High uniformity of left and right ventricular repolarization dynamics induced by an abrupt decrease in pacing cycle length in a dog is not affected by left ventricular ischemia.

INTRODUCTION: After an abrupt increase in heart rate, action potential duration (APD) will shorten. To assess the effect of ischemia on APD shortening dynamics, we compared right ventricular (RV) and left ventricular (LV) APD shortening induced by an abrupt decrease in pacing cycle length (PCL) during control and LV ischemia. METHODS AND RESULTS: In eight anesthetized AV block dogs, endocardial LV and RV APD were determined simultaneously after an abrupt PCL decrease from 800 to 350 msec. Measurements were repeated during left anterior descending coronary artery (LAD) occlusion. During control, LV and RV APD shortened 97 +/- 27 and 71 +/- 14 msec, respectively (P < 0.05). Shortening was pronounced in a short initial phase and gradual in the longer secondary phase. Linear regression analysis revealed very high uniformity of LV and RV APD shortening dynamics (r2 = 0.96 +/- 0.01). During repeated LAD occlusion, ischemia induced a gradual LV APD shortening from 314 +/- 25 msec to a new steady-state value of 251 +/- 23 msec, whereas RV APD remained stable at 289 +/- 28 msec. The additional PCL decrease resulted in LV and RV APD shortening of 72 +/- 8 and 68 +/- 15 msec, respectively, with the same high uniformity of shortening dynamics as seen during control (r2 = 0.94 +/- 0.03). CONCLUSION: There is a pronounced difference in APD shortening dynamics induced by an abrupt decrease in PCL compared with ischemia. LV shortening dynamics induced by a decrease in PCL are not affected by LV ischemia, preserving a high interventricular uniformity of repolarization dynamics.

A randomized controlled clinical trial comparing ventricular fibrillation detection time between two transvenous defibrillator models. The Acute Ventak AV investigator group.

The Ventak AV is an implantable cardioverter defibrillator with dual chamber pacing capability. Features include detection and treatment of ventricular arrhythmias, detection of atrial arrhythmias, as well as dual chamber pacing. The objective of the investigation was to verify the efficacy of the Ventak AV in detecting ventricular fibrillation in the presence of dual chamber pacing. Thirty-three patients, who were to receive an implantable defibrillator were randomized (1:1) in a paired comparison study to the Ventak AV (study device) and the Ventak Mini (control) during defibrillation threshold testing. In order to create a "worst case scenario" for sensing of ventricular fibrillation, pacing was performed at high lower rate limit values (Ventak AV DDD pacing at 150/min, Ventak Mini at VVI 100/min). Ventricularfibrillation was induced and the randomized device was allowed to detect and treat the arrhythmia. This test was repeated for each patient using the alternate device in a randomized order, such that all patients were tested with both devices. The mean ventricular fibrillation detection time for the Ventak AV was 2.0+/-0.11 seconds and for the control device the detection time was 1.8+/-0.11 seconds (P = 0.26). Appropriate tachyarrhythmia therapy decision was documented in all episodes for both devices. The study patient population demonstrated equivalent ventricular fibrillation detection time between the Ventak AV and the Ventak Mini. The Ventak AV demonstrated effectiveness in detecting ventricular fibrillation in the presence of high rate dual chamber pacing.

Rate dependent effects of procainamide on the threshold current for pacing in the setting of postrepolarization refractoriness in dogs.

Normally, ventricular APD exceeds the VERP. However, under specific circumstances this relation may change and can become inverse. This phenomenon of postrepolarization refractoriness may be caused by a decrease in excitability. The threshold current (TC) for pacing has never been quantified as a possible explanation for these observations. Using a MAP pacing catheter in the right ventricular apex, the rate dependent behavior of TC, VERP, and APD before and after procainamide (dose 20 mg/kg in 10 min + 5 mg/min infusion) was determined in 17 dogs with chronic complete AV block. Initially, TC was determined with 0.1 mA accuracy. Using a pacing current of at least twice TC, VERP and APD showed a similar, rate dependent shortening for PCLs 800, 575, and 350 ms. Procainamide treatment led to an equal, rate independent VERP and APD increase: no post repolarization refractoriness. Subsequently, accuracy for TC determination was increased to 0.01 mA. Comparing PCLs 800 and 250 ms, TC doubled from 0.05 +/- 0.01 to 0.10 +/- 0.09 mA during control and almost tripled from 0.06 +/- 0.02 to 0.17 +/- 0.10 mA (P < 0.05) after procainamide. Using a fixed pacing current of exactly twice TC found at 800 ms PCL during control, VERP exceeded APD after procainamide treatment at 300 and 250 ms PCL: postrepolarization refractoriness. Increasing the pacing current to twice the rate dependent TC, the relation between VERP and APD normalized: no postrepolarization refractoriness. We conclude that after procainamide, rate dependent TC increase is of major importance for the phenomenon of postrepolarization refractoriness.

Steady-state and dynamic behavior of ventricular repolarization and refractoriness in the dog: the effect of multiple cycle length changes and d-sotalol administration.

In anesthetized dogs with chronic, complete AV block we studied the characteristics of ventricular repolarization and refractoriness. Therefore, we determined: (1) steady-state values of ventricular effective refractory period (VERP), action potential duration (APD), and stimulus T interval (STI) before and after d-sotalol treatment at various pacing cycle lengths (PCLs); and (2) the dynamics of VERP, APD, and STI before and after d-sotalol treatment after the abrupt PCL decreases. VERP, APD, and STI showed a normal frequency dependency. All three parameters increased significantly after d-sotalol administration. During steady-state and dynamic measurements, STI was always longer than APD and APD was always longer than VERP in an individual animal, irrespective of PCL and conditions. Standard deviations of steady-state and dynamic values indicated a considerable interindividual variation. However, the dynamics of VERP, APD, and STI after an abrupt decrease in PCL were highly correlated (linear regression analysis: r2 > or = 0.93). The best mathematical model to describe these dynamics was a bi-exponential model (r2 > or = 0.98) with a very short first and a much longer second time constant. We found that there was a very consistent relation between VERP, APD, and STI, not only during steady-state but also in the dynamic situation after various abrupt PCL decreases. This relation does not change after the administration of d-sotalol. Therefore, STI could be used to predict steady-state and dynamic values of VERP and APD. Since STI can be made available online in implantable pacing systems this could lead to the development of new features in these devices.

Adverse events with transvenous implantable cardioverter-defibrillators: a prospective multicenter study. European 7219 Jewel ICD investigators.

BACKGROUND: A newly developed classification system relates adverse events to the surgical procedure or the function of the implantable defibrillator. METHODS AND RESULTS: Adverse events were monitored during prospective clinical evaluation of the Medtronic model 7219 Jewel ICD and were classified according to the definitions of the ISO 14155 standard for device clinical trials into 3 groups: severe and mild device-related and severe non-device-related adverse events. In addition, events were related to the surgical procedure, treatment with the device, or cardiac function. Seven hundred seventy-eight patients were followed up for an average of 4.0 months after ICD implantation. In total, 356 adverse events were observed in 259 patients. At 1, 3, and 12 months after ICD implantation, 99%, 98%, and 97% of the patients, respectively, survived; 95%, 93%, and 92%, respectively, were free of surgical reintervention; and 79%, 68%, and 51%, respectively, were free of any adverse event. Twenty patients died: 6 deaths were related to the surgical procedure, 12 deaths were considered unrelated to ICD treatment, and 2 patients died of an unknown cause. Of 111 nonlethal severe adverse device effects, 47 required surgical intervention, 19 times for correction of a dislodged lead. Inappropriate delivery of therapy was observed 128 times in 111 patients, and the events were typically resolved by reprogramming or drug adjustment. Nine of these required rehospitalization. CONCLUSIONS: Approximately 50% of patients experience an adverse event within the first year after ICD implantation. The observed adverse event rate depends on the definitions and the prospective monitoring. The incidence of inappropriate therapy emphasizes the need for improved detection algorithms and for quality-of-life evaluations, especially when considering ICD treatment in high-risk but arrhythmia-free patients.

Internal balloon compression: a method to achieve hemostasis when removing an inadvertently placed pacemaker lead from the subclavian artery.

One of the possible complications of subclavian vein puncture is entry into the subclavian artery. If this is not recognized, a pacemaker lead may be placed arterially. Since this may lead to systemic emboli, the pacemaker lead must be removed. This case report describes a patient in whom an atrial lead was inadvertently placed in the ascending aorta, where it had good sensing values but poor atrial capture threshold values. This lead was subsequently removed and hemostasis was achieved with intraarterial balloon compression via the brachial artery.

Cure of incessant pacemaker circus movement tachycardia by radiofrequency catheter ablation.

INTRODUCTION: Treatment of pacemaker circus movement tachycardia (PCMT) in patients with very long VA conduction times may present a problem. METHODS AND RESULTS: PCMT occurred in a 46-year-old woman with an uncommon AV nodal reentrant tachycardia who developed 2:1 AV block after fast pathway radiofrequency catheter (RF) ablation performed at another institution. Due to the long VA conduction time, PCMT could not be prevented by reprogramming the pacemaker or by the addition of antiarrhythmic drugs. Cure of the PCMT was obtained after selective RF ablation of the slow AV nodal pathway. CONCLUSION: RF ablation of the retrograde conduction offers another alternative for treatment of PCMT.

Induction of ventricular fibrillation predicts sudden death in patients treated with amiodarone because of ventricular tachyarrhythmias after a myocardial infarction.

OBJECTIVE: To examine the value of programmed electrical stimulation of the heart in predicting sudden death in patients receiving amiodarone to treat ventricular tachyarrhythmias after myocardial infarction. DESIGN: Consecutive patients; retrospective study. SETTING: Referral centre for cardiology, academic hospital. PATIENTS: 106 patients with ventricular tachycardia (n = 77) or ventricular fibrillation (n = 29) late after myocardial infarction. INTERVENTIONS: Programmed electrical stimulation was performed while on amiodarone treatment for at least one month. MEASUREMENTS AND MAIN RESULTS: In 80/106 patients either ventricular fibrillation (n = 15) or sustained monomorphic ventricular tachycardia (n = 65) was induced. After a mean follow up of 50 (SD 40) months (1-144), 11 patients died suddenly and two used their implantable cardioverter debfibrillator. By multivariate analysis two predictors for sudden death were found: (1) inducibility of ventricular fibrillation under amiodarone treatment (P << 0.001), and (2) a left ventricular ejection fraction of < 40% (P < 0.05). The survival rate at one, two, three, and five years was 70%, 62%, 62%, and 40% respectively for patients in whom ventricular fibrillation was induced, and 98%, 96%, 94%, 94% for patients with induced sustained monomorphic ventricular tachycardia. Where there was no sustained arrhythmia, five year survival was 100%. CONCLUSIONS: In patients receiving amiodarone because of life threatening ventricular arrhythmias after myocardial infarction, inducibility of ventricular fibrillation, but not of sustained monomorphic ventricular tachycardia, indicates a high risk of sudden death.

Management of electrical instability after ICD implantation.

UNLABELLED: Postoperative ventricular arrhythmias were studied in 52 patients receiving implantable cardioverter defibrillators (ICDs). A group of 9 patients was identified who experienced electrical instability (EI). The lead approach was thoracotomy in 6 and nonthoracotomy in 3 patients. In 8 of 9 patients VTs started soon after surgery. There was no evidence of ischemia, cardiac failure, electrolyte imbalance, or drug intoxication. The severity of ventricular arrhythmias varied from a considerable increase in incidence of well-tolerated VTs in 3 patients (1 incessant) to poorly tolerated frequent VTs in 6 patients (2 incessant). In 4 patients VTs led to cardiac failure. Ventricular arrhythmias during EI were refractory to antiarrhythmic drugs (AAD) in 7 of 9 patients. In 3 patients VTs accelerated into fast VT or VF with antitachycardia pacing (ATP) or cardioversion. The successful management of EI was: sedation in 4 patients (3 with midazolam 1 with temazepam), ATP and AAD in 2 patients, AAD and hemodynamic support in 2 patients, spontaneous resolution in 1 patient. All patients survived the period of postoperative EI. Two patients had a relapse of EI at 2- and 9-months postimplantation, respectively, one of whom eventually died. CONCLUSIONS: EI occurred in 17% of patients after ICD implantation, had a varying degree of severity and required an individualized approach. Control of EI with AAD was successful in only 2 of 9 patients. Sedation with midazolam was useful in the management of EI.

Initial experience with mode switching in a dual sensor, dual chamber pacemaker in patients with paroxysmal atrial tachyarrhythmias.

Mode switching algorithms have been developed to avoid tracking of atrial fibrillation (AF) or flutter (AFL) during DDD(R) pacing. Upon recognition of AF or AFL, the mode is switched to a nontracking, sensor driven mode. The Vitatron Diamond model 800 pacemaker does this on a beat-to-beat basis. Atrial events occurring within a "physiological range" (+/- 15 beats/min) calculated from a running average of the atrial rate are tracked. When atrial events are not tracked the escape interval is either determined by the sensor(s) or by a fallback algorithm thereby preventing large increases in V-V interval during mode switching. Loss of atrioventricular (AV) synchrony by atrial premature beats and after an episode of AF or AFL is prevented by atrial synchronization pulses (ASP), which are delivered after a safe interval (timed out from the sensed premature atrial event) has expired and before delivery of the next ventricular stimulus. We implanted 26 such devices in 18 men and 8 women with symptomatic second- or third-degree AV block and paroxysmal AF or AFL. Their ages ranged from 18-84 years (mean 60), and the follow-up ranged from 2-13 months (mean 8). During pacemaker check-up, exercise testing or 24-hour Holter monitoring one or more episodes of mode switching was documented in 8 patients. In these 8 patients a smooth transition (ventricular rate) from sinus rhythm to AF or AFL was documented on one or more occasions, without inappropriate increase in ventricular rate in the DDDR mode. None of the patients complained of palpitations.(ABSTRACT TRUNCATED AT 250 WORDS)

Inter- and intraindividual variations in shortening of ventricular effective refractory period after an abrupt decrease in pacing cycle length.

After an abrupt decrease in pacing cycle length (PCL), the ventricular effective refractory period (VERP) shortens. The pacing protocol needed to determine accurate and reproducible values for the VERP during this process is elaborate and time consuming. In this study, steady-state values of VERP at 800 and 350 msec PCL and dynamic values of VERP due to an abrupt change in PCL from 800 to 350 msec were determined. This was done for 11 different dogs to test the interindividual variation and repetitively in the same dog to test the intraindividual variation. The results for steady-state and dynamic values of the VERP show a wide range for both groups. This means that accurate prediction of steady-state and dynamic values of VERP based on previous measurements is not possible.

Is the ventricular effective refractory period different when determined by incremental versus decremental scanning?: the effect of pacing cycle length, d-sotalol, and levcromakalim.

In the clinical setting, the ventricular effective refractory period (VERP) is determined by an 8-beat drive train (S1S1), followed by a premature stimulus (S2), which is decremented in subsequent drive trains until capture is lost. Variation in intertrain pauses and capturing extra stimuli disturb steady-state conditions and reduce reproducibility of values found for the VERP. To increase reproducibility, a protocol without intertrain pause and incremental scanning (IS) of S2 was developed. In anesthetized dogs with chronic AV block, determination of the VERP using IS and decremental scanning (DS) without intertrain pause was compared at 800 and 350 msec pacing cycle length (PCL). The measurements were repeated after the administration of d-sotalol to lengthen the VERP and levcromakalim to shorten the VERP. The results showed no difference between IS and DS at both PCLs with or without medication. Recurrent and abrupt rate changes were avoided during IS, making this the protocol of choice when induction of arrhythmias is to be avoided.

Programming a long paced atrioventricular interval may be risky in DDDR pacing.

In patients with intermittent AV block and dual chamber pacemakers, a long paced AV interval of 200 msec or more can be selected to prolong pulse generator life (by avoiding the ventricular pace output) and to enable a more physiological and hemodynamically superior activation sequence. This case report describes the potential risks of programming a long paced AV interval in a patient with a DDDR pacemaker. T wave pacing, as described here, can occur if the conducted QRS complex is not sensed because it occurs during the ventricular blanking period (delivery of the atrial stimulus). This can be initiated by the mechanisms that induce apparent and actual P wave undersensing of the conducted QRS complex. In this case report apparent P wave undersensing and subsequent T wave pacing with ventricular capture (in a patient with intermittent AV block) occurred frequently during an exercise test done in the DDDR mode with a paced AV interval of 200 msec, according to the clinical evaluation protocol.

Improvement in left ventricular function by ablation of atrioventricular nodal conduction in selected patients with lone atrial fibrillation.

Left ventricular (LV) function was studied in 30 patients with lone atrial fibrillation (AF) (paroxysmal [n = 27] and persistent [n = 3]) before and after ablation of atrioventricular conduction. In all patients, drug treatment did not control ventricular rate during AF or prevent recurrences of the arrhythmia, or both. LV ejection fraction, and LV end-systolic and end-diastolic, and left atrial dimensions were measured by echocardiography before (mean 7 +/- 10 months, range < 1 to 37) and after (14 +/- 20 months, < 1 to 77) ablation. Before ablation, LV ejection fraction was < or = 50% in 12 patients (group I) and > 50% in 18 (group II). After ablation, LV ejection fraction increased significantly in group I from 43 +/- 8% to 54 +/- 7% (p < 0.0001). There were also significant decreases in LV-end systolic and end-diastolic, and left atrial dimensions. No changes in these parameters were observed in group II. Groups I and II had a significant difference in the duration of AF (group I: mean 11 years, range 8 to 28; and group II: 5 years, 2 to 14) (p < 0.05). No difference was present in age, sex, New York Heart Association functional class for dyspnea, or type of ablation procedure. Thus, some patients with lone AF may show deterioration of LV function, which appears to be related to the duration of the arrhythmia; in these cases, LV function may improve significantly after ventricular rate control is accomplished by ablation of atrioventricular conduction.

Artificial neural networks and ECG interpretation. Use and abuse.

The computerized interpretation of the resting electrocardiogram has reached a steady-state phase: an equilibrium between sensitivity and specificity has been reached. New computer techniques, such as expert systems and artificial neural network technology, have been proposed or are currently under evaluation. Although neural network techniques are based on complex mathematical theories and their application is full of pitfalls, progress has been made in a number of subdomains, like signal filtering, electrocardiographic classification, and compression of stress electrocardiograms. Presently, the hesitating acceptance by the human user forms one of the obstacles that needs to be overcome by convincing, well-performed studies.

Apparent P wave undersensing in a DDD pacemaker post exercise.

Wenckebach behavior of DDD pacemakers occurring when the P-P interval varies between the programmed upper rate interval and the total atrial refractory period is symmetrical in a sense that the pacemaker response during atrial rate acceleration is similar to the pacemaker response during atrial rate deceleration. This phenomenon can be observed in all patients with persistent AV block in whom a DDD pacemaker is implanted, during exercise testing when the spontaneous atrial rate exceeds the selected upper rate, i.e., the programmed upper rate interval. However, this phenomenon will not be observed in all patients with intermittent intact AV conduction during exercise. In this case report we describe a patient who showed an asymmetrical response during a bicycle exercise test. There was 1:1 atrial sensing ventricular pacing until the atrial rate exceeded the upper rate of 140 ppm, while atrial sensing was restored during recovery when the conducted sinus rhythm had decreased to 105 beats/min.

Ambulatory electrocardiography evaluation of supraventricular tachyarrhythmias and bradyarrhythmias.

Long-term ECG recordings are of great value in the diagnosis and management of patients with cardiac arrhythmias. Information from programmed stimulation studies and intracardiac recordings has markedly improved the diagnostic abilities of the person examining the long-term ECG recording. This article discusses how knowledge from intracardiac electrophysiologic studies has resulted in much better recognition of the type and mechanisms of a supraventricular arrhythmia on the Holter record.

Efficacy of automatic multimodal device therapy for ventricular tachyarrhythmias as delivered by a new implantable pacing cardioverter-defibrillator. Results of a European multicenter study of 102 implants.

BACKGROUND: Third-generation implantable cardioverter-defibrillators are devices designed to treat ventricular tachycardia (VT) and ventricular fibrillation (VF) by means of overdrive pacing, cardioversion, or defibrillation. So far, the efficacy of tiered therapy has been documented only in small series. Therefore, a European multicenter clinical evaluation study of a new tachyarrhythmia control device, the Medtronic PCD pacer-cardioverter-defibrillator with epicardial patch-lead configuration, was undertaken. METHODS AND RESULTS: We report on 102 patients (mean age, 55 +/- 13 years) from 11 European centers. PCD devices implanted between May 1989 and February 1991 were included. The patients suffered from hemodynamically significant ventricular tachyarrhythmias not suppressed by antiarrhythmic drug therapy and unrelated to acute myocardial infarction; one patient had nonsustained VT and severely depressed left ventricular function. Seventy patients had coronary artery disease with old myocardial infarctions, 23 had cardiomyopathies of various etiologies, and nine patients had no detectable heart disease. Mean ejection fraction was 36 +/- 14% (range, 10-76%). Mean intraoperative defibrillation threshold (51 patients) was 10.6 +/- 5.1 J (range, 2-18 J). The documented follow-up ranged from 1 to 21 months (mean, 9.4 +/- 5.8 months), or 79.9 cumulative patient-years. Perioperative mortality was 3.9%. The actuarial survival rate at 12 months was 91%. One sudden arrhythmic death occurred. Sixty patients (58%) received device therapy. Seventeen patients had therapies only for "VF" episodes, 16 patients only for VT, and 28 patients for VT and "VF" episodes. Based on device memory data, 1,235 spontaneous VT episodes were detected and treated in 43 patients. Twelve hundred four of these VT episodes received painless initial antitachycardia pacing therapy, restoring sinus rhythm in 91%. The 108 ongoing episodes received 209 multiple therapeutic attempts. Eighty-five additional overdrive pacing therapies restored sinus rhythm in 30%. Initial ineffective antitachycardia pacing therapies received 51 cardioversion pulses. The success rate was 61%. Seventy-three additional cardioversion pulses were delivered to backup ineffective pacing therapy as well as ineffective secondary cardioversion pulses. Their success rate was only 40%. Two hundred eighty-six spontaneous episodes were detected in 44 patients as "VF." Overall defibrillation efficacy was 97.6%. CONCLUSIONS: The implanted device nearly eliminates sudden arrhythmic death in patients with documented, potentially fatal ventricular tachyarrhythmias. Automatic tiered therapy is highly effective to restore sinus rhythm, provided that an integrated two-zone tachycardia detection algorithm is used, assigning lower tachycardia rates to overdrive pacing and/or cardioversion and higher tachycardia rates to defibrillation. In general, spontaneous VTs can be terminated by automatic overdrive pacing, and painful or disturbing countershock therapies are not required to terminate the majority of spontaneous VT episodes.

Demonstration of the feasibility of implantation of a skeletal muscle pulse generator for fecal incontinence in a patient with an implanted unipolar DDD pacemaker.

Electromagnetic fields and myopotentials from skeletal muscle may interfere with the function of a cardiac pacemaker. A 65-year-old woman with a unipolar DDD cardiac pacemaker underwent dynamic graciloplasty (transposition of the gracilis muscle around the anal canal and subsequent implantation of a bipolar pulse generator to stimulate the gracilis muscle), for the treatment of fecal incontinence. This gracilis pulse generator is turned "off" with an external magnet to allow defecation. Appropriate functioning of these two pulse generators (the cardiac pacemaker and the gracilis pulse generator) was tested during implantation of the gracilis pulse generator and afterwards. It was demonstrated that the combination could be used safely in this patient.

Applicability of the stimulus-T interval for antitachycardia pacing.

UNLABELLED: At the onset of tachycardia, the refractory period (RP) changes together with the tachycardia termination window. We evaluated dogs with total atrioventricular (AV) block to determine if stimulus-T interval (STI) can be used to adjust the coupling interval(s) of an antitachycardia pacemaker in relation to changes in RP. Endocardial STI was recorded continuously together with six surface ECG leads. Steady-state (greater than 2 min) RP was determined for drive cycle lengths (DCL) 400 msec and 900 msec. The test pulse (TP) coupling interval, with DCL 900 msec, was chosen to be equal to the RP of DCL 400 msec. DCL was then changed to 400 msec until TP captured. STI of DCL of beat before capture was gained was measured. DCL was then changed back to 900 msec and the interval determined when capture was lost. TP was then lengthened by 5 msec and the procedure repeated until TP captured immediately upon changing to DCL 400 msec. RESULTS: The difference between RP at onset of pacing at DCL of 400 msec and RP when capture was achieved with the shortest coupling interval was 35-50 (mean 40) msec. This required 35-90 (mean 62) seconds. The correlation coefficient RP to STI was greater than 0.95. CONCLUSIONS: (1) RP changed by as much as 35-50 msec at the onset of an abrupt increase in rate in a 35-90-second period; and (2) STI enables estimation of RP on a beat-to-beat basis. Capture can therefore be predicted from the previous beat and the coupling interval adjusted accordingly in an antitachycardia pacing mode.