Acceleration Of Ventricular Tachycardia Research Articles

Abstract 14364: Atrial Fibrillation With Rapid Ventricular Response Induced Ventricular Tachycardia Terminated by Intrinsic Anti-Tachycardia Pacing - A First in Literature Case Report

Background: Intrinsic anti-tachycardia pacing (iATP) is a novel tailored algorithm that has shown increased efficacy against ventricular tachycardia (VT), including fast VT. We describe a case of atrial fibrillation (AF) with rapid ventricular response (RVR) induced VT terminated by iATP. Case description: A 71-year-old male with coronary artery disease, heart failure (EF 30-35%), atrial fibrillation, VT status post biventricular implantable cardioverter defibrillator and failed renal transplant presented with syncope during dialysis. His home medications included amiodarone, metoprolol, apixaban. He was hemodynamically stable on presentation. He had bilateral pitting edema with a systolic murmur and bilateral basilar crackles on exam. His labs were consistent with anemia and end stage renal disease. His device interrogation (Figure) showed AFRVR which degenerated to VT with final cycle length (CL) of 290 msec. First round of ATP with S1x10 burst pulses (88%, CL 250msec) and S2 extra stimuli (CL 230 msec) failed to terminate the VT. Post pacing interval (PPI) was 450 msec. Given calculated remote distance, another five rounds of adaptive iATP with similar S1 pulses but faster S2 and addition of S3 extra stimuli were delivered but were unsuccessful in terminating VT. Finally, the seventh round of iATP (S1x10 at CL 260 msec, S2 at 240 msec) was successful at conversion to sinus rhythm briefly before reverting to AF with controlled ventricular pacing. Discussion: ATP decreases ICD shocks but is programmed empirically and there is less success with fast VT. iATP analyses the PPI of the prior failed sequence to adjust the subsequent ATP therapy by altering the number of burst pulses (S1) and addition of ramp extra stimuli. Computational models and early clinical experience have shown increased efficacy of iATP in terminating fast VT without concomitant increase in VT acceleration. To the best of our knowledge, this is first case report of AFRVR induced VT terminated by iATP.

Arrhythmogenicity of anti-tachycardia pacing in patients with implantable cardioverter defibrillator

BackgroundAnti-tachycardia pacing therapy (ATP) has shown comparable efficacy to shock therapy in ventricular tachycardia (VT) termination with better quality of life. However, some ATPs may lead to VT acceleration or degeneration to ventricular fibrillation (VF), which will result in more ICD shocks. The aim of this study was to investigate the predictors of VT acceleration by ATP therapy in a real-life patient cohort.ResultsWe retrospectively reviewed 448 monomorphic VT episodes that required ATP therapy in 60 patients with structural heart diseases implanted with ICD or CRTD. The clinical data of the patients and the episodes’ details were evaluated. We found that patients with a higher ejection fraction (EF) were more likely to be cardioverted by ATP therapy (P: 0.024). VT acceleration was more frequent in patients with lower EF (mean 31.24 ± 4.08) compared with the non-accelerated patients with higher EF (mean 37.00 ± 9.4, P: 0.016). The percentage of accelerated episodes was 8.5%. VT episodes with a mean cycle length (CL) < 310 ms are more likely to accelerate (sensitivity 76.3%, specificity 67.7%, PPV value 45%, NPV 86%, and AUC 0.790). There was a statistically significant difference in the accelerated VT episodes as compared to non-accelerated episodes regarding the number of ATP bursts (mean 3.66 ± 2.22 vs. 1.76 ± 1.35, P: < 0.001), ramp (23.7% vs. 4.2%, P: < 0.001), scanning (55.3% vs. 31.3%, P: 0.003) and burst adaptive cycle length (mean 83.55 ± 2.92 vs. 84.64 ± 2.61, P: 0.016). In a multivariate analysis, the VT CL, number of ATP bursts and ramp pacing predicted VT acceleration by ATP therapy.ConclusionsVentricular tachycardia in patients with low LV EF and fast VTs with a CL less than 310 ms were more likely to accelerate with ATP therapy. The number of ATP bursts and the use of ramp had a significant effect on VT acceleration. To avoid VT acceleration by ATP therapy, ramp pacing better be avoided, especially in fast VTs, and lesser number of bursts should be delivered.

Antitachycardia pacing at the His bundle is safer than conventional right ventricular antitachycardia pacing in a canine myocardial ischemic injury model.

Antitachycardia pacing (ATP) is used to terminate ventricular tachycardia (VT) by delivering rapid, low energy pacing to the right ventricle (RV). Unfortunately, ATP is not effective against all VT episodes and can result in adverse outcomes, such as VT acceleration and degeneration into ventricular fibrillation (VF). Improving ATP is therefore desirable. Our objective was to compare the efficacy and safety of ATP delivered at the His bundle to traditional ATP. Six dogs were anesthetized and pacing leads were implanted in the RV and His bundle. The left anterior descending artery was occluded for 2 h to create an ischemic injury. In a study 4-7 days later, a 128-electrode sock was placed snugly around the ventricles and VT was induced using rapid pacing. ATP was delivered from either the His bundle or RV lead, then attempted at the other location if unsuccessful. Success rates and instances of VT acceleration and degeneration into VF were calculated. We induced 83 runs of VT and attempted ATP 128 times. RV ATP was successful in 36% of attempts; His ATP was successful in 38% of attempts. RV ATP resulted in significantly more adverse outcomes. RV and His ATP induced VT acceleration in 9% and 3% of trains, respectively, and induced degeneration into VF in 5% and 1% of trains, respectively. His bundle ATP is safer, but not significantly more effective, than RV ATP.

PO-05-082 ANTITACHYCARDIA PACING IS MORE EFFECTIVE WHEN DELIVERED TO THE LEFT BUNDLE BRANCH COMPARED TO THE RIGHT VENTRICLE IN A CANINE ISCHEMIC VENTRICULAR TACHYCARDIA MODEL

Implantable cardioverter-defibrillators (ICDs) can terminate ventricular tachycardia (VT) with Antitachycardia pacing (ATP) delivered to a right ventricular (RV) pacing lead, thereby avoiding painful and damaging high-energy shocks. However, ATP efficacy is limited for fast VT, and ATP can accelerate VT or convert VT to ventricular fibrillation (VF). Physiological pacing delivered to the left bundle branch (LBB) has emerged as a clinically relevant target to minimize ventricular dyssynchrony and pacing-induced heart failure. ATP efficacy and safety delivered to the LBB are yet to be investigated. Evaluate the therapeutic efficacy and safety of ATP delivered to an LBB lead compared to ATP delivered to a conventional RV lead. In 6 anesthetized dogs, pacing leads from two ICDs (CobaltTM XT DR, Medtronic, Inc) were implanted at the RV apex (6947 Sprint Quattro SecureTM, Medtronic, Inc) and the LBB (3830 SelectSecureTM, Medtronic, Inc). A lateral thoracotomy procedure was performed, and a two-hour lateral anterior descending artery ischemia-reperfusion injury was caused. The thoracotomy was closed and on post-infarct day 4, dogs were anesthetized, and sustained VT episodes were induced by programmed electrical stimulation. ATP (up to 5 trains of 8 pulses at approximately 88% of the VT cycle length) was delivered to either the LBB or RV pacing site in a randomized fashion. The success rate of ATP in terminating the VT episodes and the rate of VT acceleration and degeneration into VF from both pacing locations were evaluated. In our canine ischemic VT model, VT was induced 80 times, with a mean VT cycle length of 178±35 ms. ATP was delivered and tested for each episode. For ATP delivered to the RV, the success rate for terminating VT was 54%. The success rate for terminating VT for ATP delivered to the LBB was 73% (Fig. A, p < 0.05). ATP resulted in VT acceleration for 10% and 5% of ATP attempts delivered to the RV and LV, respectively (Fig. B, p = Not Significant, NS). Degeneration to VF occurred for 5% of all ATP attempts delivered to the RV, and there was no such incident for ATP delivered to the LBB (Fig. B). Higher efficacy and lower incidence of VT acceleration were observed with ATP delivered to LBB compared to ATP delivered to the RV in this canine ischemic VT model. Improved performance of ATP delivered to LBB compared to RV provides additional incentive for expanded use of LBB leads for pacing and therapy delivery.

PO-05-056 FAILURE OF INTRINSIC ANTI-TACHYCARDIA PACING TO TERMINATE VENTRICULAR TACHYCARDIA AND POTENTIAL PROARRHYTHMIC EFFECTS

Intrinsic anti-tachycardia pacing (iATP™) is a novel, automated ATP algorithm that provides individualized therapy to terminate ventricular tachycardia (VT). If the first ATP attempt is unsuccessful, the algorithm analyzes the tachycardia cycle length and the post-pacing interval (PPI) and adjusts the subsequent sequence to successfully terminate VT. This algorithm was effective in a single clinical study without a comparator arm and case reports have corroborated this success in clinical practice. Despite the previously presented data, iATP™ failure has not been well documented in the literature. We present the first case series of iATP™ failure in routine clinical practice with detailed episode analysis and the apprise the electrophysiology community of the potential proarrhythmic effect of the algorithm. We retrospectively evaluated 262 patients with Medtronic Cobalt XT defibrillators followed at Mayo Clinic campuses in Minnesota, Florida, and Arizona. 119 patients had devices with the iATP™ feature turned on. 4 out of 119 patients (3.36%) had an acceleration of their ventricular arrhythmias within our cohort. Illustrative Case: A 74-year-old male with a history of idiopathic, non-ischemic cardiomyopathy (LVEF) 21%) status post-cardiac resynchronization therapy (CRT)-defibrillator for primary prevention, subsequent VT, and atrial fibrillation presented to our heart rhythm clinic for evaluation of syncope. The patient was riding an all-terrain vehicle when he felt a sudden onset of dyspnea and pre-syncope. His device interrogation revealed a presenting rhythm of VT at 200 beats per minute (bpm). The patient underwent four unsuccessful rounds of ATP. The 4th round of ATP resulted in acceleration (figure 1A) and degeneration into ventricular fibrillation (VF), followed by a successful 39.5 J shock (figure 1B). Figure 1C shows the dot plot for the entire episode with the blue box highlighting the acceleration in ventricular rate after the 4th ATP sequence. Given concern for a proarrhythmic effect, iATP™ was turned off. The patient was treated with amiodarone and mexiletine and underwent endocardial ablation with substrate modification in the inferolateral LV. He is currently doing well without a subsequent need for VT therapies. While the novel adaptive algorithm and its underlying concepts are intriguing, clinicians should be aware of the potential for acceleration and degeneration of VT by iATP™ and prepared to turn off the feature when this occurs.

Efficacy of intrinsic antitachycardia pacing for ventricular tachycardia refractory to conventional burst pacing: A case series.

Intrinsic antitachycardia pacing (iATP) is a novel automated ventricular ATP algorithm that designs ATP sequences based on the analysis of prior failed ATP. Real-world data on the efficacy and safety of iATP are lacking. Among 124 ventricular tachycardia (VT) episodes in 130 consecutive patients (mean age at implantation: 63.8 ± 14.9 years; sex, 95 male and 35 female) for whom implantable cardioverter defibrillator or cardiac resynchronization therapy defibrillator equipped with iATP algorithm was implanted, we investigated the efficacy and safety of iATP for VT refractory to conventional burst pacing.Eight patients had a total of 17 episodes of iATP therapy after failed conventional burst pacing within 11.2 ± 6.6 months of follow-up. Eleven VT episodes (64.7%) in seven patients (87.5%) were successfully terminated by iATP, and only one patient (12.5%) experienced VT acceleration.iATP might be useful for VTs refractory to conventional burst pacing with a low risk of VT acceleration.

PO-678-03 ANTITACHYCARDIA PACING AT THE HIS BUNDLE IS SAFER THAN TRADITIONAL RIGHT VENTRICULAR ANTITACHYCARDIA PACING IN A CANINE MYOCARDIAL INFARCTION MODEL

Antitachycardia pacing (ATP) therapy delivers low-energy pacing to the right ventricle (RV) to terminate episodes of ventricular tachycardia (VT). While this treatment has reduced instances of high-energy shocks in patients, some episodes of VT are less responsive to ATP, and adverse events, such as VT acceleration and degeneration into VF, remain a concern. Improving the success rate and safety of ATP is therefore desirable.

Short-time ventricular tachycardia ablation for cardiac sarcoidosis using coherent map.

A 69‐year‐old woman with isolated cardiac sarcoidosis was hospitalized for frequent appropriate implantable converter defibrillator therapies for ventricular tachycardia (VT) despite of favorably controlled condition with oral prednisolone. The patient underwent urgent catheter ablation with CARTO 3D mapping system. Although the voltage map, activation map, and propagation map during VT could not visualize the tachycardia circuit, the coherent map clarified entrance and exit sites of the tachycardia circuit with slow or nonconducting (SNO) zones, which seemed like a figure‐of‐eight circuit. Considering the risk of VT termination or acceleration to rapid unstable VT, neither entrainment nor pacing studies were performed. The VT was terminated near the exit site of the isthmus where tiny pre‐systolic potential was detected. Any diastolic potentials could not be detected. This meant that the critical isthmus might be located at the epicardium or deep incite of the left‐ventricular myocardium where the coherent map showed as SNO zones. We should recognize coherent map as artificial that may represent VT circuit as if complete endocardial reentry even if not. The procedural time from mapping to termination of VT was only 22 minutes. The patient has been free from any cardiovascular events after the procedure. Coherent map might be feasible for revealing the critical isthmus of hemodynamically stable VTs without using electrophysiological techniques, including entrainment, pacing study, and voltage map during own beats, and would enable us to achieve successful VT ablation in a short time.

RR interval variability in the evaluation of ventricular tachycardia and effects of implantable cardioverter defibrillator therapy.

BackgroundAn implantable cardioverter defibrillator (ICD) is the most reliable therapeutic device for preventing sudden cardiac death in patients with sustained ventricular tachycardia (VT). Regarding its effectiveness, targeted VT is defined based on the tachyarrhythmia cycle length. However, variations in RR interval variability of VTs may occur. Few studies have reported on VT characteristics and effects of ICD therapy according to the RR interval variability. We aimed to identify the clinical characteristics of VTs and ICD therapy effects according to the RR interval variability.MethodsWe analyzed 821 VT episodes in 69 patients with ICDs or cardiac resynchronization therapy defibrillators. VTs were classified as irregular when the difference between two successive beats was >20 ms in at least one of 10 RR intervals; otherwise, they were classified as regular. We evaluated successful termination using anti‐tachycardia pacing (ATP)/shock therapy, spontaneous termination, and acceleration between regular and irregular VTs. The RR interval variability reproducibility rates were evaluated.ResultsRegular VT was significantly more successfully terminated than irregular VT by ATP. No significant difference was found in shock therapy or VT acceleration between the regular and irregular VTs. Spontaneous termination occurred significantly more often in irregular than in regular VT cases. The reproducibility rates of RR interval variability in each episode and in all episodes were 89% and 73%, respectively.ConclusionsATP therapy showed greater effectiveness for regular than for irregular VT. Spontaneous termination was more common in irregular than in regular VT. RR interval variability of VTs seems to be reproducible.

What factors lead to the acceleration of ventricular tachycardia during antitachycardia pacing?-Results from over 1000 episodes.

IntroductionVentricular tachycardia (VT) acceleration due to antitachycardia pacing (ATP) therapy could be often observed in patients with implantable cardioverter defibrillator (ICD), which usually results in additional shock. However, few studies focused on the risk factors for VT acceleration caused by ATP therapy. The purpose of this study was to investigate risk factors for VT acceleration due to ATP delivery.MethodsWe retrospectively reviewed 1056 ATP episodes in 33 patients with structural heart diseases, of whom clinical characteristics and episodes details were evaluated.ResultsAt individual patient level, number of VT morphologies recorded in electrograms during follow‐up was a risk factor with cutoff point of 1 (AUC 0.79, sensitivity 72.7%, specificity 77.3%, P < .001) to predict ATP acceleration (OR 3.50, P = .008). From episode‐based analysis, VT cycle length (VTCL) and mean variation in VTCL were risk factors to predict ATP acceleration (OR 0.98, P < 0.001 vs OR 1.06, P < .001, respectively), with cutoff points of 347 ms (AUC 0.67, sensitivity 82.5%, specificity 47.6%, P < .001) and 7.3 ms (AUC 0.66, sensitivity 77.5%, specificity 56.7%, P < .001), respectively. In addition, VTs with cycle length less than 347 ms were more likely to be accelerated by burst stimulation with more pulse numbers (OR 3.31, P < .001).ConclusionsNumber of VT morphologies, VTCL, and mean variation in VTCL are risk factors predicting ATP acceleration. Burst stimulation with less pulse numbers should be performed in VTs with cycle length less than 347 ms.

Comparison of the “Real-life” Diagnostic Value of Two Recently Published Electrocardiogram Methods for the Differential Diagnosis of Wide QRS Complex Tachycardias

The diagnostic values of the aVR lead or "Vereckei algorithm," and the lead II R-wave peak time (RWPT) criterion, recently devised for the differential diagnosis of wide QRS complex tachycardias (WCTs), were compared. A total of 212 WCTs (142 ventricular tachycardias [VTs], 62 supraventricular tachycardias [SVT], and eight preexcitation SVTs) from 145 patients with proven electrophysiologic diagnoses were retrospectively analyzed by seven examiners blinded to the electrophysiologic diagnoses. The overall test accuracy of the Vereckei algorithm was superior to that of the RWPT criterion (84.3% vs. 79.6%; p = 0.0003). The sensitivity of the Vereckei algorithm for VT diagnosis was greater than that of RWPT criterion (92.4% vs. 79.1%; p < 0.0001). The negative predictive value (NPV) for the Vereckei algorithm was also greater (77.8%; 95% confidence interval [CI] = 73.6% to 82.1%) than that of the RWPT criterion (61.6%; 95% CI = 57.6% to 65.6%). The specificity of the Vereckei algorithm was lower than that of the RWPT criterion (64.7% vs. 80.9%; p < 0.0001). The positive predictive value (PPV) was also lower for the Vereckei algorithm (86.4%; 95% CI = 84.4% to 88.4%) than for the RWPT criterion (90.9%; 95% CI = 89.1% to 92.8%). Incorrect diagnoses made by the Vereckei algorithm were mainly due to misdiagnosis of SVT as VT (65.7% of cases), and those made by the RWPT criterion were due to the more dangerous misdiagnosis of VT as SVT (72.5% of cases). The Vereckei algorithm was superior in overall test accuracy, sensitivity, and NPV for VT diagnosis and inferior in specificity and PPV to the RWPT criterion. All of these parameters were lower in "real life" than those reported by the original authors for each of the particular electrocardiographic methods.

Saving lives and reducing inappropriate device therapy: The MADIT family of implantable cardioverter-defibrillator and cardiac resynchronization therapy trials

In 1980, Mirowski et al. [1] reported the first 3 patients treated with an automatic implantable defibrillator (AID). At that time, the AID was implanted with electrodes attached to the epicardium through a surgical thoracotomy with the battery portion of the unit placed undeer the skin in the abdominal wall. The AID detected the onset of ventricular fibrillation through a unique algorithm and the device was considered a “shock box” since shock was the only therapy delivered. The U.S. Food and Drug Administration (FDA) initially provided approval for use of the AID device in high-risk cardiac patients who had been resuscitated from a prior aborted cardiac arrest. Around the same time frame, Medtronic developed a pacing approach (antitachycardia pacing [ATP]) to terminate rapid ventricular tachycardia (VT) by delivering a series of appropriately timed pacing stimuli in the interval between the QRS and T-wave complexes of the tachycardia (review article [2]). This pacing technique was effective in terminating VT in a majority of patients with ventricular tachyarrhythmias. However, this ATP approach produced acceleration of VT and even ventricular fibrillation and sudden death in a small percentage of patients, and ATP therapy was not approved by the FDA as a stand-alone therapy. The AID was initially developed by Drs. Mirowski and Mower in association with Dr. M. Stephen Heilman at the Medrad/Intec Company in Pittsburgh, Pennsylvania, and the implantable defibrillator was subsequently sold to CPI/Guidant Corporation in 1985. Although CPI/Guidant and Medtronic were competitors in the pacemaker field, both companies recognized the need for a device with tiered therapy that would include ATP and defibrillation. Through a cooperative agreement, CPI/Guidant and Medtronic jointly agreed on a device involving ATP and shock therapy, called the automatic implantable cardioverter defibrillator (AICD) for treating patients at risk for life-threatening VT and/or ventricular fibrillation.

Efficacy and safety of different antitachycardia pacing sites in the termination of ventricular tachycardia in patients with biventricular implantable cardioverter-defibrillator

We sought to evaluate the efficacy and safety of different antitachycardia pacing (ATP) sites in heart failure (HF) patients with a biventricular implantable cardioverter-defibrillator (ICD). Between January 2003 and December 2008, 89 consecutive patients with biventricular (BiV) ICDs (Medtronic Inc., St Paul, Minnesota, USA) were enrolled. In these patients, stored electrograms of the true spontaneous ventricular tachycardia (VT) episodes with at least one ATP therapy were analysed. Out of the 89 patients, 46 experienced 259 VT episodes. When we considered all VT forms, both left ventricular (LV)-ATP (91%) and BiV-ATP (89%) were significantly better than right ventricular (RV)-ATP (72%) in terminating VTs (P = 0.03 and 0.04, respectively). In the fastVT zone, there was a trend for higher efficacy of BiV-ATP compared with RV-ATP and LV-ATP (75 vs. 60 vs. 60%, P = 0.10). Fast VT acceleration occurred to a similar extent in all ATP groups (20% in RV-ATP vs. 20% in LV-ATP vs. 20% in BiV-ATP, P = NS). In the slow VT zone, RV-ATP was significantly less effective than LV-ATP (74 vs. 100%, P = 0.001) and BiV-ATP (74 vs. 100%, P = 0.014). Incidence of acceleration was lower with LV-ATP and BiV-ATP than RV-ATP (0 vs. 0 vs. 9%, P = 0.03) in the slow VT zone. In HF patients treated with BiV ICD, overall ATP efficacy is higher when delivered from LV or BiV than from RV. Biventricular-ATP and LV-ATP are also safer than RV-ATP in the slow VT zone.

Efficacy of Chest Thump Version for Ventricular Arrhythmias

Purpose Electrical cardioversion for ventricular arrhythmias (VAs) contained of ventricular tachycardia (VT), ventricular fibrillation (VF) and torsades de pointes (TdP), was established to be effective for VAs. Little is known about which case should have an effect on chest thump version (TV) in patients with VAs. Method Subjects were 18 patients (Male: Female = 9:9, mean age 61±20 years old). TV was done for 28 episodes in VT, 8 episodes in VF, and 5 episodes in TdP. TV was performed after onset of symptoms within one minutes, and electrocardiogram (ECG) monitor was analyzed. Heart beats were averaged with 10 beats of VF and TdP. The time from Q wave to TV was measured from ECG monitoring in VT patients. Result TV successfully terminated VT in 12 of 28 episodes, VF in 1 of 8 episodes, and 1 of 5 episodes. TV terminated VT in the range between -20ms and +60ms. The mean cycle length of VT was 284±30ms, VF was 238±21ms, and TdP was 270±25ms, respectively. The mean cycle length of successful TV was significantly longer than that of failed TV in VT (358±57ms vs 289±59ms, p<0.01). There was no acceleration of VT in this study. Conclusion TV was available for slower VT at the timing in the range between -20ms and +60ms, and not for TdP and VF.

Adenosine: an effective and safe antiarrhythmic drug in pediatrics.

Adenosine is an effective, safe drug for the diagnosis and treatment of paroxysmal tachycardias in adult and pediatric patients. A starting dose of 0.05-0.10 mg/kg as a rapid bolus injection is recommended for infants and children. An electrophysiologic effect can be expected within 20 seconds after injection. Dosage may be increased up to 0.3 mg/kg in steps of 0.05-0.10 mg/kg or until conversion to sinus rhythm is reached. Due to its basic electrophysiologic properties of slowing conduction in the atrioventricular (AV) node, which may result in transient AV block, adenosine is almost always effective in terminating supraventricular tachycardias in which the AV node forms a critical part of the reentrant circuit (i.e., AV nodal reentrant tachycardia and AV reciprocating tachycardia). Based on its properties, adenosine is also advocated as a useful diagnostic tool for unmasking primary atrial tachycardias by inducing transient high grade AV block. Advantages over other antiarrhythmic agents include the agent's short half-life (<2 seconds) and minimal or no negative influence on blood pressure. Because of its short half-life, however, early recurrence of the tachycardia is observed in up to one-third of patients treated. Based on rare but serious unwanted side effects, patients with known or suspected irritable airways and sinus node dysfunction and those who have undergone orthotopic cardiac transplantation should probably not be given adenosine. Adenosine may be recommended as the drug of choice for treatment of paroxysmal tachycardia in young patients. Primary success rates range between 85% and 100% of all the tachycardia episodes treated. Termination of the tachydysrhythmia, however, does not always mean that the underlying dysrhythmia was of supraventricular origin with the AV node as a critical part of the tachycardia mechanism. Rare but possible life-threatening side effects (prolonged sinus arrest and complete AV block, atrial fibrillation, acceleration of ventricular tachycardia, apnea) necessitate proper monitoring of the patients.

Implantation and Follow‐Up of a Third‐Generation Cardioverter Defibrillator: Comparison of Epicardial and Nonthoracotomy Defibrillation Lead System

The intraoperative and follow-up results were compared in 67 patients with ventricular tachyarrhythmias who underwent implantation of the Ventritex Cadence defibrillator with either epicardial patch (EPI, 25 patients) or nonthoracotomy CPI Endotak (ENDO, 42 patients) defibrillation lead systems. There was no significant difference between groups in age, sex, structural heart disease, ejection fraction, arrhythmia history, or drug therapy. Successful implantation was accomplished in all patients using either lead system. In the ENDO group, 35 patients (83%) had a defibrillation threshold < or = 550 V and did not require a subcutaneous patch. Intraoperatively, the defibrillation threshold was 453 +/- 139 V (13 +/- 9 J) for EPI and 490 +/- 113 V (15 +/- 8 J) for ENDO (P = NS). There were no perioperative deaths in either group. At predischarge testing, the defibrillation threshold was 445 +/- 183 V (14 +/- 12 J) for EPI and 439 +/- 133 V (13 +/- 7 J) for ENDO (P = NS). During a mean follow-up of 16 +/- 8 months, there were no sudden deaths, and four patients died from congestive heart failure (3 EPI, 1 ENDO). During follow-up, 916 spontaneous arrhythmia episodes occurred in 16 of 25 EPI patients (64%) and 967 episodes occurred in 31 of 42 ENDO patients (74%) (P = NS). The number of episodes detected as ventricular fibrillation were 192 for EPI (21%) and 232 for ENDO (24%), with first shock success in 76% and 75%, respectively; all episodes were successfully terminated by the device. In the remaining episodes detected as ventricular tachycardia, antitachycardia pacing was attempted and was successful in 672 of 724 episodes (93%) with EPI and 666 of 735 episodes (91%) with ENDO lead systems (P = NS). Acceleration of ventricular tachycardia with antitachycardia pacing occurred in 21 episodes (3%) with EPI and in 37 episodes (5%) with ENDO leads (P = NS). A nonthoracotomy approach using the third generation cardioverter defibrillator Cadence V-100 is safe and effective and has clinical results that are not significantly different from epicardial defibrillation lead systems.

Effect of shock timing on efficasy and safety of internal cardioversion for ventricular tachycardia

Objectives. We examined the effect of shock timing within the QRS complex on cardioversion efficacy in a randomized crossover test of shocks delivered at two timing intervals relative to QRS onset.Background. The local ventricular electrogram is used in implantable cardioverter-defibrillators to synchronize cardioversion shocks to terminate ventricular tachycardia. However, the timing of the local electrogram relative to global ventricular depolarization is variable, depending on the site of ventricular tachycardia origin.Methods. Transvenous detibrillation leads were positioned in the right ventricular apex (cathode), coronary sinus and superior vena cava (anodes) of patients with sustained monomorphic ventricular tachycardia. After repeat ventricular tachycardia induction, sequential shocks with energy settings of 0.5 to 22 J were delivered simultaneously with QRS onset (QRS + 0 shock) or 100 ms after QRS onset (QRS + 100 shock). QRS onset was determined from the surface electrocardiogram. Cardioversion threshold, defined as the lowest shock energy for successful ventricular tachycardia termination, was measured for these two timings.Results. Fifteen patients (13 men, 2 women; mean [± SD] age 60.5 ± 7.7 years) completed testing. Cardioversion threshold was significantly lower with QRS + 100 shocks than QRS + 0 shocks (3.1 ± 3.5 vs. 10.5 ± 7.4 J, p < 0.01). Thirteen patients (87%) experienced ventricular tachycardia acceleration with QRS + 0 shocks, but only three patients (20%) had ventricular tachycardia acceleration using QRS + 100 shocks (p < 0.01). Of the 32 failed QRS + 0 shocks, 25 (78%) caused ventricular tachycardia acceleration, whereas only 5 (36%) of the 14 failed QRS + 100 shocks caused ventricular tachycardia acceleration (p < 0.05). Cardioversion threshold was not correlated with ventricular tachycardia cycle length, QRS duration, left ventricular ejection fraction or left ventricular diastolic volume (p = NS).Conclusions. Internal cardioversion shocks delivered late in the QRS complex during ventricular tachycardia are more effective and have a lower risk of ventricular tachycardia acceleration than those delivered near QRS onset.

Effects of heptanol, class Ic, and class III drugs on reentrant ventricular tachycardia. Importance of the excitable gap for the inducibility of double-wave reentry.

Double-wave reentry (DWR) can be a mechanism for acceleration of ventricular tachycardia (VT) with a large excitable gap (EG). The purpose of this study was to determine the effects of heptanol, class Ic, and class III drugs on the inducibility of DWR. In 11 Langendorff-perfused rabbit hearts, a thin ring of anisotropic left ventricular epicardium was created by a cryoprocedure. VT with a revolution time of 180 +/- 26 milliseconds and an EG of 106 +/- 8 milliseconds was induced by incremental pacing. During control, entrainment with 10 stimuli at a 99 +/- 15-millisecond interval terminated VT in seven hearts. In four hearts VT was accelerated from 205 +/- 24 to 115 +/- 14 milliseconds by introduction of a second circulating wave in the ring. In the seven VTs that could not be accelerated, 0.5 mumol/L Org7797 (class Ic) and 1.0 mmol/L heptanol (uncoupling agent) prolonged the cycle length of VT by 32% and 37%, respectively. Because the refractory period (RP) only increased by 11%, the EG prolonged by 71% and the ratio between EG and RP was increased from 0.66 to 1.00. Under these conditions, DWR could be induced in all seven hearts. In the four VTs that could be accelerated during control, administration of the class III drug D-sotalol (35 mumol/L) only slightly slowed VT by 6%. Because the RP was prolonged by 15%, the ratio between the EG and the RP decreased from 0.76 to 0.63. Entrainment now failed to accelerate VT in two of four hearts, whereas in the two other hearts, double-wave reentry self-terminated within eight cycles. Drugs that increase the ratio of EG and RP enhance the susceptibility to acceleration of VT, whereas drugs that decrease this ratio prevent induction of sustained double-wave reentry.

Interaction of acute ventricular dilatation and d-sotalol during sustained reentrant ventricular tachycardia around a fixed obstacle.

Antiarrhythmic therapy of ventricular tachycardia is associated with decreased efficacy and increased proarrhythmia in patients with congestive heart failure, but the explanation for these observations is not known. This study examined the interaction of ventricular dilatation and d-sotalol in a model of reentry ventricular tachycardia. Thin epicardial layers of anisotropic myocardium were created in Langendorff-perfused rabbit left ventricles by a cryo procedure. A fluid-filled, latex balloon was secured within the left ventricle to change ventricular volume. Sustained reentrant ventricular tachycardia, around a central cryolesion, was induced by rapid pacing in all preparations (n = 7). Epicardial mapping was performed through 248 electrodes. Single premature beats introduced within the reentry circuit were used to define the excitable gap. Dilatation did not influence ventricular tachycardia cycle length or conduction velocity. A 1.25-mL increase in left ventricular volume widened the excitable gap by 12% (range, 5% to 29%) (P < .001) because of a decrease in myocardial refractoriness. d-Sotalol (final concentration, 10 mg/L) narrowed the excitable gap 18% (range, 7% to 29%) (P = .002) in the undilated left ventricle. d-Sotalol was less effective in the dilated left ventricle, narrowing the excitable gap only 9%, a difference that was not statistically significant. During pacing to induce or terminate tachycardia, tachycardia acceleration was observed significantly more frequently in the dilated than in the undilated ventricle. Ventricular tachycardia acceleration was due to the development of double-wave reentry (two successive waves traveling in the same circuit in the same direction). d-Sotalol, which narrowed the excitable gap, prevented tachycardia acceleration and double-wave reentry. Antiarrhythmic efficacy may be decreased by dilatation because of widening of the initial excitable gap and a decrease in the gap-narrowing effect of these agents. Double-wave reentry, more likely with a widening of excitable gap, may partially explain tachycardia acceleration in the dilated ventricle.

A prospective randomized comparison of autodecremental pacing to burst pacing in device therapy for chronic ventricular tachycardia secondary to coronary artery disease

A number of modes of antitachycardia pacing therapies are available in the newer generations of implantable cardioverter/defibrillators. The efficacy of synchronized burst overdrive pacing for the termination of induced and spontaneous monomorphic ventricular tachycardia (VT) was compared with synchronized autodecremental (ramp) pacing in 21 patients who received an implantable antitachycardia pacemaker/cardioverter/defibrillator for treatment of recurrent sustained monomorphic VT. Patients undergoing serial noninvasive VT induction studies after device implantation were prospectively randomized to receive trials of burst or ramp pacing therapies in a crossover study design. Antitachycardia pacing therapies were equally efficacious in treating induced VT (68% for ramp, 76% for burst pacing trials). The efficacy of ramp (93%) and burst (96%) pacing therapies was significantly higher in terminating spontaneously occurring episodes of VT than in terminating induced episodes (p = 0.001). The incidence of tachycardia acceleration was similar for both modes of pacing. The incidence of VT acceleration was lower for spontaneously occurring episodes of VT (0.01%) than for induced episodes of VT (6%, p < 0.01). Thus, antitachycardia pacing is an effective therapy for episodes of monomorphic VT, and the risk of accelerating VT to a hemodynamically unstable form is low. Antitachycardia pacing therapies are more effective against spontaneously occurring episodes than induced episodes of VT. Differences in tachycardia cycle length and duration may contribute to these effects.