Efficacy of Ventricular Rate Stabilization by Right Ventricular Pacing During Atrial Fibrillation

To assess the effect of right ventricular pacing on rate regularity during exercise and daily life activities, 16 patients with sinoatrial disease and chronic atrial fibrillation (AF) were studied. Incremental ventricular pacing was commenced at 40 beats/min until > 95% of ventricular pacing were achieved during supine, sitting, and standing. Thirteen patients also underwent randomized paired submaximal exercise tests in either a fixed rate mode (VVI) or a ventricular rate stabilization (VRS) mode in which the pacingrate was set manually at 10 beats/min above the average AF rate duringthe last minute of each exercise stage. The pacing interval for rate regularization was shortest during standing (692 ± 26 ms) compared with either supine or sitting (757 ± 30 and 705 ± 26 ms, respectively, P < 0.05). During exercise, VRS pacing significantly increased the maximum rate (119 ± 5.2 vs 106 ± 4.2 ms, P < 0.05), percent of ventricular pacing (85%± 5% vs 23%± 7%, P < 0.05), rate regularity index (5.8%± 1.6% vs 13.4%± 1.9%, P < 0.05), and maximum level of oxygen consumption (12.4 ± 0.5 vs 11.3 ± 0.5 ml/kg, P < 0.05) compared with VVI pacing. There was no change in oxygen pulse or difference in symptom scores in this acute study between the two pacing modes. It is concluded that right ventricular pacing may significantly improve rate regularity and cardiopulmonary performance in patients with chronic AF. This may be incorporated in a pacing device for rate regularization of AF using an algorithm that is rate adaptive to postural and exercise stresses.     

Heart Rate Turbulence after Ventricular Pacing Trains During Programmed Ventricular Stimulation

Background: This study tested the hypothesis that heart rate turbulence (HRT) following ventricular pacing trains depends on train cycle length, presence of retrograde ventriculoatrial (VA) conduction, and left ventricular (LV) function.
Methods: We analyzed digital recordings of programmed ventricular stimulation (PVS) performed in 82 patients (57 men) referred for electrophysiologic studies of ventricular arrhythmias, whose mean age was 64 ± 12 years and LV ejection fraction (EF) was 47 ± 15%. Profiles of sinus RR intervals after all available 8-beat ventricular pacing trains (600-and 400-ms) were averaged. Heart rate turbulence slope (HRTS) was analyzed as the maximum positive slope of a regression line through a sequence of 2–5 (HRTS2 - HRTS5) consecutive RR intervals within the first 5 RR intervals after the pacing train.
Results: Dynamics of RR intervals had biphasic and monophasic patterns, in patients with and without VA conduction, respectively. Sinus nodal response was less prominent after 600-ms than 400-ms pacing trains. After 400-ms pacing trains, HRTS was significantly shallower in patients with LVEF ≤40% than in those with LVEF >40%. HRTS4 was the best discriminator between the two groups (6.8 ± 8.6 ms/RR vs 19.6 ± 26.0 ms/RR, P = 0.017).
Conclusion: In patients with VA conduction, HRT after ventricular pacing trains reflects a combination of vagal withdrawal due to transient hypotension and suppression of sinus node automaticity. Attenuation of vagal modulation was detected in patients with LV dysfunction during standard PVS.     

Relationship Between QT Interval Duration and Electrical Induction of Ventricular Tachycardia

The relation of inducible ventricular tachycardia (VT) to QT interval duration of ventricular paced rhythm has not been evaluated. To clarify this relation we measured corrected QT interval duration (QT_C) during sinus rhythm and QT interval duration during ventricular paced rhythm (QT-V) in patients with coronary artery disease without (non-VT group = group B) and with inducible VT (VT group = group A). Duration of QT-V was greater in the VT group (n = 20) compared with non-VT group (n = 20) during ventricular pacing at cycle lengths of 600 ms (424 ± 26 vs 396 ± 19 ms, P < 0.01), of 500 ms (407 ± 20 vs 383 ± 21 ms, P < 0.01), and of 400 ms (390 ± 21 vs 362 ± 17 ms, P < 0.001). During sinus rhythm the mean values of QT_C were similar in both groups (408 ± 25 vs 413 ± 20 ms, NSJ. During ventricular stimulation the percentage of patients with values of QT-V exceeding 380 ms was 35% in non-VT group and 95% in VT group (P <0.01) at cycle length of 500 ms and 5% versus 60%, respectively, (P < 0.01), at cycle length of 400 ms. Thus, a trend toward longer QT values of ventricular paced rhythm exists in patients with inducible VT.     

Optimized Standby Rate Reduces the Ventricular Rate Variability in Pacemaker Patients with Atrial Fibrillation

Patients with chronic atria! fibrillation (AF) and symptomatic bradycardia often receive ventricular-based pacemakers. However, many of these patients continue to have symptoms of palpitations, which may be due to ventricular rate variability. It has previously been shown that contin uous ventricular pacing during AF has a stabilizing effect on the ventricular rate. Hence, a study was initiated to determine whether a patient-specific optimal ventricular standby rate that reduces the ventricular rate variability, without over-pacing, could be predicted. A ventricular rate stabilization (VRS) pacing algorithm that increases the pacing rate until instability is reduced below a threshold was developed. The VRS algorithm was utilized to determine a patient-specific standby rate in 15 patients with chronic AF, intact AV nodal conduction, and implanted pacemakers. The computer algorithm controlled a pacemaker programmer to automatically change the pacemaker's ventricular pacing rate via telemetry. Patients were studied for 15 minutes with VRS and for 15 minutes with 50 ppm fixed rate pacing (control). The results were as follows: (1) VRS versus control = P < 0.05; (2) mean ventricular pacing rate (ppm): 77 ± 13 versus 50 ± 0; (3) mean ventricular rate (beats/mm); 82 ± 13 versus 79 ± 12; (4) ventricular rate coefficient of variation (%): 11 ± 1 versus 22 ± 5; (5) percent pacing: 75 ± 8 versus 6 ± 8; (6) percent of RR intervals less than minimum pacing interval eliminated: 58 ± 12; (8) regression analysis: mean VRS pacing rate (beats/min) = 0.96 X mean control ventricular rate + 2.3, r²= 0.85. We concluded that: (1) a moderate increase in the ventricular pacing rate was required to substantially stabilize the ventricular rate; (2) the resulting mean ventricular rate increased marginally: (3) a majority of RR cycles less than each patient's minimum pacing interval were eliminated; and (4) there was a linear relationship between the mean ventricular rate during control and the optimal ventricular pacing rate. Thus, a ventricular pacing rate close to the mean ventricular rate during control consistently reduced the ventricular variability. Although pacing at an increased ventricular standby rate reduces variability at rest, the optimal solution would likely be an adaptive rate algorithm that changes the ventricular standby rate as the mean intrinsic rate varies.     

Circadian and Sex-Dependent QT Dynamics

The dynamic QT relationship between the QT and RR intervals in normal individuals, including sex differences, has not been well examined. The aim of this Holter monitor-based study was to assess circadian and sex-related variations in QT dynamics in healthy subjects. The study population consisted of 50 healthy volunteers (mean age = 32 ± 6 years, 25 men), in whom 24-hour digital Holter monitoring and QT interactive, beat-by-beat analyses were performed. The mean lengths of QT and RR intervals were measured from the 24-hour recordings. In order to assess QT dynamics, QT/RR linear regression was performed, and the slope was calculated over 24 hour and for day and night periods, and both genders separately. In the whole population, the mean QT interval was 356.5 ± 19.2 ms and RR interval was 785.9 ± 80.7 ms. The mean value of the slope over 24 hour was 0.17 ± 0.03, though significantly steeper during the day (0.13 ± 0.03) than at night (0.09 ± 0.03, P < 0.001). The analysis of QT/RR dynamics over 24 hour revealed a significantly steeper slope in women (0.18 ± 0.03) than in men (0.16 ± 0.03, P = 0.006), as well as during daytime (0.14 ± 0.03 vs 0.12 ± 0.03, P = 0.04). Circadian variations and sex differences were observed in QT dynamics. The latter may explain the greater susceptibility of women to torsades de pointes during treatment with drugs that prolong repolarization.     

Relationship Between Global Myocardial Index and Automatic Left Ventricular Border Detection Pattern to Identify Biventricular Pacing Candidates

Objective of the Study: to evaluate the relation between global myocardial index (GMI) and the pattern of left ventricular (LV) volume curves variation, using automatic border detection (ABD), and their role in assessing LV asynchrony.
Methods: We studied 52 patients (mean age = 55 ± 17 years) with dilated cardiomyopathy. QRS duration (QRSd) and GMI were measured. Currently accepted TDI and M-mode parameters were used to indicate LV dyssynchrony. On-line continuous LV volume changes were recorded using ABD. Ejection time (ET ABD) was measured from the ABD wave-forms as time interval between maximal and minimal volume variation during LV electromechanical systole. We derived the ejection time index (ETiABD) as the ratio between ET ABD and RR interval (ETiABD = ET/RR).
Results: 31 patients had a QRSd >120 ms and 21 patients had a QRSd <120 ms. Ventricular dyssynchrony was observed in 39 patients (29 patients had a QRSd > 120 ms). GMI was significantly higher in patients with, than in patients without ventricular dyssynchrony (1.06 ± 0.18 vs 0.73 ± 0.13, P = 0.0001), while ETABD was significantly smaller (233 ± 39 ms vs 321 ± 28 ms, P = 0.0001). The corresponding difference for ETiABD was 26.9 ± 6.8% vs 6.3 ± 4%, P < 0.0001. By simple regression analysis an inverse linear correlation was observed between GMI and ETiABD (r²=–0.51, P < 0.0001). The pattern of ABD waveforms showed increased isovolumic contraction and relaxation times in patients with LV asynchrony, similar to the GMI pattern.
Conclusions: Regional delays in ventricular activation cause uncoordinated and prolonged ventricular contractions, with lengthening of the isovolumic contraction and relaxation times and shortening of the time available for filling and ejection. GMI explores these parameters and together with ABD might be useful to identify patients with ventricular asynchrony.     

Electrocardiographic and Clinical Predictors of Torsades de Pointes Induced by Almokalant Infusion in Patients with Chronic Atrial Fibrillation or Flutter: A Prospective Study

The aim of this study was to identify predictors of torsades de pointes (TdP) in patients with atrial fibrillation (AF) or flutter exposed to the Class III antiarrhythmic drug almokalant. TdP can be caused by drugs that prolong myocardial repolarization. One hundred patients received almokalant infusion during AF (infusion 1) and 62 of the patients during sinus rhythm (SR) on the following day (infusion 2). Thirty-two patients converted to SR. Six patients developed TdP. During AF, T wave alternans was more common prior to infusion (baseline) in patients developing TdP (50% vs 4%, P < 0.01). After 30 minutes of infusion 1, the TdP patients exhibited a longer QT interval (493 ± 114 vs 443 ± 54 ms [mean ± SD], P < 0.01), a larger precordial QT dispersion (50 ± 74 vs 27 ± 26 ms, P < 0.05), and a lower T wave amplitude (0.12 ± 0.22 vs 0.24 ± 0.16 mV. P < 0.01). After 30 minutes of infusion 2, they exhibited a longer QT interval (672 ± 26 vs 489 ± 74 ms, P < 0.001), a larger QT dispersion in precordial (82 ± 7 vs 54 ± 52 ms, P < 0.01) and extremity leads (163 ± 0 vs 40 ± 34 ms, P < 0.001), and T wave alternans was more common (100% vs 0%, P < 0.001). Risk factors for development of TdP were at baseline: female gender, ventricular extrasystoles, and treatment with diuretics; and, after 30 minutes of infusion: sequential bilateral bundle branch block, ventricular extrasystoles in bigeminy, and a biphasic T wave. Patients developing TdP exhibited early during almokalant infusion a pronounced QT prolongation, increased QT dispersion, and marked morphological T wave changes.     

Heart Rate Variability and Major Arrhythmic Events in Patients with Idiopathic Dilated Cardiomyopathy

This prospective study of 71 patients with idiopathic dilated cardiomyopathy (IDC) and preserved sinus rhythm was designed to evaluate the relation between heart rate variability (HRV) and subsequent major arrhythmic events. Standard time- and frequency-domain HRV parameters were obtained from analysis of 24-hour Holter ECG recordings. During a mean follow-up of 15 ± 5 months, major arrhythmic events including sustained ventricular tachycardia, ventricular fibrillation, and sudden cardiac death occurred in 10 of the 71 study patients (14%). Neither time- nor frequency-domain indices of HRV differed significantly between patients with and patients without subsequent major arrhythmic events. However, there was a trend toward a lower standard deviation of the average normal RR interval for all 5-minute segments of the 24-hour recording (68 ± 17 ms vs 80 ± 31 ms; P = 0.06) in patients with major arrhythmic events. In addition, the percentage of adjacent normal RR intervals differing > 50 ms over the recording period tended to be lower in patients with major arrhythmic events (6%± 3% vs 9%± 6%; P = 0.08). Our results indicate a tendency toward attenuated parasympathetic activity in IDC patients with subsequent major arrhythmic events compared to arrhythmia-free patients. Larger studies with longer follow-up periods are necessary to clarify the role of HRV measurements for arrhythmia risk prediction in patients with IDC.     

The Effects of Rate-Adaptive Atrial Pacing Versus Ventricular Backup Pacing on Exercise Capacity in Patients with Left Ventricular Dysfunction

Background: Atrial rate-adaptive pacing may improve cardiopulmonary reserve in patients with left ventricular dysfunction.
Methods: A randomized, blinded, single-crossover design enrolled dual-chamber implantable defibrillator recipients without pacing indications and an ejection fraction ≤40% to undergo cardiopulmonary exercise treadmill stress testing in both atrial rate-adaptive pacing (AAIR) and ventricular demand pacing (VVI) pacing modes. The primary endpoint was change in peak oxygen consumption (VO₂). Secondary endpoints were changes in anaerobic threshold, perceived exertion, exercise duration, and peak blood pressure.
Results: Ten patients, nine males, eight with New York Heart Association class I, mean ejection fraction 24 ± 7%, were analyzed. Baseline VO₂ was 3.6 ± 0.5 mL/kg/min. Heart rate at peak exercise was significantly higher during AAIR versus VVI pacing (142 ± 18 vs 130 ± 23 bpm; P = 0.05). However, there was no difference in peak VO₂ (AAIR 23.7 ± 6.1 vs VVI 23.8 ± 6.3 mL/kg/min; P = 0.8), anaerobic threshold (AAIR 1.3 ± 0.3 vs VVI 1.2 ± 0.2 L/min; P = 0.11), rate of perceived exertion (AAIR 7.3 ± 1.5 vs VVI 7.8 ± 1.2; P = 0.46), exercise duration (AAIR 15 minutes, 46 seconds ± 2 minutes, 54 seconds vs VVI 16 minutes, 3 seconds ± 2 minutes, 48 seconds; P = 0.38), or peak systolic blood pressure (AAIR 155 ± 22 vs VVI 153 ± 21; P = 0.61) between the two pacing modes.
Conclusion: In this study, AAIR pacing did not improve peak VO_2, anaerobic threshold, rate of perceived exertion, or exercise duration compared to VVI backup pacing in patients with left ventricular dysfunction and no pacing indications.     

Alteration of the QT/RR Relationship in Patients with Idiopathic Ventricular Tachycardia

It has been shown that alterations in QT/RR relationship may be associated with arrhythmogenesis in several clinical settings. In the present study the QT/RR relationship was studied in 20 patients with idiopathic ventricular tachycardia (12 men and 8 women, aged 41±14 years) compared to 20 normal subjects (9 men and 11 women, aged 39 ± 13 years). All the patients were off any antiarrhythmic drugs and had no evidence of intraventricular conduction defects. The QT intervals and their preceding RR intervals were measured on electrocardiogram strips from 24-hour Holter tapes at hourly intervals. The differences in the maximum, minimum, and mean of either the QT interval or its corrected values between patients with idiopathic ventricular tachycardia and normal subjects were not statistically significant. There was a significant correlation between the QT and RR intervals in normal subjects (γ= 0.73 ± 0.12, P < 0.05) and in patients with idiopathic ventricular tachycardia (γ= 0.80 ± 0.10, P < 0.05). However, the linear regression line of the QT interval against the RR interval were significantly (P < 0.001) altered in patients with idiopathic ventricular tachycardia (QT = 0.24 + 0.18 RR) compared to normal subjects (QT = 0.27 ± 0.12 RR). We conclude that although there is no significant change in the QT interval and its corrected values, the QT/RR relationship is significantly altered in patients with idiopathic ventricular tachycardia as compared to normal subjects. This may be of importance in the pathogenesis of idiopathic ventricular tachycardia in these patients.     

Biatrial Epicardial Pacing Prevents Atrial Fibrillation and Confers Hemodynamic Benefits After Coronary Artery Bypass Surgery

Biatrial pacing (BIP) can be more effective than standard right atrial pacing (RAP) in preventing atrial fibrillation (AF) after coronary artery bypass graft surgery (CABG). However, the mechanisms and hemodynamic benefits of BIP have not been studied in detail. This study examined the efficacy and hemodynamic benefits conferred by overdrive epicardial BIP in preventing post-CABG AF. After undergoing CABG, 72 patients (mean age = 66 ± 12 years, 48 men) were randomly assigned to triggered BIP (BIP-AAT; n = 50) versus single RAP (RAP-AAI; n = 22). The hemodynamic effects of BIP were measured by right heart catheterization and echocardiography. The patients were monitored for 8.8 ± 2.4 days after CABG to detect episodes of AF. The incidence of AF was significantly lower in the BIP-AAT group (22.0%) than in the RAP-AAI group (59.1%, P < 0.01). Cardiac output was significantly higher and pulmonary artery wedge pressure (PAWP) significantly lower during BIP-AAT than during RAP-AAI. The E-wave (65.2 ± 37.8 vs 57.8 ± 37.8 cm/s, P < 0.05) was significantly higher during BIP-AAT, and the interval between atrial pacing spike and the end of A-wave (241 ± 18.4 vs 286 ± 17.2 ms, P < 0.001) was significantly shorter during BIP-AAT than during RAP-AAI. Triggered BIP was well tolerated and significantly reduced the incidence of post-CABG AF compared to single-site RAP. The hemodynamic improvements conferred by BIP-AAT were due to a shortening of the inter-atrial conduction delay and greater contribution of left atrial contraction. These hemodynamic benefits may play a role in lowering intra-atrial pressure and in preventing AF.     

Impedance Cardiography for Atrioventricular Interval Optimization During Permanent Left Ventricular Pacing

TSE, H-F., et al. : Impedance Cardiography for Atrioventricular Interval Optimization During Permanent Left Ventricular Pacing. Left ventricular (LV) pacing is increasingly used in the management of congestive heart failure. Optimization of the atrioventricular (AV) interval is essential to maximize the hemodynamic benefits of this therapy. Although Doppler echocardiography (echo) is the most widely used method, it is time-consuming, expensive, and operator-dependent. We examined the value of an impedance cardiography (IC)-based method of cardiac output (CO) measurement to optimize the AV interval in 5 men and 1 woman (mean age   = 72 ± 11   years) during permanent LV pacing with a 4.8 Fr unipolar coronary sinus pacing lead. Simultaneous measurements of CO by IC and echo were performed at AV intervals of 50, 80, 110, 150, 180, and 225 ms during DDD pacing at 85 beats/min. The optimal AV interval varied between 110 and 180 ms. In 5 of 6 patients (83%), the optimal AV interval by echo and IC was identical. While CO measurements were higher with IC than with echo (   6.1 ± 0.4 L/min   vs 4.7 ± 0.3 L/min, P < 0.05), CO measurements by IC and echo were closely correlated   r = 0.67   , P < 0.001). In conclusion, our initial experience suggests that IC is a reliable method of AV interval optimization during LV pacing. IC and echo measurements of CO during LV pacing were closely correlated. (PACE 2003; 26[Pt. II]:189–191)     

Evaluation of Asynchronous Left Ventricular Relaxation by Doppler Echocardiography During Ventricular Pacing with AV Synchrony (VDD): Comparison with Atrial Pacing (AAI)

The effect of right ventricular pacing on left ventricular relaxation was studied in 13 patients (age 62 ± 3 years), with the atrial sensing ventricular pacing mode (VDD). A control group of similar age (64 ± 4 years) consisted of 11 patients with atrial pacing (AAI). The timing of events was determined in both groups at similar R-R intervals (921 ± 77 ms vs 967 ± 37 ms). The loading conditions as estimated by peak systolic wall stress (afterload) and end-diastolic left ventricular dimensions (preload) were approximately the same in both groups. The ratio of late to early filling velocities were similar in both groups. Dominant changes were: increased preejection period (142 ± 13 ms vs 95 ± 15 ms); and higher velocities of isovolumic relaxation flow (60 ± 34 cm/s vs 25 ± 4 cm/s) in patients with ventricular pacing. The isovolumic relaxation time was longer in patients with VDD pacing (127 ± 14 ms vs 108 ± 12 ms). Anterior systolic interventricular septal motion (paradoxal motion) was recorded in nine patients with VDD pacing and in none of the patients with AAI pacing. Isovolumic relaxation flow was detected during atrial pacing in five (45%) patients and in 13 (100%) patients during atrial sensing ventricular pacing, indicating asynchronous left ventricular relaxation. This data shows that VDD pacing compared to atrial pacing resulted in an altered activation pattern of the left ventricle, associated with delayed onset, asynchronous contraction with interventricular septal motion abnormalities and prolonged asynchronous left ventricular relaxation with abnormal motion manifested by the presence of isovolumic relaxation flow.     

Abnormal Nocturnal Heart Rate Variability and QT Dynamics in Patients with Brugada Syndrome

Background: In Brugada syndrome (BSY), most of the ventricular arrhythmic events are nocturnal, suggesting an influence of the autonomic nervous system.
Methods: In 46 patients (mean age = 41 ± 14 years, 43 men) with electrocardiograms (ECG) consistent with BSY and structurally normal hearts, we measured heart rate variability (HRV) and QT dynamics (QT/RR slopes) on 24-hour ambulatory ECG. Type 1 BSY-ECG was spontaneous in 23 (50%) and induced in 23 patients.
Results: History of syncope was present in 23 patients (50%). Programmed ventricular stimulation induced ventricular tachyarrhythmias (VTA) in 13 patients (28%). A single patient developed ventricular tachycardia during a mean follow-up of 34 months. Compared to a control group matched for age and sex, HRV was decreased over 24 hours and during nighttime in patients with BSY (SDNN 122 ± 44 vs 93 ± 36 ms, P = 0.0008 and SDANN 88 ± 39 vs 54 ± 24 ms, P < 0.0001). QTend /RR slopes were decreased over 24 hours in patients with BSY (0.159 ± 0.05 vs 0.127 ± 0.05, P = 0.003) and particularly at night (0.123 ± 0.04 vs 0.089 ± 0.04, P = 0.0001). QTend /RR slopes were significantly decreased during nighttime in patients with spontaneous versus provoked BSY-ECG patterns. By contrast, HRV and QT/RR slopes were similar in symptomatic and asymptomatic patients, whether VTA were induced or not.
Conclusions: Patients with a BSY-ECG pattern had lower HRV and QT/RR slopes than control subjects during nighttime. High-risk patients with spontaneous BSY-ECG patterns had the lowest nocturnal QTend/RR slopes. These unique repolarization dynamics might be related to the frequent nocturnal occurrence of VTA in BSY.     

Age and Gender Influences on Rate and Duration of Paroxysmal Atrial Fibrillation

The influence of age and gender on the character of paroxysmal atrial fibrillation (PAF) has not been described. Methods: The heart rate (HR) during PAF in patients receiving placebo or antiarrhythmic therapy was analyzed. Data from 177 24-hour Holter recordings were analyzed to mark the onset and termination of PAF and converted into RR interval files. PAF episodes lasting at least 2 minutes and containing ± 20% noise were included. HR during the first 30-second segment versus during the remainder of the episode, and the duration of PAF episodes were compared among groups of different ages and sex (Wilcoxon test). Results: 236 episodes from 55 recordings in 32 patients (all patients: 61.4 ± 12.8 years; men (19): 58.5 ± 12.6 years; women (13) 65.5 ± 12.4 years, P = ns for difference in age) fulfilled the inclusion criteria. Women had a higher mean heart rate at AF onset (123 ± 35 beats/min vs 115 ± 20 beats/min, P = 0.02) and during the remainder of the episode (120 ± 25 beats/min vs 112 ± 22 beats/min at the start, P = 0.01, and 116 ± 26 beats/min vs 108 ± 18 beats/min subsequently, P = 0.01). Episodes tended to be longer in women (mean 89.8 min vs 50.5 min, P = NS) and in the aged (mean 83.8 min vs 46.9 min, P = NS). Conclusion: PAF episodes are associated with faster heart rates and last longer in women, which may reflect differing autonomic responses to AF. A slower ventricular rate during PAF in older patients probably reflects an increasing prevalence of impaired atrioventricular conduction.     

Effects of Left Atrial Dilatation on the Endocardial Atrial Defibrillation Threshold: A Study in an Ovine Model of Pacing Induced Dilated Cardiomyopathy

Left atrial (LA) dilatation is a common finding in patients with chronic atrial fibrillation (AF). Progressive dilatation may alter the atrial defibrillation threshold (ADFT). In our study, epicardial electrodes were implanted on the LA free wall and right ventricular apex of eight adult sheep. Large surface area, coiled endocardial electrodes were positioned in the coronary sinus and right atrium (RA). LA dilatation was induced by rapid ventricular pacing (190 beats/min) for 6 weeks and echocardiographically assessed weekly along with the ADFT (under propofol anesthesia). LA effective refractory period (ERP) was measured every 2–3 days using a standard extra stimulus technique and 400 ms drive. The AF cycle length (AFCL) was assessed from LA electrograms. During the 6 weeks of pacing the mean LA area increased from 6.1 ± 1.5 to 21.3 ± 2.4 cm². There were no significant changes in the mean ADFT (122 ± 15 V), circuit impedance (46 ± 5 Ω), or LA AFCL (136 ± 23 ms). There was a significant increase in the mean LA ERP (106 ± 10 ms at day 0, and 120 ± 13 ms at day 42 of pacing). In this study, using chronically implanted defibrillation leads, the minimal energy requirements for successful AF were not significantly altered by ongoing left atrial dilatation. This finding is a further endorsement of the efficiency of the coronary sinus/RA shock vector. Furthermore, the apparent stability of the AF present may be a further indication of a link between the type of AF and the ADFT.     

Intracardiac echocardiography-guided his bundle pacing and atrioventricular nodal ablation

Background: His bundle pacing (HBP) results in rapid synchronous ventricular activation, but has been associated with long procedure times and compromised pacing and sensing performance. This study sought to reduce procedure time and radiation exposure, and improve electrical performance through more accurate lead placement.
Methods: Intracardiac echocardiography (ICE) was used to guide ablation and lead implantation at the His bundle, right atrial appendage (RAA), and right ventricular apex (RVA), and to assess cardiac function. Custom bipolar screw-in leads with steerable delivery sheaths and an ablation catheter were navigated using ICE (local detailed imaging) and fluoroscopy (global imaging) in anesthetized closed-chest canines (N = 6).
Results: HBP (N = 1) or His + ventricular septal pacing (N = 5) was achieved in all canines. The QRS width was 59.7 ± 5.3 ms for canines in sinus rhythm (SR) and 82.8 ± 16.6 ms for canines with HBP (P = 0.0086). The QRS width for RVA pacing was 106.3 ± 18.4 ms (P = 0.042 vs HBP; P = 0.00013 vs SR). HBP thresholds were 3.0 ± 1.0 volts at 0.5 ms (N = 5 due to a late exit block in one canine). The average procedure duration for His lead placement was 40 ± 28 minutes (range of 3–81 minutes) and the total procedural X-ray exposure was 12 ± 12 minutes (range of 2–30 minutes). Hemodynamic performance was similar for HBP and RAA pacing.
Conclusions: Feasibility of ICE guidance for His pacing and precision ablation of the atrioventricular (AV) node has been shown. This anatomic approach improved accuracy, limited X-ray exposure, and might allow His pacing in patients with preexisting AV nodal block.     

Sympathovagal Balance Prior to Onset of Repetitive Monomorphic Idiopathic Ventricular Tachycardia

Repetitive monomorphic idiopathic (RMI) ventricular tachycardia (VT) occurs typically in patients without structural heart disease, originates in most cases from the right ventricular outflow tract, and can often be induced by exercise or isoproterenol. This study analyzed the dynamic changes in autonomic tone immediately before the spontaneous onset of RMIVT using frequency-domain heart rate variability (HRV) indices. We analyzed the ambulatory electrocardiographic recordings from 6 men and 8 women (mean age: 43 ± 18 years; mean number of VT runs per day: 134 ± 213; mean VT rate: 194 ± 40 bpm; median VT run length: 4 cycles) with RMIVT. A total of 36 clusters of nonsustained episodes of RMIVT preceded by ≥1 hour of sinus rhythm without VT were analyzed (25 minutes before the onset of RMIVT divided into five 5-minute periods; 8 minutes before onset of RIMVT divided into eight 1-minute periods). During 25 minutes preceding the onset of VT, the mean RR interval decreased from 767 ± 118 to 723 ± 105 ms (P = 0.015) and the low-frequency (LF)/high-frequency (HF) ratio increased from 2.24 ± 0.79 to 2.49 ± 1.0 (P = 0.03). During the 8 minutes before VT onset, the mean RR interval decreased from 745 ± 118 to 718 ± 102 ms (P = 0.001) and the LF components increased from 205 ± 72 to 253 ± 113 ms (P = 0.014). No change in HF components was observed during the 25 or 8 minutes periods preceding the RMIVT onset. The changes in HRV indices suggest a strong time-dependent primary activation of sympathetic tone prior to the occurrence of RMIVT. Withdrawal of vagal tone does not appear essential to the initiation of RMIVT clusters.     

Extrasystolic beats affect transmural electrical dispersion during programmed electrical stimulation

BACKGROUND: Experimental studies suggest that the electrocardiographic Tpeak-Tend (TpTe) interval reflects transmural dispersion of repolarization (TDR). The genesis and role of the TpTe interval in a clinical setting have not been established. This study aimed to assess the clinical usefulness of the TpTe interval as an index of TDR and a pro-arrhythmic marker. MATERIALS AND METHODS: Endocardial monophasic action potential (MAP) duration and electrocardiographic QTp, QTe and TpTe intervals were assessed in 13 patients undergoing an electrophysiological study. Surface electrocardiograms were recorded during right ventricular pacing (Basic Cycle Length = 600 ms) before and after single extrastimuli. RESULTS: Ventricular arrhythmia was induced in six patients. During ventricular pacing, MAP duration and QTp intervals shortened in response to extrastimuli applied at progressively shorter coupling intervals. In contrast, QTe intervals increased in response to premature stimulation and QTe dispersion increased at short coupling intervals. During sinus rhythm, the TpTe interval was greater in the inducible group in leads V3-V4. Premature stimulation increased the duration of TpTe intervals, suggesting an increase in TDR. The maximum TpTe interval was greater in the inducible than in the noninducible group, both during baseline ventricular drive pacing (163 +/- 22 vs. 130 +/- 27 ms, respectively, P < 0.03) and after application of shortly coupled extrastimuli (263 +/- 66 vs. 200 +/- 47 ms, respectively, P < 0.05). CONCLUSIONS: The TpTe interval of surface ECG is likely to represent TDR. TDR is increased by premature ventricular stimulation and the magnitude of the maximum TpTe interval (i.e. maximum TDR) during ventricular pacing is greater in patients with inducible arrhythmias.