The Story of Managed Ventricular Pacing.

A significant milestone in cardiac pacing occurred approximately two decades ago, when the primary operating mode was reimagined to more closely mimic normal top-down cardiac activation. When introduced, Managed Ventricular Pacing (MVP™; Medtronic, Minneapolis, MN, USA) was an unprecedented dual-chamber mode as it preferentially paced the right atrium in the AAI/R mode and simultaneously protected against transient heart block, albeit only in the instance of dropped ventricular beats. At the time, dual-chamber DDD/R with atrial-based timing and programmable atrioventricular delay was state of the art. MVP™ "unlocked" conventional dual-chamber pacing by not consistently requiring a 1:1 atrioventricular relationship during its primary operating mode (ie, AAI/R+). Ultimately, MVP™ emerged as a primitive means to promote His-Purkinje activation, and it is not a coincidence that its roots can be traced back to first-in-man permanent His-bundle pacing.

Sinus rhythm R-wave amplitude as a predictor of ventricular fibrillation undersensing in patients with implantable cardioverter-defibrillator.

BACKGROUND: Ventricular fibrillation (VF) is induced during implantable cardioverter-defibrillator (ICD) implantation to ensure that the ICD will sense, detect, and defibrillate VF. ICD implant guidelines state that the amplitude of the sinus rhythm R wave recorded from the ventricular electrogram should have amplitude ≥5 mV. No study has tested the relationship between sinus rhythm R-wave amplitude and VF sensing using modern, transvenous sensing electrodes. OBJECTIVE: The goal of this study was to determine whether there is a sinus rhythm R-wave amplitude cutoff that can be used to determine which patients are not at risk of VF undersensing. METHODS: A retrospective analysis of induced and spontaneous VF episodes from 2 clinical trials with 2022 patients was performed. Episodes with undersensing during the initial detection of VF were identified, and the distribution of sinus rhythm R-wave amplitudes for patients with and without VF undersensing was analyzed. RESULTS: Only 3% of analyzed induced VF episodes were considered to have VF undersensing, and none had clinically significant detection delays. There was no correlation between device-measured, rectified sinus rhythm R-wave amplitude and VF undersensing at the time of implantation or during follow-up, although <4% of patients had sinus rhythm R-waves with amplitude <3 mV. CONCLUSION: We analyzed true bipolar sensing of induced VF or spontaneous ventricular tachycardia/VF detected in the ICD VF zone. Sensing of VF was so reliable that clinically significant undersensing did not occur. Our findings do not support any recommended minimum sinus rhythm R wave to ensure reliable sensing of VF or the necessity of inducing VF to verify sensing for rectified sinus rhythm R-waves with amplitude ≥3 mV.

The relationship between pacing site and induction or termination of sustained monomorphic ventricular tachycardia by antitachycardia pacing.

BACKGROUND: With the development of left ventricular pacing for cardiac resynchronization, there is an interest in the possibility of improving ventricular antitachycardia pacing (ATP) efficacy by pacing from the LV electrode(s). OBJECTIVE: This study assessed the efficacy of pacing delivered from the left coronary vein (LCV) compared to that delivered from the right ventricular apex (RVA) upon ventricular tachycardia (VT) induction and termination. METHODS: Sixty patients undergoing provocative ventricular electrophysiology (EP) studies in three centers were enrolled. Multipolar EP catheters were placed in the atrium, the RVA, and LCV. VT induction was attempted from the RVA and LCV in random order. Upon detection of monomorphic VT, burst ATP for up to 10 pulses at 88% VT cycle length was delivered from the RVA or LCV, in a random order, and crossed over when possible. Identical VT morphologies were reinduced to allow paired comparison of RVA versus LCV ATP. RESULTS: Data from 55 patients were analyzed. Thirty-four morphologically distinct monomorphic VT types were induced in 22 patients. ATP succeeded in 18 (55%) and VTs in 13 patients. RVA ATP terminated 15 of 23 (65%) VTs, and LCV ATP terminated 10 of 23 (43%) VTs (P = 0.14). ATP delivered ipsilateral to the earliest activation site required 5.0 + or - 2.6 pulses to terminate compared to 4.8 + or - 1.7 pulses when delivered from the contralateral site (P = 0.90). Paired comparison was possible for 13 VT morphologies in 11 patients. Paired RVA and LCV ATP efficacy was identical (54%vs 54%, P = 1.0). CONCLUSION: ATP delivered from a LCV lead offers no efficacy advantage over pacing from the RVA.

Severe atrioventricular decoupling, uncoupling, and ventriculoatrial coupling during enhanced atrial pacing: incidence, mechanisms, and implications for minimizing right ventricular pacing in ICD patients.

UNLABELLED: AV Decoupling During Enhanced AAIR Pacing. BACKGROUND: Enhanced AAI/R pacing minimizes right ventricular pacing but may permit or induce AV decoupling (AV-DC) due to unrestricted AV intervals (AVIs). The purpose of this study was to characterize and quantify AVI behavior in a randomized trial of enhanced AAI/R pacing in ICD patients. METHODS: One hundred twenty-one patients in the Marquis ICD MVPtrade mark Study, a randomized 1-month crossover comparison of cumulative% ventricular pacing (Cum%VP) in enhanced AAIR (MVP) vs DDD/R, were analyzed. AV-DC was defined as >or=40% AVIs >300 ms; VA coupling (VA-C) was defined as%V-atrial pace (AP) intervals <300 ms. Dynamic AVI behavior and increases in Cum%VP due to AV block (AV uncoupling, AV-UC) were characterized using Holters with real-time ICD telemetry. RESULTS: AV-DC occurred in 17 (14%) of patients. Baseline PR, amiodarone, nighttime, lower rate >60 beats/min, rate response, and Cum%AP were associated with longer AVIs. Logistic regression identified baseline PR (odds ratio [OR]= 1.024, 95% confidence interval [CI] 1.007-1.042; P = 0.005), and Cum%AP (OR = 1.089, 95% CI 1.027-1.154; P = 0.004) as predictors of AV-DC. AV-DC was associated with approximately 10-fold increases in both Cum%VP (13.6 +/- 28.3% vs 1.2 +/- 3.9%; P = 0.023) due to transient AV-UC) and VA-C (6.0 +/- 17.5% vs 0.5 +/- 1.2%, P = 0.028). AV coupling (<40% AVIs >300 ms) was preserved in 104 (86%) patients. CONCLUSIONS: AV-DC, VA-C, and AV-UC may be worsened or induced by enhanced AAI/R pacing. Conservative programming of lower rate and rate response should reduce the risk of AV-DC by reducing Cum%AP.

Automatic determination of timing intervals for upper limit of vulnerability using ICD electrograms.

BACKGROUND: Implantable cardioverter defibrillator (ICD) implant testing based on the upper limit of vulnerability, or vulnerability testing, permits assessment of defibrillation safety margins without inducing ventricular fibrillation (VF) in most patients. Vulnerability testing requires that T-wave shocks be timed at the most vulnerable intervals of the cardiac cycle, defined as intervals at which the strongest shock induces VF. Our goal was to develop and test an automated method to select these timing intervals using ICD intracardiac electrograms (EGMs). METHODS: At ICD implant in 22 patients, we determined the range of the most vulnerable intervals by scanning the T wave with shocks. Simultaneously, EGMs were recorded for 351 pacing sequences used for measurement of timing intervals or T-wave shocks. EGMs were analyzed off-line using a novel automated method to identify a stable point near the maximum slope of the T wave in the far-field (shock) EGM. Fiducial timing points based both on the EGM and on the electrocardiogram (ECG) were used to predict the most vulnerable intervals. We compared the predicted most vulnerable to the measured most vulnerable intervals determined by T-shock scans. RESULTS: Automatically determined timing points from EGMs and operator-determined timing points from the surface ECG had comparable accuracy in identifying the measured most vulnerable intervals (91% EGM vs 86% ECG, P = NS). CONCLUSIONS: An automated method based on ICD EGMs identifies the most vulnerable intervals with accuracy comparable to the operator-performed, clinical method based on the surface ECG. This EGM method can be implemented efficiently in an ICD to automate vulnerability testing.

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.

Improved defibrillation efficacy with an ascending ramp waveform in humans.

OBJECTIVES: The purpose of this study was to compare an ascending ramp waveform (RAMP) with a standard, clinically available biphasic truncated exponential waveform (BTE) for defibrillation in humans. BACKGROUND: In animal studies, RAMP had a lower defibrillation threshold (DFT) than BTE. METHODS: We studied 63 patients at implantable cardioverter-defibrillator placement using a dual-coil lead and left pectoral active can. The subjects were divided into two groups, one with a 12-ms ascending first phase and one with a 7-ms ascending first phase. Phase 2 of RAMP for both groups was a truncated exponential decay with 65% tilt and reversed polarity. The BTE had a 50% tilt in each phase. DFT and upper limit of vulnerability (ULV) were measured for both waveforms using a binary search protocol. RESULTS: The patient population was 77% male, with a mean age of 63 +/- 10 years and ejection fraction of 33 +/- 13%. Delivered energy at DFT was lower with the 7-ms RAMP vs BTE (5.4 +/- 2.6 J vs 6.5 +/- 3.4 J; P < .01) but unchanged with the 12-ms RAMP (7.4 +/- 4.5 J vs 7.1 +/- 4.9 J). Maximal voltage at DFT was significantly lower with either RAMP compared to BTE (P < .01). There was a strong correlation between ULV and DFT for both RAMP and BTE (P < .01). CONCLUSIONS: The 7-ms ascending ramp waveform significantly reduced delivered energy (18%) and voltage (24%) at DFT, whereas the 12-ms RAMP reduced only DFT voltage. This is the first report of a waveform that is superior to a BTE for defibrillation in humans. ULV correlates with DFT for RAMP, supporting the use of ULV testing for implantation of devices.

Randomized pilot study of a new atrial-based minimal ventricular pacing mode in dual-chamber implantable cardioverter-defibrillators.

OBJECTIVE: We hypothesized that a new minimal ventricular pacing mode (MVP) that provides AAI/R pacing with ventricular monitoring and back-up DDD/R pacing as needed during AV block (AVB) would significantly reduce cumulative percent ventricular pacing compared to DDD/R. BACKGROUND: Conventional DDD/R mode often results in high cumulative percent ventricular pacing that may adversely affect ventricular function and increase risk of heart failure and atrial fibrillation. METHODS: MVP was made operational in 30 patients with DDD/R implantable cardioverter-defibrillators (ICDs) and no history of AVB. Patients were randomized to one week each in DDD/R and MVP. Holter monitor recordings (ECG, intracardiac electrograms, and event markers) and device diagnostics were analyzed for cumulative % atrial paced (Cum%AP), cumulative percent ventricular pacing, and frequency and duration of DDD/R pacing back-up. Diaries were used to report symptoms. RESULTS: Age of the study population was 61 years +/- 12 years and 83% were male. Baseline PR interval was 204 ms +/- 32 ms and programmed AV intervals (DDD/R) were 200 ms +/- 50 ms (paced)/167 ms +/- 54 ms (sensed). Cum%AP was similar between MVP and DDD/R (47.9 +/- 37 vs 46.3 +/- 36). Cumulative percent ventricular pacing was significantly lower in MVP vs DDD/R (3.79 +/- 16.3 vs 80.6 +/- 33.8, P < .0001). Back-up DDD/R pacing during MVP operation due to transient AVB occurred in 10% of patients (9.3 +/- 7.4 [range 1-15] episodes/patient-day, duration 39.7 minutes +/- 156 minutes). Fifteen percent of AV intervals during MVP operation exceeded 300 ms. No significant symptoms were reported during MVP operation. CONCLUSIONS: MVP dramatically reduced cumulative percent ventricular pacing compared to DDD/R while maintaining AV synchrony and providing sensor-modulated atrial pacing support. Intermittent oscillations between MVP and DDD/R during transient AV block appeared safe and well tolerated.

Statistical accuracy of a moving equivalent dipole method to identify sites of origin of cardiac electrical activation.

While radio frequency (RF) catheter ablation (RCA) procedures for treating ventricular arrhythmias have evolved significantly over the past several years, the use of RCA has been limited to treating slow ventricular tachycardias (VTs). In this paper, we present preliminary results from computer and animal studies to evaluate the accuracy of an algorithm that uses the single equivalent moving dipole (SEMD) model in an infinite homogeneous volume conductor to guide the RF catheter to the site of origin of the arrhythmia. Our method involves measuring body surface electrocardiographic (ECG) signals generated by arrhythmic activity and by bipolar current pulses emanating from a catheter tip, and representing each of them by a SEMD model source at each instant of the cardiac cycle, thus enabling rapid repositioning of the catheter tip requiring only a few cycles of the arrhythmia. We found that the SEMD model accurately reproduced body surface ECG signals with a correlation coefficients > 0.95. We used a variety of methods to estimate the uncertainty of the SEMD parameters due to measurement noise and found that at the time when the arrhythmia is mostly localized during the cardiac cycle, the estimates of the uncertainty of the spatial SEMD parameters (from ECG signals) are between 1 and 3 mm. We used pacing data from spatially separated epicardial sites in a swine model as surrogates for focal ventricular arrhythmic sources and found that the spatial SEMD estimates of the two pacing sites agreed with both their physical separation and orientation with respect to each other. In conclusion, our algorithm to estimate the SEMD parameters from body surface ECG can potentially be a useful method for rapidly positioning the catheter tip to the arrhythmic focus during an RCA procedure.