmic symptoms were collected through patient diaries and interviews. In 11+/-3 months of follow-up, 431 episodes of FVT occurred in 98 patients, representing 32% of ventricular tachyarrhythmias and 76% of those that would be detected as ventricular fibrillation and shocked with traditional ICD programming. ATP was effective in 229 of 284 episodes in the ATP arm (81%, 72% adjusted). Acceleration, episode duration, syncope, and sudden death were similar between arms. Quality of life, measured with the SF-36, improved in patients with FVT in both arms but more so in the ATP arm.Compared with shocks, empirical ATP for FVT is highly effective, is equally safe, and improves quality of life. ATP may be the preferred FVT therapy in most ICD patients.
With the development of left ventricular pacing for cardiac resynchronization, there is an interest in the possibility of improving ventricular antitachycardia pacing (ATP) efficacy by pacing from the LV electrode(s).This study assessed the efficacy of pacing delivered from the left coronary vein (LCV) compared to that delivered from the right ventricular apex (RVA) upon ventricular tachycardia (VT) induction and termination.Sixty patients undergoing provocative ventricular electrophysiology (EP) studies in three centers were enrolled. Multipolar EP catheters were placed in the atrium, the RVA, and LCV. VT induction was attempted from the RVA and LCV in random order. Upon detection of monomorphic VT, burst ATP for up to 10 pulses at 88% VT cycle length was delivered from the RVA or LCV, in a random order, and crossed over when possible. Identical VT morphologies were reinduced to allow paired comparison of RVA versus LCV ATP.Data from 55 patients were analyzed. Thirty-four morphologically distinct monomorphic VT types were induced in 22 patients. ATP succeeded in 18 (55%) and VTs in 13 patients. RVA ATP terminated 15 of 23 (65%) VTs, and LCV ATP terminated 10 of 23 (43%) VTs (P = 0.14). ATP delivered ipsilateral to the earliest activation site required 5.0 + or - 2.6 pulses to terminate compared to 4.8 + or - 1.7 pulses when delivered from the contralateral site (P = 0.90). Paired comparison was possible for 13 VT morphologies in 11 patients. Paired RVA and LCV ATP efficacy was identical (54%vs 54%, P = 1.0).ATP delivered from a LCV lead offers no efficacy advantage over pacing from the RVA.
We evaluated the ability of propranolol and diltiazem alone and in combination to enhance the recovery of left ventricular (LV) segmental function during 1 month of reperfusion after two temporary occlusions of the left anterior descending coronary artery (LAD) in conscious dogs instrumented with ultrasonic crystals for the measurement of regional net systolic wall thickening (NET). LV segments were classified according to their contractile function after 1 hr of LAD occlusion: class 1, greater than 67% of preocclusion (control) NET; class 2, 0% to 66.9%; class 3, less than 0% (paradoxical systolic wall thinning). Propranolol (1 mg/kg iv) or diltiazem (20 micrograms/kg/min) was given 65 min after LAD occlusion in dogs that had 2 (group I) or 4 hr (group II) of LAD occlusion. Diltiazem plus propranolol (same doses) were given to another group of dogs that underwent 4 hr (but not 2) of LAD occlusion. Untreated control dogs received 25 ml of saline and underwent 2 or 4 hr of LAD occlusion. The NET of class 2 and 3 segments in group I control dogs increased significantly during 1 month of reperfusion, from 32 +/- 5% and -43 +/- 6% to 66 +/- 9% and 26 +/- 9%, respectively (p less than .05). Neither diltiazem nor propranolol enhanced the long-term recovery of these segments in group I dogs. However, diltiazem prevented further deterioration of contractile dysfunction observed in control dogs immediately after reperfusion in both segment classes. The NET of class 2 segments in group II control dogs after 4 weeks of reperfusion remained at levels observed during LAD occlusion: 30 +/- 4% to 37 +/- 12%. Class 3 NET increased from -33 +/- 5% to 12 +/- 12% with 1 month of reperfusion, but these segments were essentially akinetic. Propranolol or diltiazem alone did not produce significant overall increases in NET, but diltiazem again prevented further declines in NET of class 2 and 3 segments during early reperfusion. However, the combination of diltiazem and propranolol significantly enhanced overall recovery of class 2 NET in group II dogs (44 +/- 3% to 88 +/- 7%) and prevented the worsening of NET associated with early reperfusion. Compared with untreated dogs, propranolol plus diltiazem also significantly decreased the extent of histologic necrosis in class 2 and 3 segments as well as the macrohistochemically determined infarct size in group II dogs.(ABSTRACT TRUNCATED AT 400 WORDS)
Abstract Atrial fibrillation due to hyperthyroidism is characterized by a rapid ventricular reponse which is typically resistant to digoxin therapy. We report a patient with flutter‐fibrillation who developed cyclic sinus node dysfunction with profound ventricular pauses in response small doses of digoxin, verapamil, and propranolol, which resolved with discontinuation of the medications. Caution is necessary to avoid paradoxical ventricular when treating hyperthyroid‐induced atrial fibrillation.
The anatomical substrate for atrioventricular (AV) node reentry is unclear. To gain insights into the mechanism of cure of AV node reentry by nonpharmacological techniques, we compared AV node properties in 53 patients undergoing operative therapy (perinodal dissection) and 43 undergoing radiofrequency ablation (28 posterior approach, 15 anterior approach). Anterior radiofrequency ablation was associated with significant AH prolongation (62 ±18 msec vs 136 ± 64 msec, P < 0.0001), loss of “fast” pathway physiology, and no change in the anterograde refractory period of the AV node (273 ± 24 msec vs 268 ± 28 msec, P = NS). Posterior radiofrequency ablation did not change the AH interval (67 ± 17 msec vs 68 ± 17 msec, P = NS), prolonged AV node effective refractory period (275 ± 48 msec vs 320 ± 55 msec, P < 0.0001), and was associated with loss of “slow pathway” physiology. Operative treatment prolonged the AH interval (66 ±18 msec vs 83 ± 37 msec, P < 0.0001) and the AV node effective refractory period (264 ± 52 msec vs 364 ±112 msec, P < 0.0001), and affected dual pathway physiology inconsistently. These data support the view that the “fast” and “slow” pathways are distinct perinodal entities that can be selectively ablated. The operative approach causes more diffuse and variable injury to the AV node region.
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