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J Am Coll Cardiol, 2005; 45:460-461, doi:10.1016/j.jacc.2004.11.008
© 2005 by the American College of Cardiology Foundation
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CORRESPONDENCE: RESEARCH CORRESPONDENCE

Fast ventricular tachycardias in patients with implantable cardioverter-defibrillators: Efficacy and safety of antitachycardia pacing

A prospective and randomized study

Javier Jiménez-Candil, MD, Angel Arenal, MD*, Arcadio García-Alberola, MD, Mercedes Ortiz, PhD, Silvia del Castillo, MD, Javier Fernández-Portales, MD, Juan Sánchez-Muñoz, MD, Juan Martínez-Sánchez, MD, Esteban González-Torrecilla, MD, Felipe Atienza, MD, Alberto Puchol, MD and Jesús Almendral, MD

* Laboratory of Electrophysiology, Cardiology Department, Hospital General Universitario Gregorio Marañón, Doctor Esquerdo, 46, 28007, Madrid, Spain (Email: arenal{at}doymanet.es).


To the Editor: Between 11% and 40% of detected monomorphic ventricular tachycardias (VTs) in patients with implantable cardioverter-defibrillators (ICDs) have a cycle length (CL) of <320 ms (1,2). Antitachycardia pacing (ATP) and high-energy shocks (HES) are available for the treatment of these fast ventricular tachycardias (FVTs). High-energy shocks commonly are selected because the efficacy and safety of ATP in this setting have not been extensively proven and because a short CL is a predictor of unsuccessful therapy and acceleration (3,4). Nevertheless, the disadvantages of HES are battery drain, VT termination delay, and deterioration of quality of life (5). Although ATP has been reported to terminate as many as 80% of FVT episodes, studies have indicated that frequent, nonsustained FVT might overestimate the efficacy of ATP (1). To determine the effect of ATP in FVT treatment, we compared the HES incidence with ATP programmed on versus off. We also analyzed the impact of ATP in VT duration and VT-associated symptoms.

All patients with ICDs who presented with sustained monomorphic VT previously recorded or at risk of presenting monomorphic VT (ischemic heart disease, arrhythmogenic right ventricular dysplasia, and dilated cardiomyopathy) were enrolled after a written informed consent was obtained. Patients with long QT syndrome, Brugada syndrome, or hypertrophic cardiomyopathy at very low risk of presenting with monomorphic VT were excluded. Two programming strategies in the FVT zone were compared in a multicenter, prospective, randomized, and single-blind crossover study. Strategy A consisted of two ATP bursts followed by HES, and strategy B consisted of HES only. Patients were assigned to one strategy for six months and then crossed over to the other strategy for another six months. The primary end point was the incidence of HES; secondary end points were VT duration and incidence of syncope/near-syncope.

Only FVT detection and therapy programming was standardized. The detection of FVT was based on heart rate criteria and defined for a CL of 260 to 310 ms. Strategy A consisted of two consecutive bursts of five and eight pulses at 84% of VT CL, followed by maximum HES; strategy B consisted of HES alone. Successful ATP was defined as tachycardia terminating during the burst or within four beats after the burst if the VT CL was modified by ATP. The VT acceleration was defined as VT CL decreasing more than 10% immediately after ATP therapy.

Statistical analysis was performed using SPSS 11.5 for Windows (SPSS Inc., Chicago, Illinois). Assuming an ATP success rate of 77%, we estimated a sample size of 125 patients to detect a difference of 75% on HES incidence, statistical power of 80% (10% expected incidence of FVT in each strategy and alpha <0.05). The two-tailed Student t test and the chi-square test or Fisher exact test were used when appropriate. Multivariate analysis was performed by logistic regression method. A p value of <0.05 was considered statistically significant.

We randomly assigned all 137 eligible patients. One patient received a heart transplant for heart failure during the first assigned strategy (strategy B), and three other patients died during their first assigned strategy: one suddenly in strategy A at one week after extensive percutaneous coronary revascularization (electrograms not available) and two in terminal heart failure (one in each strategy); no FVT were recorded.

This analysis focuses on the 133 patients who finished the follow-up (65 in the treatment order strategy A-strategy B and 68 in strategy B-strategy A) (Table 1). Forty-nine FVTs occurred in 22 patients (17%), with a mean CL of 286 ± 16 ms. Twenty-seven occurred in 10 patients in strategy A and 22 in 13 patients in strategy B. One patient presented with FVT in both strategies. Antitachycardia pacing terminated 24 of 27 FVTs (efficacy, 89%), in all cases with the first burst. In strategy B, there were two non-sustained FVTs that terminated spontaneously during charging. The remaining FVTs in strategy B and the three FVTs that were unsuccessfully treated by ATP in strategy A were terminated by the first program of HES. Only one episode of FVT in strategy A was accelerated. The use of strategy A significantly reduced the HES incidence in the FVT zone (3 vs. 20, p < 0.001), as well as the proportion of patients with HES for FVT and the mean of HES for FVT per patient. Strategy A reduced the duration of FVT episodes and reduced the incidence of syncope/near-syncope for FVT (Table 2). A longer CL (289 ± 16 vs. 280 ± 0; p = 0.01) and beta-blocker treatment (50% vs. 4.3%; p = 0.04) were associated with a higher ATP efficacy by logistic regression.


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Table 1. Baseline Clinical Characteristics at Enrollment
 

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Table 2. Analysis of Events per Patient
 
This is the first randomized study designed to evaluate the effect of ATP in FVT treatment in patients with ICD. Our results suggest that a single, short ATP burst reduces the HES incidence in the FVT zone and may improve the clinical tolerance of these tachycardias.

In re-entrant VT, the ability of ATP to terminate the arrhythmia depends on the presence of an excitable gap (6) and on the capability of the impulses to penetrate this gap. The main limiting factor for penetrating the excitable gap is the distance to the circuit; therefore, a long burst or a short-pacing CL is needed to reach the FVT circuits. The first burst that we selected was shorter and faster than those previously reported; nevertheless, the efficacy and acceleration rate were similar, suggesting that the shorter CL might compensate for a lower number of beats in the initial ATP train (1). This observation may be important to decrease the delay before the rescue HES is delivered if needed.

The number of FVTs is lower than in previous studies; however, the proportion of patients with FVT is similar. The high proportion of patients treated with beta-blockers and the inclusion of nonischemic patients may explain this difference. The use of ATP also appears to reduce the incidence of syncope/near-syncope associated with an episode of FVT, presumably as a result of a reduction in the VT duration. Interestingly, beta-blockers increased the efficacy of ATP, indicating a possible influence of autonomic tone in the maintenance of the VT (7,8).

This study suggests that a single, short ATP burst is efficient and safe for the treatment of FVT, reducing the HES incidence and arrhythmia-related symptoms. Nevertheless, the small number of episodes and patients limits the power of these conclusions and, therefore, a larger prospective study is required to validate these data.


    References
 Top
 References
 
1. Wathen MS, Sweeney MO, DeGroot P, et al. Shock reduction using antitachycardia pacing for spontaneous rapid ventricular tachycardia in patients with coronary artery disease Circulation 2001;104:796-801.[Abstract/Free Full Text]

2. Schaumann A, von zur Mühlen F, Herse B, et al. Empirical versus tested antitachycardia pacing in implantable cardioverter-defibrillators Circulation 1998;97:66-74.[Abstract/Free Full Text]

3. Peinado R, Almendral J, Rius T, et al. Randomized, prospective comparison of four burst pacing algorithms for spontaneous ventricular tachycardia Am J Cardiol 1998;82:1422-1425.[CrossRef][Web of Science][Medline]

4. Newman D, Dorian P, Hardy J. Randomized controlled comparison of antitachycardia pacing algorithms for termination of ventricular tachycardia J Am Coll Cardiol 1993;21:1413-1418.[Abstract]

5. Irvine J, Dorian P, Baker B, et al. Quality of life in the Canadian Implantable Defibrillator Study (CIDS) Am Heart J 2002;144:282-289.[Web of Science][Medline]

6. Josephson ME, Horowitz LN, Farshidi A, Kastor JA. Recurrent sustained ventricular tachycardia. 1Mechanisms. Circulation 1978;57:431-440.[Abstract/Free Full Text]

7. Bänsch D, Brunn J, Castrucci M, et al. Syncope in patients with an implantable cardioverter-defibrillator: incidence, prediction and implications for driving restrictions J Am Coll Cardiol 1998;31:609-615.

8. Fries R, Heisel A, Nikoloudakis N, et al. Antitachycardia pacing in patients with implantable cardioverter-defibrillators: inverse circadian variation of therapy success and acceleration Am J Cardiol 1997;80:1487-1489.[Medline]





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