Antitachycardia Pacing Algorithms Research Articles

Patient-activated anti-tachycardia pacing in adult congenital heart disease.

IntroductionIn adults with congenital heart disease, intra‐atrial reentrant tachycardia (IART) is a common arrhythmia that causes significant morbidity and mortality. One treatment option for IART is antitachycardia pacing. Atrial antitachycardia pacing algorithms deliver therapy for IART with ≥2:1 conduction, but most algorithms will not recognize IART with 1:1 conduction. Temporary Patient Activated Rx (TPARx) is Medtronic software that can be installed in antitachycardia pacemakers allowing patients to deliver therapies on demand for IART with 1:1 conduction.MethodsRetrospective chart review at a single institution of all patients who had TPARx installed into their pacemaker.ResultsFour adults with single ventricle congenital heart disease and IART underwent Fontan conversion, arrhythmia surgery, and placement of an epicardial dual‐chamber antitachycardia pacemaker. They had recurrent IART with a long cycle length and 1:1 conduction that failed to trigger antitachycardia pacing therapies. TPARx software was programmed into their pacemakers to allow recognition and treatment of IART with 1:1 conduction. Mean follow‐up duration after TPARx programming was 4.9 years. Each patient received at least one successful antitachycardia pacing therapy via TPARx – range 0.4–26 treated IART episodes per year. There were no atrial or ventricular arrhythmias induced with antitachycardia pacing. Two patients were able to discontinue anticoagulation after TPARx installation.ConclusionThis series demonstrates the use of TPARx software as part of a long‐term IART management strategy in select patients with IART who have failed more conventional therapies.

Forecasting episodes of atrial fibrillation using a new machine learning algorithm

The performance of preventive pacing algorithms (PPA) that can reduce atrial fibrillation (AF) burden in cardiac electronic implanted devices (CEID's) has been disappointing. This can be due to the fact that the time frame between the start of AF and the implementation of preventive stimulation and anti-tachycardia pacing algorithms is too short. Nowadays, machine learning algorithms are powerful tools and have proven their ability to anticipate events. Therefore, we assessed forecasting of paroxysmal AF minutes before its onset using machine learning techniques. To forecast an oncoming AF episode in individual patients using machine learning techniques and to assess when a change in heart rate indicates the beginning of a possible forecast. We analysed retrospectively the raw data of a data set of 10484 ECG Holter monitorings searching for AF episodes of more than 30 sec. A hundred and forty patients presented paroxysmal AF (286 recorded AF episodes). We used only RR intervals to predict the presence of AF. It should be emphasized that we did not integrate clinical variables. We developed a deep and recurrent neural net machine learning algorithm. This algorithm was trained on using 90% of patients records and tested on the remaining 10%. Rather than attempting to predict the exact RR-interval at which AF would or would not happen our algorithm attempted to predict if AF would happen within windows of time of 30 RR intervals ( Table 1 ). The performance figures are summarized in the table. Based upon this retrospective study, AF can be forecasted thirty beats before its onset with a reasonable sensitivity, using our machine learning algorithm. We believe that its embedding in CEID's could lower AF burden by improving results of PPA in selected patients.

Programming Pacemakers to Reduce and Terminate Atrial Fibrillation.

The goal of this paper is to review present knowledge regarding preventive and antitachycardia pacing algorithms, aimed to reduce atrial fibrillation (AF) burden in patients when pacing is indicated. Reactive antitachycardia pacing (ATP), the new generation of ATP, is significantly associated with a reduced risk of AF. In patients with indication for pacing and history of AF, pacemakers endowed with atrial preventive pacing and atrial ATP combined with managed ventricular pacing proved superior to standard dual-chamber pacing. Managed ventricular pacing is an algorithm that minimizes unnecessary right ventricular pacing. Progression to persistent AF is prevented by ventricular pacing minimization in patients with normal PR interval. The synergistic effect of pacemakers that combine atrial preventive pacing with reactive ATP and with algorithms that minimize ventricular pacing can reduce AF incidence and decrease the combined endpoint of permanent AF, hospital admissions, and mortality.

The Australian History of Cardiac Pacing: Memories from a Bygone Era

Although Dr Albert Hyman in New York is believed to have built the first cardiac pacemaker in 1932, he acknowledges Dr Mark Lidwell in Sydney, Australia as having not only built a pacemaker, but also successfully used it to resuscitate a newborn infant in or before 1929. Fully implantable pacemakers, however, were not possible until 1958, following the development of the silicon transistor. Within three years of that first implant, a pulse generator attached to epicardial leads was implanted at the Royal Melbourne Hospital. About the same time, an engineer in Sydney with intermittent complete heart block who had received epicardial leads and an external pulse generator proposed a simple sensing circuit, leading to the design of the first demand pacing system. By the mid 1960s, physicians were inserting transvenous leads in the right ventricle attached to pulse generators implanted in the anterior abdominal wall. In 1963, an Australian pacemaker company, Telectronics, was founded in Sydney. This innovative company-designed many of the features of transvenous leads and pulse generators we take for granted today. Australia also played a leading role in the design or early evaluation of the lithium power source, lead fixation, steroid elution, automatic anti-tachycardia pacing algorithms and the minute ventilation rate adaptive sensor. This manuscript describes the challenges and frustrations of those pioneers: physicians, surgeons and biomedical engineers.

Should Catheter Ablation be the Preferred Therapy for Reducing ICD Shocks?

In 1980, Mirowski et al1 implanted the first implantable cardioverter-defibrillator (ICD) in a young female with recurrent ventricular fibrillation and provided an innovative approach to aborted sudden cardiac death (SCD). Although the ICD was considered a treatment of last resort during that incipient stage, subsequent years have witnessed prolific expansion of indications for ICD implantation.2 Several large-scale clinical trials have demonstrated its efficacy for both primary and secondary prevention of SCD in patients with ischemic and nonischemic cardiomyopathy.3,4 ICD therapy in such high-risk patients has been shown to improve survival compared with conventional antiarrhythmic drug therapy alone.3,4 The number of ICD implantations has increased significantly in the last decade, with a concurrent decrease in the use of stand-alone antiarrhythmic drugs for ventricular indications.5–7 Current ICDs have sophisticated programming capabilities, atrial and bipolar leads, and are able to deliver antitachycardia pacing algorithms (ATP) in addition to defibrillating shocks. Response by Kuck on p 705 Typically, patients who receive ICDs are at high risk for recurrent arrhythmia; hence, most patients receive 1 or more ICD therapies for spontaneous arrhythmias after implantation.3 Despite the technological evolution of ICD systems, more than 20% of shocks are due to supraventricular arrhythmia and hence are inappropriate.8–10 The ICD uses ATP or defibrillating shocks to terminate episodes of ventricular tachycardia (VT) or ventricular fibrillation (VF). Although the ICD aborts VT/VF, many patients continue to have symptoms such as dizziness, palpitations, nervousness, flushing, or syncope before receiving an ICD shock.11 When the shock is finally delivered, it is physically and emotionally painful and so noxious that 23% of patients dread shocks and 5% of patients prefer to do without an ICD and “take their chances.”12 A significant prevalence of sadness, depression, and even anxiety disorders have been reported after …

Atrial Fibrillation: Focal or Reentrant or Both?

Ablation for atrial fibrillation (AF) is a genuinely viable and increasingly used option for improving quality of life in patients with symptomatic drug-refractory AF. What is remarkable about the limited success achieved with these procedures is that progress has occurred despite a near complete lack of knowledge about what causes or maintains AF. Focal origins for AF were first demonstrated decades ago1–4 with topical application of acetylcholine to junctional tissues and atrial sites triggering AF. More recently, there has been convincing documentation of rapid tachycardia arising from the pulmonary veins inciting AF, thus supporting the concept of “trigger elimination” contributing to the success of pulmonary vein isolation. However, studies also support the presence of multiple reentrant circuits maintaining and possibly initiating AF.5, 6 The ablation era has taught us7–9 that in persistent and chronic AF, trigger elimination alone is not enough and that substrate modification is probably necessary to decrease the likelihood of reentrant wavelet continuance and thereby increase success rates. Even the most ardent supporter of either hypothesis recognizes the limitations of each. How can a focal source exist in this milieu indefinitely, producing and maintaining chronic AF, and how do multiple reentrant wavelets arise spontaneously? Article see p 384 In this issue of Circulation: Arrhythmia and Electrophysiology , Niu et al10 provide important, interesting, and novel insights into solving this age-old riddle using a previously unexplored angle-autonomic manipulation. Acetylcholine was used to induce AF in 31 canines. In 12 of the animal studies, propafenone was administered. They then ablated the ganglionated plexi (GP). Before ablation, AF could still be induced despite administration of propafenone. After ablation, there was a consistent pattern of electrogram organization and atrial synchronization. In addition, subsequent administration of propafenone resulted in the inability to induce atrial tachyarrhythmia. There are several …

Clinical trials of pacing for maintenance of sinus rhythm.

Several prospective randomized clinical trials have demonstrated that atrial-based pacing prevents the development of paroxysmal and persistent atrial fibrillation (AF) in patients with symptomatic bradycardia as the indication for a pacemaker. The greatest benefit appears to be in patients with sinus node dysfunction as the primary indication for pacing. Studies of site specific atrial pacing have not shown a consistent benefit for prevention of AF. A number of prospective studies have been undertaken to assess the role of selective atrial pacing algorithms designed for prevention of AF. These studies suggest that these AF pace prevention algorithms have modest to minimal incremental benefit compared to atrial based pacing alone for the prevention of AF. Atrial antitachycardia pacing (ATP) algorithms have been incorporated into some pacemakers and defibrillators. Overall, atrial ATP therapy has not been shown to substantially reduce the burden of AF in one randomized trial. However, there are subsets of patients e.g. those with atrial flutter as well as AF who are likely to benefit from this therapy.

Does Rapid Atrial Pacing Terminate Atrial Fibrillation? A Comparison of Laboratory and Device Termination Studies

Atrial fibrillation is understood to be a re-entrant arrhythmia and for many years electrophysiologists have attempted to pace-terminate the rhythm. Several studies have demonstrated that an excitable gap is present during atrial fibrillation and that the capture of small amounts of atrial tissue is possible. Early attempts to terminate atrial fibrillation however were unsuccessful. The rapid development of pacemaker and defibrillator technology has provided an exciting new direction for the treatment of recurrent symptomatic atrial fibrillation. Results from studies of the effectiveness of atrial anti-tachycardia pacing algorithms have suggested that 50% of atrial arrhythmias (including atrial fibrillation) can be pace-terminated. These findings conflict with data from the electrophysiology laboratory where atrial fibrillation has yet to be convincingly terminated. In this review, the current literature is discussed and possible reasons for this discrepancy are proposed.

Optimal Programming of Antitachycardia Pacing Functions

The majority of ventricular tachyarrhythmias for which implantable cardioverter de~brillators are implanted is due to reentry. In order for paced beats to entrain or terminate a tachycardia, the arrhythmia must have an excitable gap, i.e., tissue in the circuit between the activation wavefront and the tail of refractoriness that can be depolarized by an electrical impulse entering the tachycardia circuit. When reentry is the mechanism, ventricular tachycardia can often be entrained and/or terminated by pacing [1]. Entrainment occurs when impulses enter the circuit and propagate in the antegrade direction but collide with the previous impulse in the retrograde direction. Antitachycardia pacing algorithms in implantable cardioverter de~brillators are based on the principles of entrainment [2]. The tachycardia terminates when an impulse collides in the retrograde direction and blocks in the antegrade direction. Antitachycardia pacing has several advantages over shock therapy for ventricular tachycardia. First, because it does not require that capacitors be charged, antitachycardia pacing can be delivered more quickly. This decreases the likelihood that the patient will develop hypotension or myocardial ischemia from the arrhythmia. Second, antitachycardia pacing is better tolerated than shock therapy. Direct current countershocks are often associated with pain, and, when they occur frequently, can cause signi~cant patient anxiety. In contrast, antitachycardia pacing may be associated with brief palpitation or dizziness, but is rarely associated with discomfort. Many patients are not aware of antitachycardia pacing events at all. Because it is so well tolerated, antitachycardia pacing may, in selected patients, obviate the need for antiarrhythmic drugs which are sometimes necessary to decrease the frequency of ventricular tachycardia and the attendant shocks. Third, antitachycardia pacing, when successful, uses far less energy than a direct current counter shock. In some patients this may promote longer implantable cardioverter de~brillator battery life. For all of its potential bene~ts, antitachycardia pacing is not without risk. The major risk associated with antitachycardia pacing is that of proarrhythmia. Antitachycardia pacing has the potential to accelerate an hemodynamically well tolerated ventricular tachycardia into one that is associated with hemodynamic collapse or one that is more dif~cult to terminate, even with a shock [3]. Studies suggest that this may occur in 2 to 21% of cases [4]. Proarrhymia may also occur if an implantable cardioverter de~brillator misclassi~es a supraventricular tachyarrhythmia as ventricular tachycardia [3]. In such a case, antitachycardia pacing may induce ventricular tachycardia. This is most likely to occur in patients with slow ventricular tachycardia, the rate of which overlaps with that of sinus tachycardia or other atrial arrhythmias. Finally, antitachycardia pacing, if it is unsuccessful, may delay the delivery of de~nitive shock therapy for an arrhythmia. This has the potential to subject a patient to myocardial ischemia and may limit the ef~cacy of the countershock.

Relation of induced to spontaneous ventricular tachycardia from analysis of stored far-field implantable defibrillator electrograms

Predischarge testing of implantable cardioverter-defibrillators is often used to tailor antitachycardia pacing algorithms based on the response of induced ventricular tachycardia (VT) to pacing. Despite this practice, little is known about the relation between VT induced at predischarge study and VT that occurs spontaneously. To clarify this relation, we identified 19 patients with VT induced at predischarge study and compared the characteristics of the induced VT with the first episode of spontaneous VT. VT morphology, tachycardia cycle length, and response to antitachycardia pacing were measured from far-field electrograms stored by the implantable cardioverter-defibrillator. All subjects had coronary artery disease and previous myocardial infarction. The mean time from baseline study until a spontaneous VT episode was 162 ± 121 days. Analysis of far-field electrograms revealed that spontaneous VT was morphologically different from predischarge-induced VT in 13 of 19 cases (68%). The cycle length of induced VT was significantly shorter than spontaneous VT when VT morphologies were different but not when spontaneous and induced VT had an identical morphology. Antitachycardia pacing was effective in terminating 18 of 19 (95%) induced VTs and 14 of 18 (78%) spontaneous VTs. Antitachycardia pacing was effective in terminating 9 of 12 episodes of morphologically different spontaneous VTs and 5 of 6 episodes of morphologically identical spontaneous VTs (p = NS). Thus, the characteristics of VT induced at predischarge study correlate poorly with those of subsequent spontaneous VT episodes due to the induction of faster “nonclinical” VTs at predischarge testing. This may limit the applicability of predischarge testing in tailoring antitachycardia pacing algorithms.

Are More Complex Implantable Cardioverter Defibrillators Associated With an Increased Mortality? Lessons Learned from Clinical Trials

We compared 1-year survival in patients receiving implantable cardioverter defibrillators (ICDs) that provide only shock therapy with more advanced ICDs that provide antitachycardia pacing, bradycardia pacing, low-energy cardioversion, and advanced detection algorithms. Outcome in patients with advanced-generation ICD systems was similar or improved compared with outcome in patients receiving ICDs with only monophasic shock.

Characterization of return cycle responses predictive of successful pacing-mediated termination of ventricular tachycardia

Objectives. The purpose of this study was to characterize response patterns during overdrive pacing that predict successful termination of ventricular tachycardia.Background. Overdrive pacing during ventricular tachycardia typically results in entrainment at slow pacing rates and in termination or acceleration at faster rates. The factors that determine the critical paced cycle length that results in tachycardia termination have not been extensively studied.Methods. Ventricular tachycardias in 14 patients with coronary artery disease were studied with overdrive pacing at several cycle lengths. Return cycles were measured after each additional paced beat at each paced cycle length. The return cycle responses during pacing trials that resulted in tachycardia termination and those that resulted in entrainment were compared.Results. Three return cycle responses were identified: flat, plateau and increasing. Twenty trials of overdrive pacing resulted in tachycardia termination; all were characterized by an increase in the return cycle with the delivery of each successive beat in the pacing drive until the tachycardia terminated (increasing response). Thirty-four pacing trials resulted in entrainment and not termination; these were characterized either by a constant return cycle (flat response) or an initial increase in return cycle followed by a longer, constant return cycle (plateau response) with the delivery of additional paced beats. The longest paced cycle length that resulted in tachycardia termination correlated with the relative refractory period of the circuit, defined as the tachycardia cycle length minus the fully excitable gap (r2= 0.764, p = 0.0001). Tachycardia termination was not observed unless the paced cycle length was shorter than the relative refractory period of the circuit.Conclusions. The critical paced cycle length that causes termination of ventricular tachycardia depends on the relative refractory period of the circuit because this factor determines whether the nth + 1 beat of the pacing drive will encounter partially recovered tissue. These data provide insights into the mechanism of pacing-mediated tachycardia termination and entrainment and are applicable to the development of improved antitachycardia pacing algorithms.

Randomized controlled comparison of antitachycardia pacing algorithms for termination of ventricular tachycardia

Objectives. This study compared the efficacy and safety of two antitachycardia pacing algorithms in the treatment of ventricular tachycardia.Background. There is agreement that antitachycardia pacing should be adapted to tachycardia rate and be delivered in a burst, but the ideal pacing pattern is not well understood. Effective antitachycardia pacing burst patterns include those with a between-burst decrement (SCAN) with or without an additional within-burst decrement (RAMP).Methods. Prospective randomized crossover comparison of two antitachycardia pacing algorithms (RAMP vs. SCAN) on identical induced sustained ventricular tachycardias was performed.Results. Sixty-five ventricular tachycardias (mean cycle length 364 ± 74 ms) from 37 invasive studies performed in 29 patients were studied; 86% of patients had coronary artery disease and 72% were receiving antiarrhythmic therapy at the time of study. Of the 65 tachycardias, 40 were identical pairs and 25 were unpaired (including 8 with a >30-ms difference in cycle length of induced ventricular tachycardia pairs). In the paired pacing trials, conversion to sinus rhythm occurred, respectively, in 85% of SCAN versus 90% of RAMP protocols (p = 0.63, power = 93%) and within 1.4 ± 0.7 versus 1.7 ± 1.1 attempts (p = 0.41). Discordance for pacing success was seen in taree paris. In unpaired trials, conversion to sinus rhythm occurred in 73% and 57%, respectively (p = 0.68, power = 88%). Tachycardia acceleration during pacing occurred in 7 (11%) of 65 attempts (5 SCAN, 2 RAMP). Acceleration in unpaired ventricular tachycardia trials was correlated with tachycardia cycle length. Failure to convert ventricular tachycardia was associated with a shorter tachycardia cycle length (p < 0.05).Conclusions. In the patients studied, adaptive antiachysardia pacing was safe and effective and, when successful, occurred within three attempts of an 8-beat adaptive barst algorithm. Changes in burst pattern did not affect pacing safety or efficacy. Antitachycardia pacing success was dependent on induced ventricular tachycardia cycle length.

Efficacy of pacemaker tachycardia termination algorithms: is electrophysiological testing alone adequate?

Selection of an optimal pacemaker tachycardia reversion algorithm is generally performed utilizing programmed electrical stimulation (PES). Multiple tachycardias are induced and various tachycardia termination protocols are tested for reversion success. However, PES may induce nonclinical tachycardia and result in an inaccurate assessment of subsequent reversion effectiveness for spontaneous tachycardia. To investigate this question, we compared tachycardia reversion protocol success for PES-induced tachycardia versus spontaneously occurring tachycardia in 16 patients with atrially placed Intermedics 262-12 antitachycardia pacemakers. The pacemaker has tachycardia response counters, and the reversion success was calculated from these counters. This was performed by comparing the percent of time 1 degree versus 2 degrees modality use occurred; crossover to the 2 degrees modality implied failure of the 1 degree modality to convert the tachycardia. PES was used to induce multiple episodes of tachycardia and spontaneous episodes of tachycardia were recorded over time by pacemaker counters. The pacemaker 1 degree modality success was then compared for spontaneous and induced arrhythmias. A total of 53 discrete data comparisons of PES versus spontaneous tachycardia counters were performed in the 16 patients. PES reversion success occurred 85% +/- 22% of the time versus a spontaneous reversion success of 88% +/- 22%. However, the Spearman rank correlation coefficient test demonstrated nonsignficant overall correlation (P < 0.01), and Pearson correlation on an individual patient basis varied widely (r value from < 0.1 to 1.0). When utilizing the same termination algorithm, the percentage conversion of tachycardias occurring spontaneously and induced by PES is similar but does not correlate well overall. This suggests that PES may not be a good linear predictor of the long-term success of antitachycardia pacing algorithms.

Clinical experience with antitachycardia pacing and improved detection algorithms in a new implantable cardioverter-defibrillator

Objectives. This study was conducted to assess the effectiveness of antitachycardia pacing modes and detection algorithms in patients with a new third-generation implantable cardioverter-defibrillator.Methods. Twenty-three of 42 consecutive patients had coronary artery disease, 14 had dilated cardiomyopathy, 2 had prior valve replacement and 3 had arrhythmogenic right ventricular dysplasia. The mean ejection fraction was 41 ± 14%; there were 31 men (74%) and 11 women, with a mean age of 53 years. On the basis of preoperative and postoperative electrophysiologic studies, in 28 patients antitachycardia pacing was postoperatively programmed randomly as “burst” (66%) or autodecremental “ramp” (34%) stimulation with a first coupling interval of 81% of tachycardia cycle length and up to 8 sequences with 3 to 10 stimuli.Results. During a follow-up interval of 6.3 ± 2.2 months, 15 patients were treated by antitachycardia pacing for a median of 6 (range 1 to 59) hemodynamically stable ventricular tachycardias (175 ± 12 beats/min). In 5 patients, 22 ventricular tachycardias (9%) were not terminated by antitachycardia pacing but by cardioversion. Seven (3%) of these episodes accelerated (>50 ms) during antitachycardia pacing. Syncope did not occur during these episodes. In seven patients initial antitachycardia pacing in cases of supraventricular tachycardias delayed charging and redetection prevented inappropriate discharges. Additional detection algorithms were programmed only after inappropriate therapy. The sudden “onset” and “sustained rate duration” criteria were programmed in three patients and the cycle length “stability” criteria in six patients, respectively. After activation of these detection algorithms only two of the seven patients had further inappropriate device discharges.Conclusions. Thus, antitachycardia pacing by this implantable cardioverter-defibrillator effectively and appropriately terminated 91% of hemodynamically stable ventricular tachycardias. Inappropriate device discharges were prevented in some patients by antitachycardia pacing and additional detection algorithms.

The role of the automatic implantable cardioverter-defibrillator (AICD) in the treatment of medically refractory ventricular arrhythmias

After 6 years of widespread clinical use, the role of the automatic implantable cardioverter-defibrillator (AICD) is well defined in some circumstances and less well defined in others. In the next year, the second generation of this device will become available, incorporating antitachycardia pacing algorithms and programmable delivered-energy capabilities into the basic defibrillator system. As a prelude to this development, this article addresses the current status and future role of the AICD in the overall therapeutic armamentarium for the treatment of ventricular tachycardia and presentation of sudden death.