Hemodynamic Benefits of Right Ventricular Outflow Tract Pacing: Comparison with Right Ventricular Apex Pacing

To assess optimal hemodynamics in relation to stimulation site during right ventricular pacing, 17 consecutive patients who underwent cardiac catheterization were studied. In all patients, right ventricular apex and right ventricular outflow tract stimulation was performed at 85, 100, and 120 beats/min. Cardiac index at both pacing sites was compared using the left ventricular outflow tract continuous wave Doppler technique. Comparison of the two stimulation sites demonstrated that right ventricular outflow tract pacing resulted in a higher cardiac index at 85 beats/min (2.42 ± 1.2 vs 2.04 ±1.0 L/min per m², P < 0.002) at 100 beats/min (2.78 ± 1.4 vs 2.35 ± 1.1 L/min perm², P < 0.001) and 120 beats/min (3.00 ± 1.5 vs 2.61 ± 0.9 L/min perm², P < 0.001). From a total of 51 paired observations, 45 showed an increase in cardiac index during outflow tract pacing as compared to apex pacing. Right ventricular outflow tract pacing at 120 beats/min resulted in a lower cardiac index than right ventricular apex pacing in patients with significant coronary artery disease and/or impaired left ventricular function (ejection fraction ≤ 50%), whereas right ventricular outflow tract pacing produced higher cardiac indices in the absence of these abnormalities. Right ventricular outflow tract pacing resulted in higher cardiac indices as compared to apex pacing in all other subgroups at all other pacing sites tested. It is concluded that stimulation of the right ventricular outflow tract offers a significant hemodynamic benefit during single chamber pacing as compared to conventional apex pacing, particularly in the absence of significant coronary artery disease and/or left ventricular dysfunction.     

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.     

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.     

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.     

Hemodynamic Responses to Rapid Pacing: A Model for Tachycardia Differentiation

The hemodynamic responses to rapid atrial and ventricular pacing were examined in 10 closed-chest anesthetized dogs in an attempt to distinguish hemodynamically stable from unstable tachycardias. Pressure monitoring catheters were placed in the femoral artery, right atrium, and right ventricle to measure mean arterial pressure, mean right atrial pressure, and mean right ventricular pressure at baseline heart rate and after rapid high right atrial and right ventricular apex pacing. Pressures recorded during rapid pacing (average of the pressures at 30 and 60 seconds of pacing) at pacing rates of 180, 250, and 280/minute were compared to those recorded initially at baseline heart rates. Rapid right ventricular apex pacing resulted in significant increases in mean right atrial pressure (from 6 ± 1 mmHg (mean ± standard error) to 12 ± 1 mmHg, a 100% increase, P < 0.001) and mean right ventricular pressure (from 11 ±1 mmHg to 16 ± 1 mmHg, a 45% increase, p < 0.02) with marked hemodynamic compromise (mean arterial pressure decreased from 85 ± 6 mmHg to 50 ± 6 mmHg, a 41% decrease, P < 0.01). These parameters remained stable (no statistically significant difference from baseline) during high right atrial pacing. In half of the dogs high right atrial pacing at rates 250 resulted in atrioventricular Wenckebach. Thus, it is concluded that mean right atrial pressure and mean right ventricular pressure may be useful in distinguishing hemodynamically significant tachycardias, and in the future design of antitachycardia devices.     

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.     

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)     

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.     

Successful treatment of idiopathic left ventricular outflow tract tachycardia by catheter ablation or minimally invasive surgical cryoablation

Idiopathic right ventricular outflow tract tachycardia is readily amenable to radiofrequency catheter ablation. However, treatment modalities for left ventricular outflow tract tachycardia are not well defined. Out of 37 patients with idiopathic outflow tract tachycardia referred for catheter ablation, in 3 patients tachycardia originated from the left ventricular outflow tract. On the surface ECG, all left ventricular tachycardias exhibited an inferior axis with a predominant negative QRS complex in lead I. Heart rate during tachycardia ranged from 115 to 170 beats/min. During electrophysiological testing, 1 patient had inducible tachycardia on orciprenaline challenge, 1 patient had inducible tachycardia at baseline, and 1 patient had incessant tachycardia. In two patients, earliest ventricular activation was recorded from the endocardial left ventricular outflow tract at an anterolateral and an anterior site, respectively. A distinct high frequency spike preceded the QRS onset by 66/78 ms. Application of radiofrequency energy successfully eliminated tachycardia at these sites. In one patient, tachycardia originated from the epicardial left ventricular outflow tract. Mapping of the anterior interventricular vein revealed a fractionated low amplitude signal occurring 46 ms before QRS onset. After failure of catheter ablation from the corresponding endocardial site, successful minimally invasive surgical focal cryoablation of the epicardial target region was performed. During a follow-up period ranging from 7 to 12 months, all patients remained free of tachycardia. In conclusion, ventricular tachycardia arising from the left ventricular outflow tract may require endo- and epicardial mapping. Successful treatment is achieved by radiofrequency catheter ablation or minimally invasive surgical cryoablation.     

Comparison of Resting Hemodynamic Indices and Exercise Performance During Atrial Synchronized and Asynchronous Ventricular Pacing

Resting hemodynamic indices and exercise tolerance were measured during atrial synchronized (VAT) and asynchronous ventricular pacing (VOO) in 35 patients with implanted pacemakers which could be externally programmed to function in either pacing mode. Cardiac output and mean systemic arterial pressure were significantly greater during VAT pacing (VAT: 4.5 ± 1.21 /min, 115 ± 28 mmHg; VOO: 3.7 ± 0.8 1/min 105 ± 25 mmHg respectively), although there was no difference in pulmonary artery end-diastolic pressure. Maximal exercise performance was assessed using the Bruce protocol in both pacing modes. Neither the patient nor the supervising physician was aware of the preselected pacing mode; a second physician monitored the electrocardiogram and blood pressure but influenced the point of exercise termination only if a potentially dangerous arrhythmia or hypotension occured. Blood pressure responses were superior and atrial rates lower during VAT pacing, In all but five patients, exercise tolerance was improved by VAT pacing. This amounted to 33 percent or more in 23/35 patients. This improvement was shown to be maintained in the 20 patients who had repeat exercise tests several weeks later. Ventricular arrhythmias, hypotension, and lightheadedness frequently complicated exercise during asynchronous pacing but occurred rarely with atrial synchronized pacing. Resting hemodynamic indices did not predict the extent of improvement gained by physiological pacing.     

Effects of proximal ventricular septal pacing on hemodynamics and ventricular activation

Recently the use of alternate site pacing to improve cardiac function in patients with bradyarrhythmias has increased. In the present study, hemodynamics of right ventricular septal pacing were studied in seven dogs. A bipolar screw-in lead and endocardial lead were placed in the proximal right ventricular septum and right ventricular apex, respectively. The right ventricle was paced from each site. A conductance catheter and Millar catheter were inserted into the left ventricle to determine the left ventricular pressure and the pressure-volume loop. Cardiac output was measured using the thermodilution method. In five of the seven dogs, ventricular activation was documented by isochronal epicardial activation mapping during each pacing mode. Mean arterial pressure and cardiac output during septal pacing were significantly higher than during apical pacing (110 +/- 17 mmHg vs 100 +/- 18 mmHg; 1.00 +/- 0.39 L/min vs 0.89 +/- 0.33 L/min). The positive dp/dt during septal pacing was significantly higher than during apical pacing (2137 +/- 535 mmHg/s vs 1911 +/- 404 mmHg/s). End-systolic elastance during septal pacing was significantly higher compared to apical pacing (13.1 +/- 0.3 mmHg/mL vs 8.9 +/- 4.0 mmHg/mL). The ventricular activation time during septal pacing was significantly shorter than during apical pacing. The epicardial maps generated during septal pacing were similar to those from atrial pacing. We conclude that hemodynamics and interventricular conduction are less disturbed by proximal right ventricular septal pacing than apical pacing in dogs with normal hearts.     

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.     

Entrainment of Ventricular Tachycardia in Postoperative Tetralogy of Fallot

The mechanism of ventricular tachycardia (VT) in postoperative tetralogy of Fallot has been ascribed to both reentry and triggered automaticity. We performed electrophysiologic studies on a patient with this condition and induced sustained uniform ventricular tachycardia by programmed extrastimulation. Pacing during the tachycardia at multiple cycle lengths from the right ventricular apex (RVA) and outflow tract (RVOT) produced constant but progressive fusion between the paced and tachycardia QRS. With termination of pacing, the last captured complex was unfused but coupled at the paced cycle length and then the tachycardia resumed at its intrinsic rate. Therefore, the VT was entrained. In addition, an area of slow conduction between the RVOT and RVA was demonstrated. These findings support a reentrant mechanism of this arrhythmia.     

Atrial and Ventricular Pressures in Atrial Flutter

The hemodynamic effects of atrial flutter (AF) are unknown. The purpose of the present study was to investigate the changes in atrial and ventricular pressures after induction of AF. In 23 patients with paroxysmal AF (age 59 ± 9 years), a hemodynamic study was performed both during sinus rhythm and after induction of the tachyarrhythmia. During AF, 13 patients showed a fixed 2:1 AV conduction and 10 patients showed variable conduction. Mean right and left atrial pressures increased (P < 0.001) and right and left ventricular end-diastolic pressures decreased (P < 0.001) after induction of AF. Roth the increase in mean atrial pressures and the decrease in ventricular end-diastolic pressures were present either in the patients with fixed 2:1 AV (heart rate: 133 ± 15 beats/min) or in those with variable conduction (heart rate 96 ± 15 beats/min), but were more marked in the former. AF produces an impairment of atrial function, as evidenced by the increase in mean atrial pressures and reduction in ventricular end-diastolic pressures in the absence of an elevated heart rate. The mechanisms responsible for the increase in mean atrial pressures are unknown; however, atrial contractions against closed AV valves seem to play an important role.     

Distinct Activation Patterns of Idioventricular Rhythms and Sympathetically-Induced Ventricular Tachycardias in Dogs with Atrioventricular Block

To investigate mechanisms of ventricular impulse formation in response to sympathetic stimulation in the healthy canine heart in situ, we compared the patterns of ventricular activation during the idioventricular rhythms arising after complete atrioventricular (AV) block and ventricular tachycardias induced by RSG or LSG stimulation. Isochronal maps were generated by computer from 116-127 unipolar electrograms recorded from the entire ventricular epicardium in 15 open chest, anesthetized dogs. In eight of these, bipolar electrograms were recorded with plunge electrodes from 11 selected endocardial sites located below epicardial breakthrough areas. Intracardiac recordings from the His-Purkinje system were made with electrode catheters. After electrograms were recorded during sinus rhythm, complete AV block was induced by injecting formaldehyde into the AV node and idioventricular rhythms occurred spontaneously at a rate of 37 +/- 12 beats/min (mean +/- SD, n = 25). During idioventricular rhythms, endocardial activation preceded the earliest epicardial breakthrough, which occurred in either the right anterior paraseptal region, antero-apical left ventricle, or postero-apical left ventricle. These sites were consistent with a focal origin in the subendocardial His-Purkinje system. Total epicardial activation times lasted for 47 +/- 13 msec (n = 40). Idioventricular rhythms were suppressed by overdrive pacing (intermittent trains of ten beats with decremental cycle length from 500 to 200 msec) or by intravenous calcium infusion (to plasma levels of 10.1-15.2 mM). Right or left stellate ganglion stimulation increased idioventricular rhythm rates (to 52 +/- 13 beats/min, n = 28) and also induced, in all preparations, ventricular tachycardias that had significantly faster rates (189 +/- 55 beats/min, n = 27, P less than 0.005). Ventricular fibrillation was induced after brief runs of ventricular tachycardia in five of the preparations. During ventricular tachycardias, epicardial activation occurred on the right ventricular outflow tract or the postero-lateral wall of the left ventricle, and preceded endocardial activation in 50% of cases. Total epicardial activation times (103 +/- 29 beats/min) were significantly longer than during idioventricular rhythms (P less than 0.005). Ventricular tachycardias displayed overdrive excitation at critical pacing cycle lengths (360-280 msec) and were not suppressed by calcium infusion. Thus, differential mechanisms of impulse formation with distinct localizations can be elicited from healthy ventricular myocardium.     

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)     

Contribution of Atrioventricular Synchrony to Left Ventricular Systolic Function in a Closed-Chest Canine Model of Complete Heart Block: Implications for Single-Chamber Rate-Variable Cardiac Pacing

This study assessed the impact of atrioventricular (AV) synchrony on characteristics of left ventricular (LV) systolic function during ventricular pacing over a wide heart rate range in a conscious closed-chest canine model of complete AV block. Ten healthy adult dogs underwent thoracotomy during which complete AV block was created by formaldehyde injection, and paired ultrasonic sonomicrometers were positioned on the LV anterior-posterior minor axis. Following recovery from surgery, peak and end-diastolic LV transmural pressure, maximum dP/dt, stroke work, end-diastolic minor axis dimension, and maximum velocity of shortening, were quantitated at heart rates of 80, 100, 120, 140, and 160 beats per minute (bpm) during both ventricular pacing alone and AV sequential pacing with increasing AV intervals (0, 50, 100, 150, 200, 250, and 300 ms). Over the heart rate range tested, parameters of LV systolic function did not differ significantly during ventricular pacing with or without AV synchrony. For example, during ventricular pacing alone maximum LV dP/dt varied from 2110 +/- 70 mmHg/s to 2463 +/- 567 mmHg/s, a range essentially identical to that observed in the presence of AV synchrony. On the other hand, although the impact on LV performance of varying AV interval from 0 to 300 ms was small, differences tended to become more pronounced at higher pacing rates. At 80 bpm, neither stroke work nor maximum LV dP/dt were affected by change in AV interval, while at heart rates greater than or equal to 120 bpm both stroke work and LV dP/dt tended to maximize at AV intervals of 50 and 100 ms and thereafter declined.(ABSTRACT TRUNCATED AT 250 WORDS)     

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)     

Differentiation Between Monomorphic Ventricular Tachycardia and Sinus Tachycardia Based on the Right Ventricular Evoked Potential

The differentiation between ventricular tachycardia (VT) and smus tachycardia (ST) is problematic in some patients with implantable defibrillators and/ or antitachycardia pacemakers. The Integral of the ventricular endocardial evoked response, or paced depolarization integral (PDI), has been demonstrated to undergo characteristic changes with a variety of stimuli including catecholamines, pacing rate, and exercise. We hypothesized that the PDI recorded from a unipolar transvenous right ventricular endocardial catheter would differentiate VT from ST. The PDI was calculated from a unipolar pacing stimulus, delivered via a cathode in the right ventricular apex, and the reference electrode, a quadripolar catheter positioned in the superior vena cava. PDIs were measured in 22 patients during VT and sinus rhythm. The PDI measured during sinus rhythm was 579 ± 240 μV-sec and the PDI during VT was 894 ± 411 μV-sec (P < 0.001). In a subset of seven patients, PDIs were measured during VT, sinus rhythm, and ST induced by catecholamine infusion or exercise. In this subset, the PDI during sinus rhythm was 645 ± 295 μV-sec, during ST 588 ± 308 μV-sec (9% decrease from sinus, P = 0.05), and during VT 863 ± 342 μV-sec (33.9% increase, P = 0.01). These data indicate that the measurement of the PDI is potentially useful in differentiating VT from ST.     

Hemodynamics of Idiopathic Paroxysmal Atrial Fibrillation

The hemodynamics of induced atrial fibrillation (AF) was investigated in 15 patients (ages 58 ± 11 years) with paroxysmal AF presenting without organic heart disease or hypertension. A hemodynamic study was performed both during sinus rhythm and after the induction of AF. The mean heart rate increased from 73 ± 11 to 128 ± 18 beats/min (P < 0.001) after AF. Systolic and mean aortic pressures did not significantly change, and diastolic aortic pressure increased (78 ± 11 vs 89 ± 12 mmHg, P < 0.01). Left ventricular enddiastolic pressure decreased during AF (9 ± 3 vs 6 ± 2.6 mmHg, P < 0.005), whereas mean pulmonary wedge pressure increased (8 ± 2 vs 12 ± 4 mmHg, P < 0.001). Systolic pulmonary arterial pressure did not show significant variations, and there was a slight but statistically significant increase in the diastolic and mean pulmonary arterial pressures (P < 0.01). The right ventricular end-diastolic pressure decreased during AF (5.6 ± 2 vs 3.8 ± 2 mmHg, P < 0.01 j, whereas mean right atrial pressure showed a trend toward an increase. Stroke volume markedly decreased (P < 0.001) while the cardiac index did not significantly change. Systemic vascular resistance, pulmonary arteriolar resistance, and the arteriovenous O₂ difference showed no significant variations after the induction of AF. These results suggest that in subjects without organic heart disease, paroxysmal AF is well tolerated hemodynamicaily, and the rise in the atrial pressures during AF is not related to an increase in the ventricular end-diastolic pressure.