Importance of the Site of Ventricular Tachycardia Origin on Left Ventricular Hemodynamics in Humans

Experimental animal data have indicated that the site of ventricular tachycardia origin and, hence, the degree of asynchronous contraction, may influence the hemodynamic tolerance during sustained ventricular tachycardia. However, data in man are scarce. We studied patients with preserved left ventricular function and absence of significant coronary artery disease. Ventricular tachycardia was simulated with rapid pacing (at 120 and 150 beats/min), performed randomly, from the right ventricular apex or the right ventricular outflow tract. Following pacing from one site, it was repeated from the alternate site. Compared to outflow tract pacing, QRS duration was significantly longer during rapid pacing from the apex. Left ventricular pressure was recorded using a micromanometer-tipped catheter. During sinus rhythm, peak systolic pressure was 142 ± 14 mmHg: at 120 beats/min, it decreased to 109 ± 12 mmHg during pacing from the apex and to 127 ± 21 mmHg during pacing from the outflow tract (P = 0.008). This difference diminished at 150 beats/min (101 ± 16 mmHg vs 112 ± 16 mmHg, respectively, P = 0.21). During sinus rhythm end-diastolic pressure was 13 ± 1 mmHg, which did not change significantly during pacing at 120 beats/min. During pacing at 150 beats/min, end-diastolic pressure increased to 21 ± 3 mmHg during pacing from the apex and to 16 ± 2 mmHg during pacing from the outflow tract (P = 0.005). Changes in first derivative of pressure and in isovolumic relaxation time constant were comparable during pacing from the two sites. Thus, it seems that tachycardias originating from the right ventricular outflow tract result in more favorable left ventricular hemodynamics, compared to those from the right ventricular apex     

Acute Hemodynamic Effects of Atrioventricular Pacing at Differing Sites in the Right Ventricle Individually and Simultaneously

We hypothesized that pacing, which provided a rapid uniform contraction of the ventricles with a narrower QRS, would produce a better stroke volume and cardiac output (CO). We sought to study whether pacing simultaneously at two sites in the right ventricle (right ventricular apex and outflow tract) would provide a narrower QRS and improved CO in 11 patients undergoing elective electrophysiology studies. Patients were studied by transthoracic echocardiography measurement of CO using the Doppler flow velocity method in normal sinus rhythm, AOO pacing (rate 80), DOO pacing in the right ventricular apex (AV delay 100 ms). DOO pacing in the right ventricular outflow tract, and DOO pacing at both right ventricular sites simultaneously in random order. The COs were 5.42 ± 1.83, 5.61 ± 1.97. 5.67 ± 1.6. 5.84 ± 1.68. and 5.86 ± 1.52 L/min, respectively (no significant difference by repeated measures analysis of variance [ANOVA]). The QRS durations were 0.09 ± 0.02, 0.09 ± 0.02. 0.13 ± 0.027, 0.13 ± 0.03, and 0.11 ± 0.03 sees respectively. Repeated measures ANOVA showed that the QRS duration significantly increased with right ventricular apex or right ventricluar outflow tract pacing compared to sinus rhythm and AOO pacing (P < 0.001) but then diminished with pacing at both sites (P < 0.01). QRS duration was not correlated with CO, however the change in QRS duration correlated significantly with the change in CO when pacing was performed at the two right ventricular sites simultaneoasly. In conclusion, during DOO pacing, there was a trend for pacing in the right ventricular outflow tract or both sites to improve the CO compared to the right ventricular apex. With simultaneous pacing at both ventricular sites, the QRS narrowed. Further studies will be required to see if this approach has value in patients with poor left ventricular function or congestive heart failure.     

Is Right Ventricular Outflow Tract Pacing an Alternative to Left Ventricular/Biventricular Pacing?

The right ventricular apex has been used as the traditional pacing site since the development of transvenous pacing in 1959. Some studies suggest that pacing the right ventricular apex may cause remodeling and is harmful. In the past decade, there have been a multitude of studies of the hemodynamic, electrophysiological, electrocardiographic, and clinical effects of ventricular pacing at other sites. Pacing of the left ventricle singly or with biventricular pacing has emerged as an effective and safe therapy for moderate to severe congestive heart failure in patients with prolonged QRS complexes. Studies of alternate right ventricular sites, like the right ventricular outflow tract, have given mixed results. Not all patients can be treated with left ventricular pacing, which is a time-consuming and difficult procedure. Right ventricular pacing is easier and less expensive than left ventricular pacing and further study of additional right ventricular sites seems warranted. (PACE 2004; 27[Pt. II]:871–877)     

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.     

Multisite Pacing for End-Stage Heart Failure: Early Experience

Our objective was to improve hemodynamics by synchronous right and left site ventricular pacing in patients with severe congestive heart failure (CHF). Previous studies reported a benefit of dual chamber pacing with a short AV delay in patients with severe CHF. Other works, however, show contradictory results. Deleterious effects due to a desynchronization of right (RV) and left ventricular (LV) contractions have been suggested. This study included eight subjects with widened QRS and end-stage heart failure despite maximal medical therapy, who refused, or were not eligible to undergo heart transplantation. Each patient underwent a baseline, invasive hemodynamic evaluation with insertion of three temporary leads to allow different pacing configurations, including RV apex and outflow tract pacing, and biventricular pacing between the RV outflow tract and LV and RV apex and LV. According to the results of this baseline study, the configuration of preexistent pacemakers was modified or new systems were implanted to allow biventricular pacing, which, in patients with sinus rhythm, was atrial triggered. Biventricular pacing increased the mean cardiac index (CI) by 25% (from a baseline of 1.83 ± 0.30 L/min per m², P < 0.006), decreased the mean V wave by 26% (from a baseline of 36 ± 12 mmHg, P < 0.004), and decreased pulmonary capillary wedge pressure by 17% (from a baseline of 31 ± 10 mmHg, P < 0.01). Four patients died (1 preoperatively, 1 intraoperatively, 2 within 3 months, and 1 of a noncardiac cause). The four surviving patients have clinically improved from New York Heart Association Functional Class IV to Class II. In these survivors, CI decreased by 15% (P < 0.007) when multisite pacing was turned off during follow-up. In patients with end-stage heart failure, multisite pacing may be associated with a rapid and sustained hemodynamic improvement.     

右心室不同部位起搏对心脏结构和左心功能的影响

[目的]对比研究右心室不同部位起搏对患者心脏结构和左心功能的影响.[方法]90例Ⅲ度或高度房室传导阻滞患者, 随机分为三组, A组行右室流入道（RVIS）间隔部起搏,B组行右室流出道（RVOT）间隔部起搏,C组行右心室心尖部（RVA）起搏. 观察三组手术中情况,监测术中血流动力学变化及手术曝光时间,比较三组术后随访的起搏器工作情况,心电图QRS波宽度,左心功能及血浆中B型钠尿肽（BNP）的差异.[结果]术中监测血流动力学,A组及B组明显优于C组.术后随访观察,A组及B组心电图QRS波宽度明显窄于C组,A组及B组具有更好的心脏功能.[结论]右心室间隔部起搏无论右室流出道起搏还是右室流入道间隔部起搏都是安全,有效的,比右室心尖部起搏更有利于双心室电激动的同步性,且长期对心脏结构及心功能影响也较少.     

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.     

Cardiac Pacing in Fetal Lambs: Intrauterine Transvenous Cardiac Pacing for Fetal Complete Heart Block

To evaluate the feasibility of intrauterine transvenous cardiac pacing, the right ventricular output was measured during pacing in six fetal lambs. Under maternal anesthesia, the uterus was opened, and, under local anesthesia, the pacing lead (Medtronic Capsure SP4023) was inserted via the fetal left internal jugular vein. Right ventricular output was estimated using an Aloka SSD-730 ultrasound device, and tricuspid valve regurgitation was evaluated with an Aloka SSD-880 using the transuterine approach. The ultrasonic right ventricular cardiac output was measured under three different conditions: (1) with the tip of the pacing lead in the superior vena cava (control); (2) with the tip of the pacing lead in the right ventricle; and (3) with pacing at 200 beats/min. The right ventricular output decreased when the pacing lead was inserted into the right ventricle, as well as during pacing at 200 beats/min ([1] = 107 ± 13.2 ml/kg per min; [2] = 73.8 ± 17. 5 ml/kg per min; and [3] = 78.3 ± 23.6 ml/kg per min), Tricuspid regurgitation did not change under any of the conditions tested. Intrauterine transvenous cardiac pacing was successfully achieved. Insertion of the pacing lead into the right ventricle decreased the ventricular output without increasing tricuspid valve regurgitation.     

Acute Changes in Left Atrial and Left Ventricular Diameters After Physiological Pacing

The present study examined alterations in left atria! diameter (LAD) and diastolic left ventricular diameter (LVDd) in 37 patients (72.2 ± 9.8 years old) who received physiological pacemakers; 22 with atrioventricular (AV) block and 15 with sick sinus syndrome (SSS). After pacemaker implantation, LAD and LVDd were serially measured using echocardiography, and their diameters ware expressed per body surface area (LADI and LVDdl; mm/m). Pulmonary capillary wedge pressure (PCWP) and cardiac output (CO) were measured in ten patients with SSS and ten with AV block during both right ventricular and AV sequential pacing. After AV sequential pacing, CO increased in 19 of 20 patients (3.2 ± 0.9 L/min to 3.9 ± 1.0 L/min: P < 0.001). LADI decreased from 24.9 ± 4.2 mm/m² to 21.8 ± 4.4 mm/m² (P < 0.001) in 22 patients with AV block and from 24.1 ± 3.4 mm/m² to 20.4 ± 3.8 mm/m² (P < 0.001) in 15 SSS patients. However, LVDdl did not change significantly in either group of patients. The changes in LAD after the implantation of a physiological pacemaker occurred rapidly, i.e. LAD began to decrease within 1 minute after the procedure, and then reached a plateau. This plateau phase continued for at least 7 days during physiological pacing. There was a positive correlation between the changes in LADI after pacemaker implantation and those in PCWP observed during the AV sequential pacing performed prim- to the implantation (r = 0.86; P < 0.001). The reduction in LAD following pacemaker implantation was rapid and seemed to be accompanied by improvement of cardiac function. Thus, it is suggested that the serial measurement of LADI is useful to predict the efficacy of physiological pacemaker implantation.     

Rate-Responsive Ventricular Pacing: Clinical Experience With the RS4-SRT Pacing System

Eighteen patients (11 men and 7 women) with symptomatic second or third degree atrioventricular block underwent implantation of the rate-responsive RS4-SRT pacing system. Exercise tolerance in RS4 mode was compared to that in VVI mode by randomized double-blind treadmill stress testing. Following hospital discharge, HS4 function was assessed by repeat exercise testing and 24-hour Holter monitoring. Difficulty in obtaining satisfactory P-wave amplitudes at implonfation (mean 3.1 ±1.5 mV) resulted in prolonged implantation times (mean 79.4 ± 26.4 minutes). Following implantation, 10 patients (58%) showed a significant ventricular rate response to exercise, seven did not, and one remained in sinus rhythm. For responders, peak ventricular paced rate and double product were significantly greater in RS4 than in VVI mode, being 101.8 ± 5.8 vs. 74.3 ± 0.4 beats per minute and 20.1 ± 2.9 vs. 15.5 ± 3.7 beats per minute ± mmHg ± 10⁻³, respectively (p < 0.001). However, treadmill times (10.5 ± 2.6 vs. 9.7 ± 3.3 minutes) and work done (5.51 ± 2.01 vs. 4.97 ± 2.33 joules ± 10⁻⁵) were not significantly different (p = 0.22). Following hospital discharge, repeat exercise testing and 24-hour Holter monitoring demonstrated RS4 junction in 11 of 16 and 15 of 18 patients, respectively. We conclude that, due to unreliable atrial sensing, the RS4-SRT pacing system does not provide the reliable rate-responsiveness required to improve exercise tolerance.     

Adequacy of Pacing Rate During Exercise in Rate Responsive Ventricular Pacing

Our objective was to determint; the adequate pacing rate during exercise in ventricular pacing by measuring exercise capacity, cardiac output, and sinus node activity. Eighteen patients with complete AV block and an implanted pacemaker underwent cardiopulmonary exercise tests under three randomized pacing rates: fixed rate pacing (VVJ) at 60 beats/min and ventricular rate-responsive pacing (VVIR) programmed to attain a heart rate of about 110 beats/min ar 130 beats/min (VVIR 110 and VVIR 130, respectively) at the end of exercise. Compared with VVI and VVIR 130, VVIR 110 was associated with an increased peak oxygen uptake(VVIR 110:20.3 ± 4.5 vs VVI: 16.9 ± 3.1; P < 0.01; and VVIR 130: 19.0 ± 4.1 mL/min per kg, respectively; P < 0.05) and a higher oxygen uptake at anaerobic threshold (15.3 ± 2.7, 12.7 ± 1.9; P < 0.01, and 14.6 ± 2.6 mL/min per kg; P < 0.05). The atrial rate during exercise expressed as a percentage of the expected maximal heart rate was lower in VVIR 110 than in VVI or VVIR 130 (VVIR 110: 75.9%± 14.6% vs VVI: 90.6%± 12.8%; P < 0.01; VVIR 110 vs VVIR 130: 89.1%± 23.1%; P < 0.05). There was no significant difference in cardiac output at peak exercise between VVIR 110 and VVIR 130. We conclude that a pacing rate for submaximal exercise of 110 beats/min may be preferable to that of 130 beats/min in respect to exercise capacity and sympathetic nerve activity.     

Right Ventricular Outflow Tract Septal Pacing: Long-Term Follow-Up of Ventricular Lead Performance

Background: The detrimental effects of right ventricular apical pacing on left ventricular function has driven interest in selective site pacing, predominantly on the right ventricular outflow tract (RVOT) septum. There is currently no information on long-term ventricular lead electrical performance from this site.
Methods: A total of 100 patients with ventricular lead placement on the RVOT septum undergoing pacemaker implantation for bradycardia indications were analyzed retrospectively. Lead positioning was confirmed with the use of fluoroscopy. Long-term (1 year) follow-up was obtained in 92 patients. Information on stimulation threshold, R-wave sensing, lead impedance, and lead complications were collected.
Results: Lead performance at the RVOT septal position was stable in the long term. Ventricular electrical parameters were acceptable with stable long-term stimulation thresholds, sensing, and impedance for all lead types. One-year results demonstrated mean stimulation threshold of 0.71 ± 0.25 V, mean R wave of 12.4 ± 6.05 mV, and mean impedance values of 520 ± 127 Ω. There were no cases of high pacing thresholds or inadequate sensing.
Conclusions: This study confirms satisfactory long-term performance with leads placed on the RVOT septum, comparable to traditional pacing sites. It is now time to undertake studies to examine the long-term hemodynamic effects of RVOT septal pacing.     

Physiology of Cardiac Pacing in Children: The Importance of the Ventricular Pacing Site

Children with congenital or acquired atrioventricular block are provided with ventricular rate support from a pacing lead that traditionally is positioned at the right ventricular (RV) apex. However, RV apical pacing causes dyssynchronous electrical activation and left ventricular (LV) contraction, resulting in decreased LV function. Chronic RV apical pacing leads to deterioration of LV function and morphology, resulting in cardiac failure in approximately 7% of children. This review describes the pathophysiology of pacing-induced dyssynchronous LV activation and contraction, especially as a result of chronic RV apical pacing. Furthermore, this review provides an overview of the possible alternative pacing sites, such as the RV outflow tract, His-bundle, LV apex, and biventricular pacing.     

The Right Ventricular Outflow Tract as an Alternative Permanent Pacing Site: Long-Term Follow-Up

The long-term characteristics of the right ventricular outflow tract have been assessed as an alternative permanent pacing site to the right ventricular apex. Thirty-three consecutive patients requiring ventricular pacing were randomized to be paced from one of the two sites. Pacing was performed using a screw-in lead, and a programmable pacemaker was used to facilitate threshold testing. There was no significant difference in the lead positioning time or any acute implant measurement (e.g., threshold at 0.5 msec 0.4 +/- 0.2 V for both sites, P = 0.99). Chronic measurements were also comparable during follow-up (mean 73 months) with a mean threshold at most recent follow-up of 0.15 +/- 0.2 msec (apex) and 0.13 +/- 0.21 msec (outflow tract) at 5 V, P = 0.81. There was only one pacing related complication, a lead dislodgment (outflow tract) in a pacemaker twiddler. Overall, both sites were highly satisfactory.     

Atrial Pacing Lead Location Alters the Hemodynamic Effects of Atrial-Ventricular Delay in Dogs with Pacing Induced Cardiomyopathy

HETTRICK, D.A., et al .: Atrial Pacing Lead Location Alters the Hemodynamic Effects of Atrial Ventricular Delay in Dogs with Pacing Induced Cardiomyopathy. The role of atrial lead location in cardiovascular function in the presence of impaired ventricular dysfunction is unknown. We tested the hypothesis that left atrial (LA) and left ventricular (LV) hemodynamics are affected by alterations in AV delay and are influenced by atrial pacing site in dogs with dilated cardiomyopathy. Dogs   (n = 7)   were chronically paced at 220 beats/min for 3 weeks to produce cardiomyopathy and then instrumented for measurement of LA, LV end diastolic pressure (LVEDP) and mean arterial pressure (MAP), LA volume, LV short-axis diameter, and aortic and pulmonary venous blood flow. Hemodynamics were measured after instrumentation and during atrial overdrive pacing from the right atrial appendage (RAA), coronary sinus ostium (CSO) and lower LA lateral wall (LAW). The AV node was then ablated, and hemodynamics were compared during dual chamber AV pacing (right ventricular apex) from each atrial lead location at several AV delays between 20 and 350 ms. Atrial overdrive pacing from different sites did not alter hemodynamics. Cardiac output (CO), stroke volume, LVEDP, MAP and +dLVP/dt demonstrated significant (P < 0.05) variation with AV delay during dual chamber pacing. CO was higher during LAW pacing than RAA and CSO pacing (   2.3 ± 0.4   vs   2.1 ± 0.3   vs   2.0 ± 0.3 l/min   , respectively) at an AV delay of 120 ms. Also, MAP was higher in the LAW than RAA and CSO (   65 ± 9   vs   59 ± 9   vs   54 ± 11 mmHg   , respectively) at an AV delay of 350 ms. Atrial lead location affects indices of LV performance independent of AV delay during dual chamber pacing in dogs with cardiomyopathy. (PACE 2003; 26[Pt. I]:853–861)     

Clinical Comparison of Acute Single to Dual Chamber Pacing in Chronotropically Incompetent Patients with Left Ventricular Dysfunction

Dual chamber, rate responsive (DDDR) pacing is felt to be superior to ventricular, rate responsive (VVIR) pacing since it more closely mimics the normal electrical and hemodynamic activity of the heart. This reasoning has been used to justify the higher initial costs and increased complexity of dual chamber systems. This study was designed to determine if objective criteria could be identified during acute testing to justify implanting a dual chamber instead of a single chamber system in patients with left ventricular dysfunction. Eight patients with DDDR pacemakers (implanted for chronotropic incompetence) and left ventricular dysfunction underwent exercise radionuclide angiography and graded exercise treadmill testing. Each patient performed the tests in the single (VVIR) and dual (DDDR) chamber modes in a randomized, blinded fashion. We found that objective parameters such as ejection fraction (31%± 13% vs 31%± 10%), exercise tolerance (6.1 ± 2.7 min vs 6.3 ± 2.9 min), oxygen consumption (VO₂) (941 ± 286 mL/min vs 994 ± 314 mL/min), carbon dioxide production (VCO₂) (995 ± 332 mL/min vs 1054 ± 356 mL/min), and maximum attainable workload (43 ± 24 W vs 46 ± 22 W) did not differ between the single and dual chamber pacing modes. These findings suggest that in the acute setting, the additional cost and complexity of dual chamber, rate responsive pacing cannot be justified by objective improvements in exercise tolerance in patients with underlying left ventricular dysfunction.     

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.     

Optimization of Ventricular Function by Improving the Activation Sequence During Ventricular Pacing

Abnormal electrical activation occurring during ventricular pacing reduces left ventricular (LV) pump function. Two strategies were compared to optimize LV function using ventricular pacing, minimal asynchrony and optimal sequence of electrical activation. ECG and hemodynamics aortic flowpmbe, thermodilution cardiac output, LV pressure and its maximal rates of rise (LVdP/dtpos) and fall (LVdP/dtneg) were measured in anesthetized open-chest dogs (n = 7) with healthy hearts. The QRS duration (a measure of asynchrony of activation) was 47 ± 5 ms during sinus rhythm and increased to 110 ± 12 ms during DDD pacing at the right ventricular (RV) apex with a short AV interval. During pacing at the LV apex and LV base, the QRS duration was 8%± 7% and 15%± 7% (P < 0.05) longer than during RV apex pacing, respectively. Stroke volumes, LVdP/dtpos and LVdP/dtneg, however, were higher during LV apex(15%± 16%, 10%± 12% [P<0.05], and 15%± 10%, respectively) and LV base pacing (11%± 12% [P<0.05], 3%± 12%, and 3%± 11%, respectively) than during RV apex pacing. Systolic LV pressure was not influenced significantly by the site of pacing. Biventricular pacing (RV apex together with one or two LV sites) decreased the QRS duration by approximately 20% as compared with RV apex pacing, however, it did not improve stroke volumes, LVdP/dtpos and LVdP/dtneg beyond those during pacing at the LV apex alone. In conclusion, the sequence of electrical activation is a stronger determinant of ventricular function than the synchrony of activation. For optimal LV function the selection of an optimal single pacing site, like the LV apex, is more important than pacing from multiple sites.     

Direct His-Bundle Pacing:

Direct His-bundle pacing (DHBP) produces rapid sequential multisite synchronous ventricular activation and, therefore, would be an ideal alternative to right ventricular apical (RVA) pacing. In 54 patients with cardiomyopathy, ejection fraction (EF) 0.23 ± 0.11, persistent atrial fibrillation, and normal QRS < 120 ms. DHBP was attempted. This was successful in 39 patients. In seven patients, the effect of increasing heart rate on contractility (Treppe effect) was investigated. Twelve patients who also received a RVA lead underwent cardiopulmonary testing. After a mean follow-up of 42 months, 29 patients are still alive with EF improving from 0.23 ± 0.11 to 0.33 ± 0.15. Functional class improved from 3.5 to 2.2. DP/dt increased at each pacing site (P < 0.05) as the heart rate increased to 60, 100, and 120 beats/min. Rise in dP/dt by DHBP pacing at 120 beats/min was at least 170 ± mmHg/s, greater than any other site in the ventricle (P < 0.05). Cardiopulmonary testing revealed longer exercise time (RVA 255 ± 110 s) (His 280 ± 104 s) (P < 0.05), higher O₂ uptake (RVA 15 ± 4 mL/kg per minute) (His 16 ± 4 mL/kg minute) (P < 0.05), and later anaerobic threshold (RVA 126 ± 71 s) (His 145 ± 74 s) (P < 0.05) with DHBP compared to RVA pacing. Long-term DHBP is safe and effective in humans. DHBP is associated with a superior Treppe effect and increased cardiopulmonary reserve when compared to RVA pacing. (PACE 2004; 27[Pt. II]:862–870)     

The Effects of Pacing Site on Left Ventricular Epicardial Surface Velocity Patterns During Systole

Changes in epicardial LV velocity patterns during isovolumic contraction and ejection as induced by ventricular pacing were studied in 15 canines. A noninvasive imaging technique that provided high temporal resolution was used to study the timing of an outward expansion of the LV during isovolumic contraction and the propagation pattern of an inward LV velocity wavefront during ejection. With this technique, surface displacements were measured (± 0.1 mm SD) at 50–70 locations on the LV free wall at 5-msec intervals. Velocities were calculated by differentiating the surface displacement waveforms and an interpolation procedure was used to provide detailed color coded velocity maps of the LV surface. LV surface velocities were determined from data obtained during closed-chest endocardial pacing from each of four sites: right atrium, right ventricular apex, left ventricular apex, and right ventricular outflow tract. These surface velocities showed a distinct spatial and temporal pattern for each pacing site. The results show that this noninvasive mapping procedure has potential for determining the location of an ectopic ventricular focus.