Initial clinical experience with the pacemaker-cardioverter-defibrillator

The implantation of a new multiprogrammable pacemaker-cardioverter-defibrillator is reported in four patients suffering from drug-refractory ventricular tachycardia or fibrillation. The generator (PCD 7215; Medtronic Inc) was interfaced to the epicardium by three countershock patch electrodes and one ventricular myocardial screw-in lead for sensing/pacing. The device employs separate rate detection criteria for ventricular tachycardia and ventricular fibrillation with automatic delivery of up to four therapies per episode. Therapeutic options include: antitachycardia burst or autodecremental pacing, synchronized cardioversion, defibrillation and ventricular demand pacing at 30 to 90 beats/min. Four men and one woman (ages 29 to 75 years) underwent intraoperative implant evaluation, and the device was implanted in the four men. Over a follow-up of 1.5 to 23 months, 161 spontaneous episodes of ventricular tachycardia and nine episodes meeting ventricular fibrillation criteria (cycle length less than 280 to 290 ms) were detected and treated by the device. Ramp pacing was initially employed to terminate 140 ventricular tachycardia episodes and was successful 88.5% of the time while 10 (7.2%) required low energy epicardial cardioversion (4 to 10 J). Six (4.3%) episodes terminated spontaneously prior to therapy delivery. All nine spontaneous episodes of ventricular fibrillation were defibrillated using 10 to 15 J. Two patients continue to do well with the device functioning reliably. The device was removed at the time of heart transplant in one patient, while another patient died suddenly from drug overdose. No other complications, device malfunctions or inappropriate therapy delivery have been observed. These early results demonstrate the potential usefulness of a programmable device which provides graded therapy for ventricular tachycardia with added defibrillation and bradycardia pacing capability.     

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.     

Determinants of reperfusion cardiac electrical activity after cold cardioplegic arrest during coronary bypass surgery

In a prospective study of 99 patients with coronary artery disease, reperfusion of the heart after a period of ischemia (protected by contemporary techniques of myocardial preservation) resulted in spontaneous resumption of cardiac electrical activity in 53%, spontaneous defibrillation in 10%, reperfusion ventricular fibrillation (VF) in 32% and indeterminate rhythm in 5%. In hearts spontaneously developing rhythms excluding VF (as opposed to hearts requiring direct-current shock), factors significantly associated were a higher plasma potassium concentration (5.2 vs 4.8 mEq/liter), shorter reperfusion time (1 vs 4 minutes), higher plasma magnesium concentration (1.36 vs 1.25 mg/dl) and a lower myocardial temperature (27 vs 32 degrees C). The duration of ischemia, arterial blood gas levels, plasma catecholamine levels, plasma ionized calcium levels, volume of cardioplegia and mean arterial pressure did not relate to occurrence of spontaneous episodes. However, VF developed in 39 of 52 patients (75%) with spontaneous resumption of electrical activity. This event was associated with lower myocardial temperature. Thus, direct-current shocks were ultimately required in 77 of the 99 patients (78%). Although certain thermal, biochemical and hemodynamic variables facilitate spontaneous resumption of cardiac rhythm, the development of VF may negate the potential benefit of this event in the prevention of myocardial damage from direct-current defibrillation.     

How Can We Facilitate Spontaneous Termination of Ventricular Fibrillation and Prevent Sudden Cardiac Death? A Working Hypothesis

Spontaneous Ventricular Defibrillation. Ventricular fibrillation (VF) is one of the most life-threatening arrhythmias encountered in daily clinical practice. Its occurrence cannot be completely prevented by currently used antiarrhythmic drugs, and, in most instances, VF is sustained and leads lo the patient's death unless a successful DC defibrillation is applied. However, spontaneous reversion of VF to sinus rhythm has been observed in various animals and occasionally even in man. Hence, facilitation of self ventricular defibrillation must be explored as an alternative therapeutic approach. In experimental studies using several mammalian species, we have found that self ventricular defibrillation requires a good intercellular coupling and well synchronized electrical activity in the ventricles, which, in untreated animals, depend on their myocardial catecholamine content. It can then be hypothesized that any agent that elevates the catecholamine level during VF would facilitate spontaneous ventricular defibrillation, and drugs inhibiting extraneuronal catecholamine reuptake have indeed been shown to possess this ability. It is suggested that their effects are mediated by an increase in the intracellular cAMP level, and any compounds sharing this property could well prove efficacious in making VF transient and in reducing sudden cardiac death.     

Ventricular self-defibrillation in mammals: age and drug dependence

Ventricular fibrillation (VF) was electrically induced in cats, rabbits, guinea pigs and rats. In young animals of all species and also in old rats short transient VF (TVF) was followed by spontaneous reversion to normal sinus rhythm. Old cats, rabbits and guinea pigs had episodes of sustained VF (SVF) which did not terminate spontaneously; artificial electro-defibrillation was required. Dibenzepin converted the sustained response of old animals to a transient one. Verapamil antagonized the effect of dibenzepin in old animals and also changed the TVF in young animals to SVF. The effect of calcie age of the animal is an important factor in determining whether the fibrillatory red to an alteration in the properties of the cell membrane.     

Spectral and correlation analyses of the verapamil-induced conversion of ventricular fibrillation to tachycardia in isolated rat hearts

Ventricular tachycardia (VT) is considered to be the most common precursor of ventricular fibrillation (VF). However, the mechanisms underlying the transition from VT to VF remain unclear. Here, we investigated whether and how perfusion of the heart with verapamil, a blocker of L-type calcium channels, changed the macro-dynamics of the heart between VT and VF. The experiments were performed with Langendorff perfused isolated rat hearts, in which left ventricular pressure and left ventricular cardiomyogram were measured. Sustained VT or VF was induced by burst pacing of the left ventricular muscles. During sustained VF, verapamil perfusion resulted in the conversion of VF to VT. A cross-correlation analysis between left ventricular cardiomyogram and left ventricular pressure revealed that the correlation coefficient was small during VF, but became larger during VT. This study showed that inactivation of L-type Ca(2+) channels occurred during verapamil-induced conversion of pacing-induced sustained VF to VT, and characterized the changes in macro-dynamics of the heart associated with the transition.     

Ventricular fibrillation and transient arrhythmias after defibrillation in patients with acute myocardial infarction

Ventricular fibrillation (VF) and transient arrhythmias after defibrillation were analyzed from the recordings of 28 patients containing at least one episode of ventricular fibrillation. An R-on-T extrasystole initiated VF in 60% of the episodes. Other initiating factors were a late premature beat (24%), stable ventricular tachycardia (VT) (7%), accelerating idioventricular rhythm (5%) and cardioversion of VT (5%) with a sinusoidal waveform. After the initiating beat, in most cases, evidence was found of a transient ventricular tachycardia which then deteriorated into VF. With a stable VT this may occur after a long time; in the case of apolymorphic VT (with changing amplitude) it generally occurred within 30 s. The main transient arrhythmias generated by circulatory arrest during VF and by the defibrillation shock were: total arrest, total AV-block and/or bradycardia. The combination of a longer duration of VF and a high energy level generally resulted in an increase in the duration of these arrhythmias (P less than 0.01, N = 30). Comparison of episodes of VT and VF recorded in a single patient also shows that arrhythmias are more unfavourable and of longer duration after VF than after VT. These data emphasize fast defibrillation, initially with stored energy levels less than 250J.     

The effect of calcium concentration on spontaneous ventricular defibrillation and VF threshold

Summary In order to investigate the influence of the effective refractory period on spontaneous ventricular defibrillation, isolated rat hearts were perfused with Krebs-Henseleit solution containing 0.5, 2.7 and 5.1 mM calcium. After measuring the fibrillation threshold at spontaneous rate (SR), ventricular fibrillation (VF) was induced during basic ventricular pacing of 110% SR, or the highest rate permitting 11 electromechanical coupling. The VF threshold was significantly reduced from 13.6±3.5 to 7.9±5.3 and 5.1±3.4 mA at 0.5, 2.7 and 5.1 mM Ca⁺⁺ concentrations, respectively. The incidence of spontaneous recovery from VF, induced during basic pacing, was 100%, 83% and 50% at calcium concentrations of 0.5, 2.7 and 5.1 mM, respectively, (p<0.01 for the incidences at 0.5 mM versus 5.1 mM Ca⁺⁺). The incidence of spontancous defibrillation decreased when the hearts were driven rapidly, with spontaneous recovery rates of 92%, 58% and 0% (p<0.0001)) for corresponding increases in Ca⁺⁺ concentration. Induced ventricular fibrillation of fine morphology was frequently observed at 5.1 mM Ca⁺⁺. It appears that progressive impairment of spontaneous defibrillation is caused by an increase in calcium concentration, this effect being more pronounced at high ventricular rates. Variations in the effective refractory period, caused by alterations in extracellular calcium concentration and differences in intracellular Ca⁺⁺ accumulation, may account for the above results.     

Cardioprotection: intermittent ventricular fibrillation and rapid pacing can induce preconditioning in the blood-perfused rat heart

The aim of the study was to use the isolated blood-perfused rat heart to: (i) determine whether brief intermittent rapid pacing and ventricular fibrillation are able to mimic preconditioning by ischemia and thereby protect the isolated blood-perfused heart against ischemia-induced injury and (ii) characterize the effects of these interventions on cardiac metabolism. To this end, isolated, blood-perfused (2.4 ml/min), paced (360 beats/min) rat hearts (n = 6/group), were aerobically perfused for 20 min. Hearts were then randomized to four groups: (i) a further 16 min aerobic perfusion (UC, untreated controls), (ii) ischemic preconditioning (IP, 3 min ischemia + 3 min reperfusion followed by 5 min ischemia + 5 min reperfusion), (iii) electrically induced ventricular fibrillation (VF, 3 min fibrillation + 3 min sinus rhythm followed by 5 min fibrillation + 5 min sinus rhythm) and (iv) rapid pacing at > or = 600 beats/min (RP, 3 min rapid pacing + 3 min normal heart rate followed by 5 min rapid pacing + 5 min normal heart rate). Hearts were then subjected to 35 min of zero-flow, global ischemia (37 degrees C) and 40 min reperfusion. In parallel studies, blood samples were collected during the first 3 min of treatment and plasma taken for the analysis of noradrenaline. The hearts were then immediately frozen and assayed for high energy phosphates and noradrenaline content. Time-to-50% contracture during ischemia was 13.2 +/- 0.8 min in controls; this was reduced to 6.3 +/- 1.1 min by IP but was unaffected by VF or RP (12.4 +/- 1.1 and 12.8 +/- 1.2 min respectively). Post-ischemic left ventricular developed pressure (LVDP) in untreated controls recovered to only 19.9 +/- 8.4% of its pre-ischemic value whereas with IP, VF and RP substantial and similar improvements were observed (60.3 +/- 7.4, 56.2 +/- 5.7 and 45.3 +/- 10.3%, respectively, P < 0.01). This protection was achieved without any significant depletion of high energy phosphates during VF or RP. Noradrenaline was essentially unchanged in controls and with RP, but VF caused a loss from tissue and a large elevation in the plasma. Our results suggest that both RP and VF are as effective as brief ischemia in protecting the heart against injury during ischemia and reperfusion. In contrast to IP, this protection can be achieved without the exacerbation of ischemic contracture and without inducing ischemia during the preconditioning period.     

Ventricular fibrillation during programmed ventricular stimulation: Incidence and clinical implications

Ventricular fibrillation occurred in 10 (3.3 percent) of 300 patients consecutively studied with programmed ventricular stimulation. One hundred twenty-five of these patients were studied with double ventricular extrastimuli including 68 patients with and 57 patients without documented or suspected ventricular tachycardia or fibrillation, or both. Ventricular fibrillation did not develop in response to a single ventricular extrastimulus delivered during sinus rhythm, ventricular pacing or ventricular tachycardia or in response to ventricular pacing at cycle lengths of 300 msec or greater and occurred only in response to double ventricular extrastimuli. All 10 patients who manifested ventricular fibrillation during programmed stimulation were in the group of patients with suspected or documented ventricular tachycardia or fibrillation. Ventricular fibrillation was initiated in seven patients with double ventricular extrastimuli delivered during sinus rhythm or ventricular pacing and in three patients with double ventricular extrastimuli delivered during ventricular tachycardia. Four patients had spontaneous conversion to sinus rhythm and the remainder underwent defibrillation without sequelae. Recurrent ventricular fibrillation occurred clinically in 7 of the 10 patients. This study suggests that ventricular fibrillation occurs uncommonly during programmed ventricular stimulation and only in response to double ventricular extrastimuli in patients in whom spontaneous episodes are likely to occur.     

Electrophysiologic manifestations of ventricular tachyarrhythmias provoking appropriate defibrillator interventions in high-risk patients with hypertrophic cardiomyopathy

Introduction: Our objective was to determine features of ventricular tachyarrhythmias triggering appropriate implantable cardioverter-defibrillator (ICD) interventions in hypertrophic cardiomyopathy (HCM).
Methods and Results: The study cohort was 68 high-risk HCM patients who received ICDs for primary sudden cardiac death prevention from 1995 to 2003. All episodes of sustained ventricular tachyarrhythmias identified by stored intracardiac electrograms were analyzed. Nine patients had 51 episodes of sustained ventricular tachyarrhythmic events that required device therapy (mean follow-up, 3.4 ± 2.2 years; cumulative event rate, 3.2% per year): five had 47 episodes of monomorphic ventricular tachycardia (VT); four each had one episode of ventricular fibrillation (VF). Sinus tachycardia or atrial fibrillation was the initiating rhythm in five of nine patients and in 43 of 51 episodes of events. Of the 17 episodes of monomorphic VT detected in the VT zone, 16 (94%) were terminated by antitachycardia pacing. Thirty episodes of monomorphic VT were detected in the VF zone and were terminated by defibrillation.
Conclusion: Sustained monomorphic VT is common in a high-risk cohort with HCM. Sinus tachycardia is often the initiating rhythm, suggesting that high sympathetic drive may be proarrhythmic when a susceptible substrate is present. Antitachycardia pacing is highly effective in terminating VT in this patient population.     

Pacing following shocks stronger than the defibrillation threshold: impact on defibrillation outcome

INTRODUCTION: A recent study of shocks near defibrillation threshold (DFT) strength demonstrated that at least three rapid cycles always occur after failed shocks but not after successful shocks, suggesting that the number and rapidity of postshock cycles are important in determining defibrillation success. To test this hypothesis, rapid pacing was performed following a shock stronger than the DFT that by itself did not induce rapid cycles and ventricular fibrillation (VF). METHODS AND RESULTS: Epicardial activation was mapped in six pigs using a 504-electrode sock. The DFT was determined by an up/down protocol with S1 shocks (right ventricle-superior vena cava, biphasic). Ten shocks that were 100 to 200 V above the DFT (aDFT) were delivered after 10 seconds of VF to confirm they always defibrillated. Then, S2, S3, etc., pacing at 5 to 10 times diastolic threshold was performed from the left ventricular apex after aDFT shocks during VF. First, the postshock interval after aDFT shocks was scanned with an S2 stimulus to find the shortest S1-S2 coupling interval (CI) that captured. This was repeated for S3, S4, etc., until VF was induced. To induce VF after aDFT shocks, three pacing stimuli (S2, S3, S4) with progressively shorter CIs were always required; S2 or S2,S3 never induced VF. For the S2-S4 cycles, the intercycle interval was shorter (P < 0.01), and the wavefront conduction time was longer (P < 0.01) for episodes in which VF was induced (n = 57) than for episodes in which it was not (n = 60). Following the S4 cycle that induced VF, two types of spontaneous activation patterns appeared: focal (88%) and reentrant (12%). CONCLUSION: VF induction after aDFT shocks always required at least three rapid successive paced-induced cycles. Thus, the number and rapidity of the first several postshock cycles rather than just the first postshock cycle may be determining factors for defibrillation outcome.     

Correlation of Acute and Chronic Defibrillation Threshold with Upper Limit of Vulnerability Determined in Normal Sinus Rhythm

Background: The upper limit of vulnerability (ULV) is the stimulus strength above which ventricular fibrillation cannot be induced, even when the stimulus occurs during the vulnerable period of the cardiac cycle. Determination of ULV using T-wave shocks during ventricular pacing has been shown to closely correlate with the defibrillation threshold (DFT) at ICD implantation. However, there are no data correlating ULV determined in sinus rhythm at ICD implantation, with DFT determined at implantation or during long-term follow-up. This is of clinical importance since ULV may be used to estimate DFT during ICD implantation, both during ventricular pacing or sinus rhythm.Methods and Results: Twenty-one patients receiving a transvenous ICD system were studied prospectively. There were 16 males and 5 females, mean age 68 ± 15 years, with mean ejection fraction 37.4 ± 17.4%. All had structural heart disease. The ULV was defined as the lowest energy that did not induce ventricular fibrillation with shocks at 0, 20 and 40ms before the peak of the T-wave, using a step-down protocol. The initial energy tested was 15J and the lowest energy 2J. DFT was determined following a similar step-down protocol. The DFT was defined as the lowest energy that successfully defibrillated the ventricles. The linear correlation coefficient between ULV and DFT was r = 0.73 (p < 0.001). At implant, mean ULV was 9.2 ± 5J, not statistically different from mean DFT 9.4 ± 4J. ULV plus 5J successfully defibrillated 19 of 21 patients. During long-term follow-up of 10.1 ± 1.8 months in eight patients, DFT was 8.8 ± 5.8J, not significantly different than the DFT of 7.5 ± 4.1J or ULV of 8.0 ± 5.3 at implant.Conclusion: 1) When determined during normal sinus rhythm the ULV significantly correlates with DFT. 2) ULV testing might be used in lieu of standard DFT testing to confirm adequate lead placement thus minimizing or eliminating VF inductions, particularly in hemodynamically unstable patients. 3) Since ULV + 5J has a high probability of successful defibrillation in most patients, programming ICD first shock energy for VF at ULV + 5J may result in lower first shock energies compared to the standard methods of programming first shock energy at twice DFT.Condensed Abstract. The purpose of this study was to determine if the upper limit of vulnerability (ULV) determined during normal sinus rhythm correlates with the defibrillation threshold (DFT), as has been previously shown when determined during ventricular pacing. The linear correlation coefficient between the ULV and DFT was r = 0.73 (p < 0.001). Mean ULV at implant was 9.2 ± 5J, not statistically different from mean DFT of 0.4 ± 4J. During long-term follow-up of 10.1 ± 1.8 months in 8 patients, DFT was 8.75 ± 8J, not significantly different than the DFT of 7.5 ± 4.1J or ULV of 8.0 ± 5.3 at implant. Shocks energies of ULV + 5J successfully defibrillated 19 of 21 patients at implant and 8 of 8 at follow-up. This study indicates that the ULV determined in normal sinus rhythm closely correlates with the DFT, and that ULV + 5J defibrillated most patients. ULV testing could be used to predict DFT and reduce or eliminate the need for DFT testing and VF induction. Programming ICD first shock energy for VF to ULV + 5J will result in lower energy than that used with standard DFT testing.     

Attenuation of reperfusion-induced ventricular fibrillation in the rat isolated hypertrophied heart by preischemic diltiazem treatment

Summary The ability of the calcium antagonist diltiazem to protect against reperfusion-induced arrhythmias in hypertrophied myocardium was studied. Hearts from normotensive and DOCA-salt hypertensive rats were Langendorff perfused and subjected to 10 minutes of stabilization, 10 minutes of left coronary artery occlusion, and 5 minutes of reperfusion. The incidence and duration of ventricular tachycardia (VT) and ventricular fibrillation (VF) during reperfusion were determined and the effects of diltiazem or vehicle (given as a single bolus 3 minutes before coronary artery occlusion) were assessed in hypertrophied and normal hearts. In vehicle-treated (control) hypertrophied hearts, VF incidence was 91% compared with 67% in normal hearts, and the median duration of VF was 272 seconds (mean 207.4±32.3) compared with 27 seconds (mean 110.6±36.6; p<0.05), respectively, suggesting that reperfusion VF is more severe in hypertrophied hearts. In normal hearts, diltiazem 18 µg reduced VT incidence from 92% to 55%, reduced VF from 67% to 27%, and sustained VF from 42% to 9%. In hypertrophied hearts, 18 µg diltiazem reduced the VT incidence from 100% to 58%, reduced VF from 91% to 25% (p<0.01), and sustained VF from 82% to 8% (p<0.01). Median VF duration in this group was reduced to 0 seconds (p<0.05; mean 24.7±22.6). Diltiazem did not significantly affect heart rate or coronary flow rate decreases during ischemia. However, developed tension, at the onset of ischemia, was lower in diltiazem-treated groups than in the control groups. We suggest that the attenuation by diltiazem of reperfusion-induced arrhythmias observed in this model was related to an energy-sparing effect during ischemia. This study shows that diltiazem administered acutely before the onset of ischemia attenuates reperfusion-induced arrhythmias in the hypertrophied myocardium, despite its greater susceptibility to reperfusion-induced arrhythmias.     

Bradycardia pacing-induced short-long-short sequences at the onset of ventricular tachyarrhythmias: a possible mechanism of proarrhythmia?

OBJECTIVES: The purpose of this study was to characterize interactions between normal pacing system operation and the initiating sequence of ventricular tachycardia (VT)/ventricular fibrillation (VF). BACKGROUND: Abrupt changes in ventricular cycle lengths (short-long-short, S-L-S) might initiate VT/VF. The S-L-S sequences might be passively permitted or actively facilitated by bradycardia pacing. METHODS: Initiating sequences of 1,356 VT/VF episodes in the PainFree Rx II (n = 634) and EnTrust Trial (n = 421) were analyzed with stored electrograms and by pacing mode (DDD/R, VVI/R, and Managed Ventricular Pacing [MVP]). Interactions between pacing and VT/VF initiation were classified as: non-pacing associated, pacing associated, pacing permitted, and pacing facilitated. RESULTS: Non-pacing associated (no pacing, no S-L-S) and pacing associated (ventricular pacing without S-L-S) onset accounted for 44.0% and 29.8% of all VT/VF, respectively. Pacing permitted (S-L-S sequences without ventricular pacing) episodes accounted for 6.4% (DDD/R), 20.0% (MVP), and 25.6% (VVI/R) of 1,356 VT/VF episodes. Pacing facilitated onset (S-L-S sequences actively facilitated by ventricular pacing including the terminal beat after a pause) accounted for 8.2% (MVP), 9.4% (VVI/R), and 14.8% (DDD/R) of 1,356 VT/VF episodes. Pacing facilitated S-L-S VT/VF occurred in 2.6% (MVP), 3.3% (VVI/R), and 5.2% (DDD/R) of patients with episodes and was the sole initiating sequence in approximately 1% of patients. Pause durations during pacing facilitated S-L-S differed between modes (DDD/R 793 +/- 172 ms vs. MVP 865 +/- 278 ms vs. VVI/R 1180 +/- 414 ms, p = 0.002). The majority of these episodes were monomorphic VT. CONCLUSIONS: Ventricular tachycardia/VF in some implantable cardioverter-defibrillator patients might be initiated by S-L-S sequences that are actively facilitated by bradycardia pacing operation and might constitute an important mechanism of ventricular proarrhythmia.     

Sudden Cardiac Death Despite a Functional Cardioverter‐Defibrillator: The Case for Early and Aggressive Therapy for Ventricular Tachycardia in Selected Patients

We present three cases within 11 months at a single institution of sustained VT that fell below the programmed detection rate of the patients’ implantable cardioverter‐defibrillators (ICDs), two of which continued until converting to an agonal VF that did not meet criteria for detection, and a third case that could not be successfully defibrillated after a prolonged period of VT. These episodes may be under‐recognized due to the dependence of device diagnostic storage on programming and the post‐mortem effort that is often required to review these events. Some patients, likely those with the most advanced heart failure, may not tolerate sustained ventricular tachycardia (VT) and may even die from ventricular arrhythmias without ever having a rhythm that meets detection criteria in a ventricular fibrillation (VF) zone.     

Laplacian electrograms and the interpretation of complex ventricular activation patterns during ventricular fibrillation

INTRODUCTION: During ventricular fibrillation (VF), interpretation of a local electrogram and determination of the local activation moment are hampered by remote activity or intervening repolarization waves. Successful defibrillation depends on critical timing of the shock relative to local activation. We tested the applicability of Laplacian electrograms for detection of the moment of local activation during VF. METHODS AND RESULTS: From isolated perfused porcine intact hearts, 247 local unipolar electrograms were recorded simultaneously (13 x 19 matrix, interelectrode distance 0.3 mm) from the left ventricular wall during sinus rhythm, following pacing or during VF. Activation maps were constructed based on local unipolar electrograms, and Laplacian electrograms were calculated from local electrograms and its eight neighbors. The Laplacian electrogram displayed a sharp R/S complex with local activation indicated by the moment of zero crossing without interference from remote activity or repolarization waves. Its amplitude increased with decreasing interelectrode distance. Following epicardial stimulation, Laplacian amplitude was significantly larger than during a breakthrough pattern. During VF, identical unipolar electrograms corresponded to Laplacian complexes with different morphology. Collision of wavefronts was associated with entirely positive Laplacian waveforms; "focal" appearance of activity was associated with an entirely negative waveform. Activation block in the activation maps was correlated with the appearance of sustained episodes of negativity or positivity in the Laplacian electrogram (depending on the location of the recording site relative to the line of block). CONCLUSION: Laplacian electrograms allow detection of the moment of local activation without interference from remote activity or repolarization, especially during complex arrhythmias. The technique applied to automatic sensing devices, such as the internal defibrillator, may optimize defibrillation success.     

Induction of clinical ventricular tachycardia using programmed stimulation: value of third and fourth extrastimuli

Initiation of ventricular tachycardia (VT) by right ventricular extrastimulation was analyzed in 142 consecutive patients, 53 with electrocardiographically documented episodes of spontaneous VT or ventricular fibrillation (VF) and 68 with no spontaneous VT or VF; 21 patients with a history of sudden death but no documented arrhythmia were excluded from further analysis. All patients received 1 to 4 extrastimuli (S2, S3, S4 and S5) during pacing at fixed cycle lengths of 600 or 500 msec at 1 or 2 right ventricular sites. Clinical VT was reproduced by extrastimulation in 28 of 43 patients (65%) with sustained VT and in 0 of 10 patients with nonsustained VT. Clinical VT was induced by S2 or S3 in 16 patients and by S4 or S5 in 12 patients. Ventricular burst pacing reproduced clinical VT in 3 other patients. Nonclinical VT, which was most often polymorphic and nonsustained, was induced in 24 of 121 patients (20%), in 11 by S2 or S3 and in 13 by S4 or S5. Ventricular burst pacing induced nonclinical VT in 4 other patients. In patients with spontaneous sustained VT, the use of S4 and S5 in the right ventricle increases the yield of inducible clinical VT compared with use of S2 and S3 alone, but at a cost of increased induction of nonclinical VT. Frequent induction of nonclinical VT limits the interpretation of the results of such stimulation in patients without previously documented VT.     

Determinants of ventricular defibrillation in adults.

Conventional defibrillators which stored no more than 400 J and used damped sine wave pulses defibrillated 240 of 253 (95%) episodes of ventricular fibrillation (VF) in 94 prospectively assessed resuscitations in 88 adults. Shocks of 80--240 J (under 3 J/kg) delivered to the chest wall defibrillated more often than higher energy levels. Defibrillation rate did not correlate with weight. Defibrillation was determined by the diagnosis and setting in which VF occurred. Patients with acute myocardial infarction (AMI) and primary VF or with coronary disease and no AMI defibrillated more easily than patients with AMI and secondary VF or with no coronary disease. VF in a terminal patient (agonal VF) defibrillated less often than VF in other clinical situations. Age, weight, delivered energy, duration of pulse wave, and duration of VF had little, if any, influence on rate of defibrillation. These data fail to support the use of more expensive, high-output defibrillators sold by 11 or 14 American manufactures.