© 2003 by European Society of Cardiology
Quality of life and exercise capacity in patients with prolonged PQ interval and dual chamber pacemakers: a randomized comparison of permanent ventricular stimulation vs intrinsic AV conduction
Division of Cardiology, Stadtspital Triemli Zurich, Switzerland
Manuscript submitted 23 January 2003. Accepted after revision 22 June 2003.
Correspondence: Dominik E. Maurer, MD, Division of Cardiology, Stadtspital Triemli, Birmensdorferstrasse 497, CH-8063 Zurich, Switzerland. Tel.: +41-1-466-1520; Fax: +41-1-466-2599. E-mail: dominik.maurer{at}triemli.stzh.ch
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Abstract |
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AIMS: The aim of this study was to assess quality of life (QoL) and exercise capacity during permanent ventricular stimulation (PVS) compared with intrinsic atrioventricular conduction (IAVC) in patients with dual chamber pacemakers (PMs) and an intrinsic PQ interval >210 ms. Dual chamber PMs in patients with atrioventricular (AV) block are usually programmed to PVS in VDD or DDD mode, although IAVC is preserved, but prolonged. This results in PVS, although long periods of IAVC may occur.
METHODS AND RESULTS: Fourteen consecutive patients (age 76±6 years; intermittent high degree AV block in six patients, binodal disease in eight patients) were enroled in a prospective, randomized, single blind, crossover study of IAVC vs PVC. To permit IAVC, programmed AV delays were prolonged. At the end of each phase, QoL scores were assessed using a questionnaire and echocardiography and cardiopulmonary stress tests were performed. During the study period with IAVC, 95±10% of the beats were conducted intrinsically. QoL scores (28.3±11 vs 29.3±13; P=0.68), peak exercise capacity (5.4±2.4 vs 5.2±2.9 METs; P=0.35) and peak oxygen uptake (19.8±4.5 vs 18.8±5.2 ml/kg/min; P=0.16) were comparable during IAVC and PVS, respectively. Similar echocardiographic values were found for left ventricular (LV) ejection fraction (50±9% vs 51±10%; P=0.67) and velocity time integral at the left ventricular outflow tract (24±5 vs 22±6 cm; P=0.20), respectively.
CONCLUSIONS: We conclude that in patients with dual chamber PMs and intermittent high degree AV block neither PVS nor IAVC is superior with respect to QoL or exercise capacity. Therefore, pulse generators may be programmed to IAVC to extend their longevity.
Key Words: Pacemaker, intrinsic AV conduction, quality of life, exercise capacity
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Introduction |
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Many patients with dual chamber pacemakers and intermittent high degree atrioventricular (AV) block or binodal disease have preserved but prolonged intrinsic atrioventricular conduction (IAVC). Although these patients depend on ventricular stimulation only during short periods of high degree AV block, pacemakers are commonly programmed to permanent ventricular stimulation (PVS; VDD or DDD mode) by choosing a shorter AV delay. While PVS normalizes prolonged AV conduction times, the resulting abnormal left bundle branch block-like pattern of right ventricular activation leads to asynchronous contraction, which potentially reduces regional myocardial blood flow and ventricular performance[1
–3]. Conversely, marked prolongation of intrinsic AV conduction interferes with optimal timing of atrial contraction and may reduce cardiac output[4–6]. Occasionally it causes symptoms, previously described as pseudopacemaker syndrome[7,8]. Many studies have, therefore, concentrated on defining optimal AV delays during PVS in patients with dual chamber pacemakers[9–19]. However, there are few data on quality of life (QoL) and exercise capacity comparing intrinsic AV conduction with permanent ventricular pacing. Thus, the present study was designed to compare PVS with intrinsic AV conduction in patients with a dual chamber pacemaker. |
Methods |
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Study patients
Fourteen consecutive patients with a dual chamber pacemaker (DDDR or VDD) were selected from the pacemaker clinic. Inclusion criteria were binodal disease or intermittent high degree AV block, intrinsic AV conduction time between 210 and 350 ms, left ventricular ejection fraction
30% and physical capability to perform a treadmill exercise test. Patients were excluded if there was a history of a recent myocardial infarction, a history of limiting pulmonary disease, or if they were in New York Heart Association (NYHA) class IV. All patients gave written informed consent.
Study design
A prospective single-blinded randomized crossover design was used (Figs. 1 and 2). At enrolment clinical baseline characteristics were assessed. In each patient a 12 lead surface ECG during intrinsic AV conduction was obtained to determine underlying conduction abnormalities. Intrinsic AV conduction time was measured on the intracardiac ECG using the telemetry features of the pacemaker. A complete transthoracic echocardiographic study was performed. After enrolment, patients were randomized either to intrinsic AV conduction or to PVS with their optimal AV delay for a period of 2 weeks. Thereafter, patients crossed over to the opposite pacing mode for another period of 2 weeks. At the end of each period, patients underwent a cardiopulmonary stress test, a transthoracic echocardiographic study, a Holter ECG and a pacemaker telemetry interrogation. Furthermore, a questionnaire was completed to assess functional class, QoL and patients' preference of stimulation mode. Medical treatment was not changed during the whole study.
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Echocardiographic studies
Two experienced operators performed all echocardiographic studies using commercially available imaging systems (Sonos 2500, Hewlett–Packard, Inc., Andover, MA, U.S.A.; GE Vingmed System Five, Horten, Norway). Patients were examined at rest in the left lateral decubitus position. All studies were performed in the patients' currently programmed mode and AV interval. M-mode echocardiography from a parasternal long axis view was used to define left ventricular (LV) mass index. Biplane LV ejection fractions were determined using the Simpson method[20]
. Velocity time integrals in the LV outflow tract were obtained from an apical five chamber view by pulsed wave Doppler measurements and the mean value was determined from five measurements. The optimal AV delay was defined as the AV delay resulting in the highest velocity time integral at the LV outflow tract during atrially triggered ventricular stimulation or AV sequential pacing. It was determined by 25 ms increments of the AV interval from 100 to 250 ms or by the appearance of fusion beats or intrinsically conducted beats. Paper printouts were obtained to document all measurements.
Pacemaker programming
To allow intrinsic AV conduction, programmed sensed and paced AV delays were prolonged to the shortest time interval necessary for complete inhibition of ventricular stimulation. If hereby the 2:1 block rate fell below the preset maximal tracking limit, the postventricular atrial refractory period was shortened by the same amount of time. In one chronotropically competent patient the maximal programmable AV delay available was not sufficient for intrinsic AV conduction and, therefore, the pacemaker was set to the DDI mode. In all other patients current pacemaker modes were left unchanged (DDDR or VDD). For PVS, the sensed AV delay was programmed at the optimal interval determined as described above. Paced AV delays were set 30 ms longer according to the mean difference between optimal paced and sensed AV delays found in previous studies[14,21]. All other programmable parameters were left unchanged.
Confirmation of intrinsic AV conduction
The percentage of intrinsically conducted beats was assessed by Holter monitoring and pacemaker telemetry data during the last 24 h of each period. Ninety or more percent of intrinsically conducted beats were required for the period of intrinsic AV conduction.
Cardiopulmonary stress tests
Symptom limited cardiopulmonary stress tests were performed using a Marquette treadmill device (Max-1TM, Marquette Electronics, Milwaukee, WI, U.S.A.) and breath-to-breath respiratory gas analysis was carried out with a cardiorespiratory diagnostic system (CardiO2TM, MedGraphics Corporation, St. Paul, MN, U.S.A.). A standardized exercise protocol was applied (modified Naughton protocol)[22]. Exercise duration, maximal exercise capacity and maximal oxygen uptake were measured.
Quality of life questionnaire
At the end of each 2-week period patients were interviewed by an examiner who was unaware of the actual pacemaker settings. Goldmann's Specific Activity Scale Functional Class questionnaire[23] was used to determine NYHA functional class. In a second questionnaire a variety of cardiovascular symptoms and self-perceived health were assessed as previously described[24]. An overall QoL score was obtained. The range of achievable points for each item was from 0 (no symptoms) to 10 points (maximal intensity and frequency of symptoms). In addition, at the end of the study all patients were asked to indicate their preferred period.
Statistical analysis
Results are expressed as mean values±SD. Student's two-tailed t-test was used to analyse paired differences. P-values of less than 0.05 were considered to be statistically significant. All analyses were performed using the statistical program StatView 4.02 (Abacus Concepts Inc., Berkeley CA, U.S.A.).
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Results |
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Patient characteristics (Table 1)
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Fourteen patients (11 men, 3 women) with a mean age of 76±6 years were randomized. Ten (71%) patients had a history of hypertension. Seven (50%) patients suffered from coronary artery disease, two (14%) had valvular heart disease and one (7%) had idiopathic cardiomyopathy. Mean LV ejection fraction was 46±13% at enrolment (permanent ventricular pacing with normal AV delays). LV hypertrophy was present in six (43%) patients. Eight (57%) patients showed intraventricular conduction abnormalities: left bundle branch block in two, left anterior fascicular block (LAFB) in three and right bundle branch block/LAFB in three patients (see Table 1 for abbreviations). The mean intrinsic AV conduction time measured on the intracardiac ECG was 259±38 ms compared with 138±40 ms of the mean optimal paced AV delay (P=0.0001). Medications included amiodarone in five (36%), sotalol in four (29%) and other beta-blockers in one (7%) patient. The indication for pacemaker implantation was binodal disease in eight (57%) and intermittent high degree AV block in six (43%) patients. Pacemaker models are indicated in Table 1. Programmed modes at baseline were VDD in one (7%), DDDR in five (36%) and DDD in eight (57%) patients.
Confirmation of intrinsic conduction
During periods of intrinsic AV conduction, 94.8±10% of all registered beats resulted in an intrinsic ventricular rhythm by the predefined pacemaker programmation, confirmed by Holter ECG and telemetry data. The predefined percentage of 90% or more was achieved in all but one patient (range 62–100%).
Functional class and quality of life (Table 2)
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Mean NewYork heart association (NYHA) class was 1.5±0.8 and 1.6±0.9 for IAVC and PVS, respectively. Most patients remained in the same NYHA class in both periods, and in two patients the NYHA class worsened from II during IAVC to III during PVS. QoL scores were 28.3±11 for IAVC and 29.3±13 for PVS.
Cardiopulmonary stress test data (Table 3)
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For IAVC and PVS maximal exercise capacity (5.4±2.4 vs 5.2±2.9 METs), exercise duration (456±180 vs 404±159 s) and peak oxygen uptake (19.8±4.5 vs 18.8±5.2 ml/kg/min), respectively, were similar (P=ns). One patient did not tolerate the mask for respiratory gas analysis, and his oxygen uptake data are missing.
Echocardiographic data (Table 4)
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Doppler derived velocity time integrals in the left ventricular outflow tract were 24.1±5.1 cm with IAVC and 22.6±6.8 cm with PVS (P=ns) and LV ejection fractions were 50.2±9.4% and 51.1±10.1% (P=ns), respectively.
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Discussion |
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The optimal AV delay in patients with dual chamber pacemakers has been investigated by many researchers[5,
9,10,1924–27]. In these studies different techniques (radionuclide ventriculography, echocardiography, impedance cardiography and invasive catheterization) have been used to determine the haemodynamic effect of various AV delays. A wide range of the optimal AV delay has been observed, making individual determination necessary. Although many dual chamber pacemakers are programmed to be atrially triggered or AV sequential pacing with permanent right ventricular stimulation, the normal intrinsic activation sequence may be preferred in patients with only short periods of high degree AV block.
The favourable haemodynamic effect of the normal AV activation sequence has been demonstrated by many investigators in animal models and various groups of patients[21,28–32]. In comparison with atrially triggered or AV sequential pacing (VDD or DDD mode), atrial pacing with intrinsic ventricular activation (AAI mode) was found to be superior with respect to cardiac output and parameters of exercise capacity[21,29–32]. There are conflicting results concerning LV ejection fraction assessed by radionuclide ventriculography. While in the study of Shefer and coworkers LV ejection fraction in patients with primary conduction defects was not dependent on pacing mode (AOO, DVI, VVI), Leclercq and coworkers found significantly higher ejection fractions during AAI pacing when compared with DDD pacing[29,32]. Animal studies have demonstrated lower myocardial oxygen consumption and higher cardiac efficiency during AOO pacing when compared with DVI or VVI pacing[28,33]. The negative effect of AV sequential and ventricular pacing has been attributed to the abnormal ventricular activation due to right ventricular apical stimulation[28,33–36]. This results in an activation pattern comparable to that seen in left bundle branch block, which has been shown to impair left ventricular ejection fraction and myocardial blood flow[37]. By programming dual chamber pacemakers to AAI or DDD mode with a prolonged AV delay, the intrinsic ventricular activation sequence can be preserved.
Recent studies assessing short-term changes in cardiac output determined by Doppler echocardiography in patients with prolonged intrinsic conduction demonstrated the superiority of AAI over DDD mode at moderately prolonged AV conduction times[38–40]. However, at conduction times exceeding 220–270 ms, DDD pacing showed improved haemodynamics, which underlines the negative effects of a markedly prolonged first degree AV block[7,8,36,38,40,41]. In a study of patients with sick sinus syndrome, Vardas and coworkers[39] found no differences in cardiopulmonary performance during submaximal stress test between AAI and DDD mode, although patients with an intrinsic conduction time of more than 220 ms had a higher cardiac output with DDD pacing at rest.
In patients with intermittent high degree AV block and otherwise preserved but prolonged AV conduction there are two possibilities for programming a dual chamber pacemaker: VDD or DDD pacing may either be programmed to a relatively short AV delay resulting in PVS or to a prolonged AV delay permitting intrinsic AV conduction. The latter mode of programming may be preferred because energy expenditure of the pulse generator is less and longevity can be extended. Based on previous data, it cannot be concluded for this specific patient group, to which mode dual chamber pacemakers should be programmed to ensure optimal long-term cardiopulmonary performance and QoL. In the present study QoL scores and functional NYHA class were comparable for IAVC and PVS. Exercise duration, maximal exercise capacity in METs and maximal oxygen uptake during cardiopulmonary stress test, again, were not significantly different, when IAVC was compared with PVS, although patients had relatively long intrinsic AV conduction times (mean 259 ms). These results are in contrast to previous acute studies with long intrinsic AV conduction times[38,40]. However, in the present study we did evaluate a longer lasting effect of the different pacing modes, since all measurements were taken at the end of each 2-week period. Thus, this study adds important data for the management of patients with intermittent high degree AV block and prolonged, but preserved, AV conduction.
In conclusion, IAVC and PVS show similar medium-term effects with respect to LV ejection fraction, cardiac output, QoL, functional class and exercise capacity in patients with intermittent high degree AV block and prolonged, but preserved, AV conduction. In these patients dual chamber pacemakers may be safely programmed to IAVC to prolong longevity of the device by reducing energy expenditure.
Limitations
Our study included a relatively small number of patients with various underlying cardiac diseases. Group statistics showed no significant differences, nor was there trend in favour of one of the tested pacemaker settings. It is, therefore, unlikely that a similar study including a considerably higher number of patients would produce a statistically significant difference. We still cannot exclude that some patients might profit from individually tailored pacemaker settings. This may particularly apply to patients with complete bundle branch block (36% of the patients included in our study).
Although 2 weeks appear to be a short period to evaluate medium- to long-term effects of various pacemaker settings on QoL and exercise capacity we consider it long enough since prior studies have shown that acute haemodynamic changes seen with different pacemaker settings are representative of changes seen with long-term pacing[42,43]. Furthermore, other authors have used the same time interval to reveal differences of various pacemaker settings[44,45]. The fact that changes in pacemaker settings immediately translate into sustained haemodynamic effects argues against a carryover effect that is potentially involved in the crossover design. The analysis of the data revealed no such effect in the present study.
The relatively short study period of 2 weeks will, however, not give an impression of the possible adverse effects of development of permanent AV block in patients programmed to preserve IAVC[46].
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References |
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[1] Askenasi J, Alexander JH, Koenigsberg DI, Belic N, Lesch M. Alterations of left ventricular performance by left bundle branch block stimulated with atrioventricular sequential pacing. Am J Cardiol 1984; 53: 99–104.[CrossRef][Web of Science][Medline]
[2] Nielsen JC, Bottcher M, Nielsen TT, Pedersen AK, Andersen HR. Regional myocardial blood flow in patients with sick sinus syndrome randomized to long-term single chamber atrial or dual chamber pacing — effect of pacing mode and rate. J Am Coll Cardiol 2000; 35: 1453–1461.
[3] Tantengco M, Thomas R, Karpawich P. Left ventricular dysfunction after long-term right ventricular apical pacing in the young. J Am Coll Cardiol 2001; 37: 2093–2100.
[4] Ishikawa T, Kimura K, Miyazaki N, et al. Diastolic mitral regurgitation in patients with first-degree atrioventricular block. Pacing Clin Electrophysiol 1992; 15: 1927–1931.[CrossRef][Medline]
[5] Ovsyshcher I, Zimlichman R, Katz A, Bondy C, Furman S. Measurements of cardiac output by impedance cardiography in pacemaker patients at rest: effects of various atrioventricular delays. J Am Coll Cardiol 1993; 21: 761–767.[Abstract]
[6] Ishikawa T, Sumita S, Kimura K, et al. Critical PQ interval for the appearance of diastolic mitral regurgitation and optimal PQ interval in patients implanted with DDD pacemakers. Pacing Clin Electrophysiol 1994; 17: 1989–1994.[CrossRef][Medline]
[7] Barold SS. Indications for permanent cardiac pacing in first-degree AV block: class I, II, or III? Pacing Clin Electrophysiol 1996; 19: 747–751.[CrossRef][Medline]
[8] Kim YH, O'Nunain S, Trouton T, et al. Pseudo-pacemaker syndrome following inadvertent fast pathway ablation for atrioventricular nodal reentrant tachycardia. J Cardiovasc Electrophysiol 1993; 4: 178–182.[Web of Science][Medline]
[9] Modena MG, Rossi R, Carcagni A, Molinari R, Mattioli G. The importance of different atrioventricular delay for left ventricular filling in sequential pacing: clinical implications. Pacing Clin Electrophysiol 1996; 19: 1595–1604.[CrossRef][Medline]
[10] Kindermann M, Fröhlig G, Doerr T, Schieffer H. Optimizing the AV delay in DDD pacemaker patients with high degree AV block: mitral valve Doppler versus impedance cardiography. Pacing Clin Electrophysiol 1997; 20: 2453–2462.[CrossRef][Medline]
[11] Eugene M, Lascault G, Frank R, Fontaine G, Grosgogeat Y, Teillac A. Assessment of the optimal atrio-ventricular delay in DDD paced patients by impedance plethysmography. Eur Heart J 1989; 10: 250–255.
[12] Frielingsdorf J, Gerber AE, Dur P, Vuilliomenet A, Bertel O. Importance of an individually programmed atrioventricular delay at rest and on work capacity in patients with dual chamber pacemakers. Pacing Clin Electrophysiol 1994; 17: 37–45.[CrossRef][Medline]
[13] Gessner M, Blazek G, Kainz W, Gruska M, Gaul G. Application of pulsed-Doppler tissue imaging in patients with dual chamber pacing: the importance of conduction time and AV delay on regional left ventricular wall dynamics. Pacing Clin Electrophysiol 1998; 21: 2273–2279.[CrossRef][Medline]
[14] Janosik DL, Pearson AC, Buckingham TA, Labovitz AJ, Redd RM. The hemodynamic benefit of differential atrioventricular delay intervals for sensed and paced atrial events during physiologic pacing. J Am Coll Cardiol 1989; 14: 499–507.[Abstract]
[15] Mest'an M, Kvasnicka J, Rejchrt P. A new method of estimation of the optimal AV delay by using pulse oximetry in DDD paced patients. Acta Med 1998; 41: 135–139.
[16] Mohan JC, Sethi KK, Pandit N, Bhargava M, Arora R, Khalilullah M. Acute hemodynamic effects of different atrioventricular intervals in dual chamber pacemakers: is there an optimum atrioventricular delay. Indian Heart J 1992; 44: 79–85.[Medline]
[17] Rossi R, Muia N, Turco V, Sgura FA, Molinari R, Modena MG. Short atrioventricular delay reduces the degree of mitral regurgitation in patients with a sequential dual-chamber pacemaker. Am J Cardiol 1997; 80: 901–905.[CrossRef][Web of Science][Medline]
[18] Wish M, Fletcher RD, Gottdiener JS, Cohen AI. Importance of left atrial timing in the programming of dual-chamber pacemakers. Am J Cardiol 1987; 60: 566–571.[CrossRef][Web of Science][Medline]
[19] Ishikawa T, Sumita S, Kimura K, et al. Prediction of optimal atrioventricular delay in patients with implanted DDD pacemakers. Pacing Clin Electrophysiol 1999; 22: 1365–1371.[CrossRef][Medline]
[20] Schiller NB, Shah PM, Crawford M, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr 1989; 2: 358–367.[Medline]
[21] Daubert C, Ritter P, Mabo P, Varin C, Leclerq C. AV delay optimization in DDD and DDDR pacing. New Perspectives in Cardiac Pacing 1993; Mount Kisco Futura Publishing Co pp. 259–287.
[22] Naughton JP and Maider R. Methods of exercise testing. In Naughton JP and Hellerstein HR (Eds.). Exercise Testing and Exercise Training in Coronary Artery Disease 1973; New York Academic Press pp. 79–91.
[23] Goldman L, Hashimoto B, Cook EF, Loscalzo A. Comparative reproducibility and validity of systems for assessing cardiovascular functional class: advantages of a new specific activity scale. Circulation 1981; 64: 1227–1234.[Medline]
[24] Frielingsdorf J, Deseo T, Gerber AE, Bertel O. A comparison of quality-of-life in patients with dual chamber pacemakers and individually programmed atrioventricular delays. Pacing Clin Electrophysiol 1996; 19: 1147–1154.[CrossRef][Medline]
[25] Leonelli FM, Wang K, Youssef M, Hall R, Brown D. Systolic and diastolic effects of variable atrioventricular delay in patients with complete heart block and normal ventricular function. Am J Cardiol 1997; 80: 294–298.[CrossRef][Web of Science][Medline]
[26] Von Knorre GH, Ismer B, Voss W, Petzsch M, Pulya K. What range of programmable AV delays is necessary in antibradycardia DDD stimulation? Pacing Clin Electrophysiol 1998; 21: 264–267.[CrossRef][Medline]
[27] Kolb HJ, Böhm U, Rother T, Mende M, Neugebauer A, Pfeiffer D. Assessment of the optimal atrioventricular delay in patients with dual chamber pacemakers using impedance cardiography and Doppler echocardiography. J Clin Basic Cardiol 1999; 2: 237–240.
[28] Prinzen FW and Peschar M. Relation between the pacing induced sequence of activation and left ventricular pump function in animals. Pacing Clin Electrophysiol 2002; 25: 484–498.[CrossRef][Medline]
[29] Shefer A, Rozenman Y, Ben David Y, Flugelman MY, Gotsman MS, Lewis BS. Left ventricular function during physiological cardiac pacing: relation to rate, pacing mode, and underlying myocardial disease. Pacing Clin Electrophysiol 1987; 10: 315–325.[CrossRef][Medline]
[30] Harper GR, Pina IL, Kutalek SP. Intrinsic conduction maximizes cardiopulmonary performance in patients with dual chamber pacemakers. Pacing Clin Electrophysiol 1991; 14: 1787–1791.[CrossRef][Medline]
[31] Rosenqvist M, Isaaz K, Botvinick EH, et al. Relative importance of activation sequence compared to atrioventricular synchrony in left ventricular function. Am J Cardiol 1991; 67: 148–156.[CrossRef][Web of Science][Medline]
[32] Leclercq C, Gras D, Le Helloco A, Nicol L, Mabo P, Daubert C. Hemodynamic importance of preserving the normal sequence of ventricular activation in permanent cardiac pacing. Am Heart J 1995; 129: 1133–1141.[CrossRef][Web of Science][Medline]
[33] Baller D, Wolpers HG, Zipfel J, Bretschneider HJ, Hellige G. Comparison of the effects of right atrial, right ventricular apex and atrioventricular sequential pacing on myocardial oxygen consumption and cardiac efficiency: a laboratory investigation. Pacing Clin Electrophysiol 1988; 11: 394–403.[CrossRef][Medline]
[34] Owen CH, Esposito DJ, Davis JW, Glower DD. The effects of ventricular pacing on left ventricular geometry, function, myocardial oxygen consumption, and efficiency of contraction in conscious dogs. Pacing Clin Electrophysiol 1998; 21: 1417–1429.[CrossRef][Medline]
[35] Chirife R. Left heart function during right heart pacing. Pacing Clin Electrophysiol 1994; 17: 1451–1455.[CrossRef][Medline]
[36] Ovsyshcher IE. Toward physiological pacing: optimization of cardiac hemodynamics by AV delay adjustment. Pacing Clin Electrophysiol 1997; 20: 861–865.[CrossRef][Medline]
[37] Grines CL, Bashore TM, Boudoulas H, Olson S, Shafer P, Wooley CF. Functional abnormalities in isolated left bundle branch block. The effect of interventricular asynchrony. Circulation 1989; 79: 845–853.[Medline]
[38] Jutzy RV, Feenstra L, Pai R, et al. Comparison of intrinsic versus paced ventricular function. Pacing Clin Electrophysiol 1992; 15: 1919–1922.[CrossRef][Medline]
[39] Vardas PE, Simantirakis EN, Parthenakis FI, Chrysostomakis SI, Skalidis EI, Zuridakis EG. AAIR versus DDDR pacing in patients with impaired sinus node chronotropy: an echocardiographic and cardiopulmonary study. Pacing Clin Electrophysiol 1997; 20: 1762–1768.[CrossRef][Medline]
[40] Iliev II, Yamachika S, Muta K, et al. Preserving normal ventricular activation versus atrioventricular delay optimization during pacing: the role of intrinsic atrioventricular conduction and pacing rate. Pacing Clin Electrophysiol 2000; 23: 74–83.[CrossRef][Medline]
[41] Hayes DL. Evolving indications for permanent pacing. Am J Cardiol 1999; 83: 161D–165D.[CrossRef][Web of Science][Medline]
[42] Kappenberger L, Gloor HO, Babotai I, Steinbrunn W, Turina M. Hemodynamic effects of atrial synchronization in acute and long-term ventricular pacing. Pacing Clin Electrophysiol 1982; 5: 639–645.[CrossRef][Medline]
[43] Kruse I, Arnman K, Conradson TB, Ryden L. A comparison of the acute and long-term hemodynamic effects of ventricular inhibited and atrial synchronous ventricular inhibited pacing. Circulation 1982; 65: 846–855.
[44] Lukl J, Doupal V, Heinc P. Quality-of-life during DDD and dual sensor VVIR pacing. Pacing Clin Electrophysiol 1994; 17: 1844–1848.[CrossRef][Medline]
[45] Sulke AN, Chambers JB, Sowton E. The effect of atrio-ventricular delay programming in patients with DDDR pacemakers. Eur Heart J 1992; 13: 464–472.
[46] Nielsen JC, Pedersen AK, Mortensen PT, Andersen HR. Programming a fixed long atrioventricular delay is not effective in preventing ventricular pacing in patients with sick sinus syndrome. Europace 1999; 1: 113–120.
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