CLINICAL RESEARCH: HEART RHYTHM DISORDERS
Right Atrial Pacing Impairs Cardiac Function During Resynchronization Therapy
Acute Effects of DDD Pacing Compared to VDD Pacing
Alain Bernheim, MD,
Peter Ammann, MD,
Christian Sticherling, MD,
Peter Burger, MD,
Beat Schaer, MD,
Hans Peter Brunner-La Rocca, MD,
Jens Eckstein, MD,
Stephanie Kiencke, MD,
Christoph Kaiser, MD,
Andre Linka, MD,
Peter Buser, MD,
Matthias Pfisterer, MD and
Stefan Osswald, MD*
Division of Cardiology, University Hospital, Basel, Switzerland.
Manuscript received August 16, 2004;
revised manuscript received October 12, 2004,
accepted January 11, 2005.
* Reprint requests and correspondence: Dr. Stefan Osswald, Cardiac Unit, University Hospital, CH 4031-Basel, Switzerland. (Email: sosswald{at}uhbs.ch).
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Abstract
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OBJECTIVES: We aimed to compare the hemodynamic effects of right-atrial-paced (DDD) and right-atrial-sensed (VDD) biventricular paced rhythm on cardiac resynchronization therapy (CRT).
BACKGROUND: Cardiac resynchronization therapy improves hemodynamics in patients with severe heart failure and left ventricular (LV) dyssynchrony. However, the impact of active right atrial pacing on resynchronization therapy is unknown.
METHODS: Seventeen CRT patients were studied 10 months (range: 1 to 46 months) after implantation. At baseline, the programmed atrioventricular delay was optimized by timing LV contraction properly at the end of atrial contraction. In both modes the acute hemodynamic effects were assessed by multiple Doppler echocardiographic parameters.
RESULTS: Compared to DDD pacing, VDD pacing resulted in much better improvement of intraventricular dyssynchrony assessed by the septal-to-posterior wall motion delay (VDD 106 ± 83 ms vs. DDD 145 ± 95 ms; p = 0.001), whereas the interventricular mechanical delay (difference between onset of pulmonary and aortic outflow) did not differ (VDD 20 ± 21 ms vs. DDD 18 ± 17 ms; p = NS). Furthermore, VDD pacing significantly prolonged the rate-corrected LV filling period (VDD 458 ± 123 ms vs. DDD 371 ± 94 ms; p = 0.0001) and improved the myocardial performance index (VDD 0.60 ± 0.18 vs. DDD 0.71 ± 0.23; p < 0.01).
CONCLUSIONS: Our findings suggest that avoidance of right atrial pacing results in a higher degree of LV resynchronization, in a substantial prolongation of the LV filling period, and in an improved myocardial performance. Thus, the VDD mode seems to be superior to the DDD mode in CRT patients.
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Abbreviations and Acronyms
| | AV = atrioventricular | | AVD = atrioventricular delay | | CRT = cardiac resynchronization therapy | | ET = ejection time | | ICT = isovolumic contraction time | | IVRT = isovolumic relaxation time | | LV = left ventricle/ventricular | | LVOT-TVI = time velocity integral in the left ventricular outflow tract | | SPWMD = septal-to-posterior wall motion delay | | TDI = tissue Doppler imaging |
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In patients suffering from severe systolic heart failure, abnormal electrical conduction contributes to asynchrony between right and left ventricular (LV) contraction and discordant wall motion within the LV (1–3). Left-bundle-branch-block-type conduction delay results in early activation of the LV septal wall and delayed activation of the LV free wall (intraventricular delay) (4–6). This intraventricular dyssynchrony impedes the mechanical systolic function of the LV (7). Additionally, the inhomogeneous course of contraction within the LV leads to a delayed onset of relaxation, which results in shortening of diastole and an impaired LV filling, which further aggravates LV dysfunction (8–13). Cardiac resynchronization therapy (CRT) has been shown to resynchronize contraction and to improve hemodynamics and clinical outcome (14–17).
To a large part, the beneficial effect of CRT depends on an appropriate atrioventricular (AV) timing delay (14,15). If the atrioventricular timing delay (AVD) is set too long, pacing-induced resynchronization of the LV lateral wall may be lost. Conversely, exceedingly short AV intervals may cause premature valve closure and result in an interruption of transmitral LV inflow during atrial contraction. Consequently, LV filling is diminished, and atrial pressure rises. The impact of right atrial pacing on these parameters is unknown.
By using the VDD pacing mode, both atria are activated via the intrinsic conduction system. In contrast, pacing of the right atrial appendage in the routinely used DDD mode leads to a delayed electrical and mechanical activation of the left atrium (18). The resulting delay of the left atrial contraction may compromise transmitral inflow during late diastole and impede LV preload compared to intrinsic left atrial activation in the VDD mode. This effect may counteract the beneficial effects of premature LV stimulation required for proper resynchronization of both ventricles.
To test this hypothesis, we analyzed the hemodynamic effects of right atrial pacing using Doppler echocardiographic assessment of the LV filling and LV systolic function in CRT patients with chronic heart failure due to LV systolic dysfunction, normal sinus rhythm, and left-bundle-branch-type intraventricular conduction delay.
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Methods
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Study population.
Seventeen consecutive patients with an atriobiventricular pacemaker were enrolled in the study. Indications for CRT were severe heart failure due to dilated or ischemic cardiomyopathy, New York Heart Association dyspnea class  III, an LV ejection fraction of <35%, and presence of a left bundle branch block with a QRS interval on the surface electrocardiogram (ECG) 150 ms. Exclusion criteria were unstable cardiac condition and permanent atrial fibrillation. All patients gave written informed consent for participation in the study.
Implanted devices.
Eleven patients were implanted with a CRT defibrillator, and the remaining patients received a CRT pacemaker system. The operation was performed under conscientious sedation using the standard technique (19). All atrial leads were placed in the right atrial appendage. All right ventricular leads were positioned in the right ventricular apex. The coronary sinus lead was positioned in the middle cardiac vein in 1 patient, the posterior/left marginal veins in 15 patients, and in the anterior interventricular vein (diagonal branch) in 1 patient.
Protocol.
All patients underwent clinical examination and received a 12-lead ECG during biventricular-paced rhythm. Subsequently, transthoracic echocardiography was performed. At baseline, the programmed AVD was optimized by Doppler measurements ensuring a proper beginning of mechanical LV contraction at the end of the atrial contraction (1,20). The device was then randomly programmed into the VDD and DDD mode, respectively, and all Doppler echocardiographic measurements were repeatedly obtained in both pacing modes. In the DDD mode, a standard additional AVD of 40 ms was programmed ("pace compensation") in order to compensate the delay of left atrial activation induced by right-atrial-appendage pacing (18,21). Additionally, in a subset of patients, the pace compensation was turned off to investigate its influence in DDD pacing. In order to ensure continuous right atrial pacing in the DDD mode, the pacing rate was set 10 beats/min above the intrinsic atrial rate. In both pacing modes, monodimensional and two-dimensional echocardiographic evaluations as well as Doppler measurements were obtained.
Echocardiographic examination.
Transthoracic echocardiography was performed using a standard echocardiographic Doppler system (Toshiba Aplio 80, Tokyo, Japan). Patients were examined in the left lateral recumbent position. Standard parasternal long- and short-axis as well as apical views were used for data acquisition. Time velocity integral in the left ventricular outflow tract (LVOT-TVI) was acquired from the apical long-axis view by placing the pulsed-wave Doppler at the center of the LVOT and measured by tracing the Doppler spectral profile. Left ventricular ejection time (ET) was calculated by measuring the time from aortic valve opening to aortic valve closure. Isovolumic contraction time (ICT), the time from mitral valve closure to aortic valve opening, and isovolumic relaxation time (IVRT), the interval from aortic valve closure to mitral valve opening, were measured by simultaneous Doppler recording of the aortic and mitral flow. For assessment of the LV filling phase, pulsed-wave Doppler was used with the Doppler sample volume set at the tip of the mitral valve leaflets. From the recorded Doppler pattern, the LV filling time (E + A dur) was measured, and LV filling delay was calculated from the delay between the beginning of the Q-wave on the surface ECG and the onset of the E-wave (E-delay). All systolic and diastolic time intervals were adjusted for differences in heart rate ([time intervalDDD in ms] x [RR intervalVDD/RR intervalDDD]).
Intraventricular asynchrony was assessed by two methods: 1) M-mode echocardiographic imaging was used in the short-axis view at the papillary muscle level. The difference of the maximal inward motion of the septum and of the maximal displacement of the left posterior wall was used to calculate the intraventricular delay on the midventricular level (septal-to-posterior wall motion delay [SPWMD]) (22); and 2) tissue Doppler imaging (TDI) was performed from the apical four-chamber view placing the sample in the lateral and septal mitral annulus, respectively. The time from the onset of the Q-wave on the surface ECG to the onset of the regional systolic motion was measured in the basal segments of the interventricular septum and the left lateral wall and the difference calculated to assess TDI-derived intraventricular delay on the mitral annular level.
Interventricular electromechanical delay was evaluated using the delay between the onsets of pulmonary and aortic outflow, calculated as the difference between the time from the onset of the Q-wave on the surface ECG to simultaneously recorded onset of aortic flow and the time from the beginning of the Q-wave to the onset of pulmonary artery flow (22).
Myocardial performance index was calculated as the sum of ICT and IVRT divided by the ET (23).
Echocardiographic data were digitally stored and independently analyzed by two investigators with an interobserver variability of 7%. Reported is the average of the two.
Statistical analysis.
Data are presented as the mean value ± one SD or as frequencies (percentage). The method of Kolmogorov and Smirnov was used to test if measured data were distributed nomally. In case of normally distributed data, the paired student t test was used for calculations. In case of a non-normal distribution, the Wilcoxon signed rank test was performed. A p value of <0.05 was considered statistically significant. All calculations were performed with a commercially available statistical package (Statview 5.0, SAS Institute Inc., Cary, North Carolina).
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Results
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Study population.
Baseline clinical characteristics of the patients enrolled in the study are depicted in Table 1. Seventeen patients with a mean age of 64 ± 10 years were included. Twelve patients were male. Seven patients suffered from coronary artery disease and 10 from dilated cardiomyopathy. Eleven patients (65%) were in New York Heart Association funtional class III before device implantation; the other six (35%) were in New York Heart Association functional class IV. The mean QRS duration of the left bundle branch block without pacing was 179 ± 21 ms; the LV ejection fraction was 18 ± 6% before CRT. The intrinsic inter- and intraventricular delays were 49 ± 20 ms and 181 ± 98 ms, respectively. The mean ventricular cycle length was 904 ± 161 ms in the VDD group and 763 ± 100 ms in the DDD group.
Acute effects of VDD and DDD pacing on Doppler echocardiographic parameters.
After a median of 10 months (range 1 to 46 months), an optimized AV delay of 111 ± 34 ms (range 40 to 150 ms) was determined echocardiographically in the VDD pacing mode as previously described.
Differences between VDD and DDD pacing with respect to systolic and diastolic time intervals are depicted in Table 2. Isovolumic contraction time, systolic ET, and IVRT were significantly shorter in VDD as compared to DDD mode even after adjustment to changes in heart rate. Shortening of these time intervals resulted in an earlier onset of the E-wave (E-delay: VDD 526 ± 55 ms vs. DDD 638 ± 114 ms; p < 0.0001). Importantly, as a consequence, the rate-adjusted LV filling time was significantly prolonged with VDD compared to DDD pacing, contributing by 50 ± 6% to the cardiac cycle in the VDD compared to 41 ± 8% in the DDD mode (p = 0.0002) (Figs. 1 and 2).
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Figure 1 Depicts the time periods of the entire cardiac cycle (electrocardiogram [ECG] and Doppler flow) in DDD pacing mode (A) compared to the VDD pacing mode (B). Note the prolongation of the mitral inflow time (E + A dur) secondary to the shorter isovolumic contraction time (IVT), isovolumic relaxation time (IVRT), and aortic ejection time (ET) in the VDD as compared to the DDD pacing mode. Data of time intervals are presented as the mean value (ms) ± SD. *p < 0.01 VDD versus DDD. ECG labeling: P = P-wave; R = R-wave; T = T-wave. Doppler inflow labeling: A = A-wave (late transmitral inflow during left atrial contraction); E = E-wave (early transmitral flow).
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In a subset of five patients (29%), measurements were repeated without pace compensation in the DDD mode. When pace compensation was inactivated, LV filling times remained significantly shorter than in the VDD mode (VDD 483 ± 97 ms vs. DDD pace compensation "off" 442 ± 103 ms; p = 0.048). There was a nonsignificant difference in the LV filling period in the DDD mode with and without pace compensation (DDD pace compensation "off" 442 ± 103 ms vs. DDD pace compensation "on" 407 ± 85 ms; p = 0.08).
In five patients (29%) a complete fusion of early diastolic and atrial filling was observed in the DDD mode, whereas in the VDD mode no patients showed a fusion between the E- and A-wave (Figs. 3A and 3B). This finding precluded quantitative E/A ratio comparisons between the modes, because the A-wave could not be differentiated in all patients in the DDD mode.
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Figure 3 Pulsed-wave Doppler echocardiographic recordings of the left ventricular inflow measured at the tips between the mitral leaflets. The cycle length during DDD pacing was mathematically adjusted to the cycle length of the tracing in VDD mode (A). Note the complete fusion of early diastolic and atrial filling observed in the DDD mode (A), whereas in the VDD mode the peak of the E- and the A-wave are still clearly separated (B). These Doppler tracings are representative for the findings observed in five (29%) patients.
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Myocardial performance index was significantly lower with VDD pacing, indicating an amelioration of LV function in this mode (VDD 0.60 ± 0.18 vs. DDD 0.71 ± 0.23; p = 0.0044). Furthermore, a beneficial effect of VDD pacing was observed on LVOT-TVI (VDD 21.3 ± 3.7 cm vs. DDD 18.3 ± 3.3 cm, p < 0.0001).
While the interventricular delay did not differ between both modes (VDD 20 ± 21 ms vs. DDD 18 ± 17 ms; p = NS), we found significant differences in the intraventricular delays in favor of the VDD mode when assessed by the SPWMD on the midventricular level (VDD 106 ± 83 ms vs. DDD 145 ± 95 ms; p = 0.001) and by TDI-derived measures of the interventricular septum and the left lateral wall performed on the mitral annular level (VDD 38 ± 39 ms vs. DDD 83 ± 52 ms; p = 0.03).
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Discussion
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The main finding of our study is that right atrial pacing abolished some of the beneficial effects of CRT. This was reflected by a worsening of LV synchronization and a highly significant reduction of LV filling times in the DDD compared to the VDD mode. Complete fusion of early (passive) and late (atrial) transmitral inflow was a common observation during active right atrial pacing. Overall, cardiac performance was significantly better in the VDD pacing mode with avoidance of right atrial pacing.
Hemodynamic consequences of conduction abnormalities.
Early activation of the septal wall and delayed inward motion of the LV free wall caused by intraventricular conduction delay worsens systolic dysfunction in chronic heart failure (24). Apart from deteriorating systolic LV function, these conduction abnormalities also add to diastolic dysfunction. The LV filling period is shortened because the mitral valve is kept closed at the time of left atrial contraction by a delayed intraventricular pressure decay, which is caused by the prolonged LV lateral wall contraction. These mechanisms were extensively explored in previous studies in patients with heart failure due to dilated cardiomyopathy. The investigators found that the LV filling time was significantly diminished, when left bundle branch block or a first-degree AV block were present (11,12). Furthermore, intraventricular conduction delays not only contribute to delayed LV activation but also to slowed and delayed muscle relaxation, which further aggravates passive LV filling. As a consequence, the overall duration of LV diastole is shortened significantly (8,12,24,25).
The fact that early LV filling (represented by the E-wave in transmitral Doppler) is delayed, but atrial contraction and the resulting late filling phase (corresponding to the A-wave) are not, results in a "single-phase" transmitral diastolic flow pattern due to fusion of the two diastolic flow components (Fig. 3A). This further compromises LV filling and the preload of the LV as a consequence of a decreased left atrial contraction efficacy (8,11,12). In patients with critical heart failure, where appropriate LV filling may be crucial to maintain hemodynamic stability via the Frank-Starling mechanism, this fusion phenomenon is likely to have a deleterious effect on cardiac performance (26).
Effect of biventricular pacing on LV performance.
The influence of CRT on LV filling has previously been investigated (27,28). Compared to intrinsic rhythm, active biventricular pacing resulted in a significantly increased LV filling time. This finding was mainly attributed to a shortening of the ICT. This effect on ICT was obtained by an optimization of the left-sided AV delay. Furthermore, the increase in diastolic filling time gained by advancing LV systole led to a better separation of the early (passive) and the late (atrial) filling period (27,28).
Our data comparing VDD versus DDD biventricular pacing also showed a significant difference in ICT between the two modes with a prolongation during DDD pacing. However, the shortening of ICT achieved in the VDD mode was substantially smaller than the observed additional prolongation of LV diastole. This suggests that the shortening of ICT was not the only component of the cardiac cycle that contributed to the improved LV filling observed during VDD pacing. In fact, we found that the ET as well as the IVRT were also shorter in the VDD compared to the DDD mode (Figs. 1A and 1B).
Suggested mechanisms for the observed adverse effects of DDD pacing.
There are basically two mechanisms by which the adverse hemodynamic effects of DDD pacing may be explained. First, by atrial pacing via the implanted lead in the right atrial appendage, activation of the left atrium is artificially delayed by at least 60 to 100 ms. This is shifting the A-wave towards the onset of systole, which results in an A-wave cutoff and decreased LV filling (Fig. 4A). Second, activation of an AVD "pace compensation" of 40 ms in the DDD mode, which was basically programmed to prevent the above mechanism and to preserve left atrial contribution to LV filling, resulted in some loss in LV synchronization due to fusion activation of the LV between intrinsic- and biventricular-paced rhythm. This effect also accounted for less beneficial hemodynamic effects of CRT in the DDD mode (18,20). This hypothesis is supported by the observed prolongation of intraventricular delay during DDD pacing, although the interventricular delays remained similar in the two pacing modes.
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Figure 4 (A and B) Show pulsed-wave Doppler recordings of the left ventricular inflow mathematically adjusted for the difference in heart rate between the two pacing modes. Note the significantly prolonged mitral inflow time and the more physiological E and A traces in the VDD mode (B). In the DDD mode, there is incomplete fusion between E-wave (passive mitral inflow) and A-wave (active atrial filling). Note that there is a beginning cutoff of the A-wave in the DDD mode, although there is a lower degree of left ventricular synchronization compared to VDD pacing as suggested by the mitral flow impairment (see text).
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Given the two competing mechanisms, the main dilemma of DDD pacing using right atrial appendage pacing cannot be solved; pacing from the right atrial appendage inevitably delays left atrial activation, which has to be compensated one or the other way. Therefore, either way, LV inflow time will be shortened if the right atrium is being paced; if "pace compensation" is inactivated, atrial contribution to LV filling will be significantly impaired (A-wave cutoff) with the benefit of fully preserved LV synchronization. If "pace compensation" is activated, the onset of passive mitral inflow (E-wave) will be delayed with the hemodynamic benefit of preserved atrial contribution to LV filling (Figs. 4A and 4B). As a consequence, LV filling time remains always shorter in the DDD mode when the right atrium is paced from the appendage, whether a pace compensation is programmed or not. However, other right atrial lead placements (e.g., in a septal position) may not be associated with such a delay of left atrial activation and, therefore, might be preferable if DDD pacing is envisioned (29).
As suggested by the present acute study, by active right atrial appendage pacing, the previously reported amelioration of LV filling and myocardial performance achieved by biventricular pacing (27,28) may substantially be diminished. Based on our findings, it can be speculated that an important part of the beneficial hemodynamic effects achievable with CRT may be abolished by the inappropriate use of DDD pacing.
Study limitations.
One limitation of our study is that we only tested the different pacing modes in the acute setting. Hence, the chronic effects on LV performance cannot be predicted by our study. This needs further evaluation in the long-term.
Furthermore, all measurements were obtained at rest. We did not study the response to exercise, but it may be expected that the complex timing and flow interrelations of LV diastole are influenced in a similar way under exercise conditions. Finally, the potential drawbacks of VDD programming, such as possible occurrence of symptomatic sinus bradycardia or, as recently reported, a possible increase in atrial arrhythmias (30) remains to be considered. Therefore, for a subgroup of patients (i.e., those with relevant sinus bradycardia), DDD pacing still may be indicated. However, one should be aware that prolongation of the programmed AVD by programming any kind of automatic "pace-compensation" feature might have deleterious effects on the degree of achievable LV resynchronization. In order to resolve these issues and to prove the clinical implications of our findings, further studies with clinical cross-over design comparing the two pacing modes over time are warranted.
Clinical implications and conclusions.
Our data provide strong evidence that intrinsic atrial activation is important to improve diastolic filling and is superior to right atrial paced rhythm for maximization of the beneficial effects of CRT. Based on our results, assessed in an acute setting, the VDD mode seems to be the superior pacing mode in CRT patients. However, long-term clinical follow-up trials are needed to confirm a lasting hemodynamic benefit.
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Figure 2 Comparison of the left ventricular (LV) filling time achieved with DDD versus VDD pacing. The graphically presented data are mean values ± SD. *p = 0.0001 between the two groups.
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Footnotes
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Drs. Bernheim and Ammann contributed equally to this work.
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References
|
|---|
- Cazeau S, Leclercq C, Lavergne T, et al. Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay N Engl J Med 2001;344:873-880.[Abstract/Free Full Text]
- Shamim W, Francis DP, Yousufuddin M, et al. Intraventricular conduction delaya prognostic marker in chronic heart failure. Int J Cardiol 1999;70:171-178.[CrossRef][ISI][Medline]
- Wilensky RL, Yudelman P, Cohen AI, et al. Serial electrocardiographic changes in idiopathic dilated cardiomyopathy confirmed at necropsy Am J Cardiol 1988;62:276-283.[CrossRef][ISI][Medline]
- Kass DA. Ventricular resynchronizationpathophysiology and identification of responders. Rev Cardiovasc Med 2003;4(Suppl 2):S3-S13.
- Murkofsky RL, Dangas G, Diamond JA, et al. A prolonged QRS duration on surface electrocardiogram is a specific indicator of left ventricular dysfunction J Am Coll Cardiol 1998;32:476-482.[Abstract/Free Full Text]
- Hamby RI, Weissman RH, Prakash MN, et al. Left bundle branch blocka predictor of poor left ventricular function in coronary artery disease. Am Heart J 1983;106:471-477.[CrossRef][ISI][Medline]
- Park RC, Little WC, O’Rourke RA. Effect of alteration of left ventricular activation sequence on the left ventricular end-systolic pressure-volume relation in closed-chest dogs Circ Res 1985;57:706-717.[Abstract/Free Full Text]
- Xiao HB, Brecker SJ, Gibson DG. Effects of abnormal activation on the time course of the left ventricular pressure pulse in dilated cardiomyopathy Br Heart J 1992;68:403-407.
- Xiao HB, Lee CH, Gibson DG. Effect of left bundle branch block on diastolic function in dilated cardiomyopathy Br Heart J 1991;66:443-447.[Abstract/Free Full Text]
- Seidl K, Rameken M, Vater M, et al. Cardiac resynchronization therapy in patients with chronic heart failurepathophysiology and current experience. Am J Cardiovasc Drugs 2002;2:219-226.[CrossRef][Medline]
- Xiao HB, Roy C, Fujimoto S, et al. Natural history of abnormal conduction and its relation to prognosis in patients with dilated cardiomyopathy Int J Cardiol 1996;53:163-170.[CrossRef][ISI][Medline]
- Nishimura RA, Hayes DL, Holmes Jr. DR, et al. Mechanism of hemodynamic improvement by dual-chamber pacing for severe left ventricular dysfunctionan acute Doppler and catheterization hemodynamic study. J Am Coll Cardiol 1995;25:281-288.[Abstract]
- Shinbane JS, Chu E, DeMarco T, et al. Evaluation of acute dual-chamber pacing with a range of atrioventricular delays on cardiac performance in refractory heart failure J Am Coll Cardiol 1997;30:1295-1300.[Abstract]
- Auricchio A, Stellbrink C, Block M, et al. Effect of pacing chamber and atrioventricular delay on acute systolic function of paced patients with congestive heart failure. The Pacing Therapies for Congestive Heart Failure Study Group. The Guidant Congestive Heart Failure Research Group Circulation 1999;99:2993-3001.[Abstract/Free Full Text]
- Kass DA, Chen CH, Curry C, et al. Improved left ventricular mechanics from acute VDD pacing in patients with dilated cardiomyopathy and ventricular conduction delay Circulation 1999;99:1567-1573.[Abstract/Free Full Text]
- Leclercq C, Cazeau S, Le Breton H, et al. Acute hemodynamic effects of biventricular DDD pacing in patients with end-stage heart failure J Am Coll Cardiol 1998;32:1825-1831.[Abstract/Free Full Text]
- Nelson GS, Berger RD, Fetics BJ, et al. Left ventricular or biventricular pacing improves cardiac function at diminished energy cost in patients with dilated cardiomyopathy and left bundle-branch block Circulation 2000;102:3053-3059.[Abstract/Free Full Text]
- Cha YM, Nishimura RA, Hayes DL. Difference in mechanical atrioventricular delay between atrial sensing and atrial pacing modes in patients with hypertrophic and dilated cardiomyopathyan electrical hemodynamic catheterization study. J Interv Card Electrophysiol 2002;6:133-140.[CrossRef][ISI][Medline]
- Daubert JC, Ritter P, Le Breton H, et al. Permanent left ventricular pacing with transvenous leads inserted into the coronary veins Pacing Clin Electrophysiol 1998;21:239-245.[CrossRef][Medline]
- Kindermann M, Frohlig G, Doerr T, et al. Optimizing the AV delay in DDD pacemaker patients with high degree AV blockmitral valve Doppler versus impedance cardiography. Pacing Clin Electrophysiol 1997;20:2453-2462.[CrossRef][Medline]
- Janosik DL, Pearson AC, Buckingham TA, et al. 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]
- Pitzalis MV, Iacoviello M, Romito R, et al. Cardiac resynchronization therapy tailored by echocardiographic evaluation of ventricular asynchrony J Am Coll Cardiol 2002;40:1615-1622.[Abstract/Free Full Text]
- Tei C, Ling LH, Hodge DO, et al. New index of combined systolic and diastolic myocardial performancea simple and reproducible measure of cardiac function—a study in normals and dilated cardiomyopathy. J Cardiol 1995;26:357-366.[Medline]
- Grines CL, Bashore TM, Boudoulas H, et al. Functional abnormalities in isolated LBBBthe effect of intraventricular asynchrony. Circulation 1998;79:845-853.
- Gillebert TC, Sys SU, Brutsaert DL. Influence of loading patterns on peak length-tension relation and on relaxation in cardiac muscle J Am Coll Cardiol 1989;13:483-490.[Abstract]
- Holubarsch C, Ruf T, Goldstein DJ, et al. Existence of the Frank-Starling mechanism in the failing human heart. Investigations on the organ, tissue, and sarcomere levels Circulation 1996;94:683-689.[Abstract/Free Full Text]
- Yu CM, Chau E, Sanderson JE, et al. Tissue Doppler echocardiographic evidence of reverse remodeling and improved synchronicity by simultaneously delaying regional contraction after biventricular pacing therapy in heart failure Circulation 2002;105:438-445.[Abstract/Free Full Text]
- St John Sutton MG, Plappert T, Abraham WT, et al. Effect of cardiac resynchronization therapy on left ventricular size and function in chronic heart failure Circulation 2003;107:1985-1990.[Abstract/Free Full Text]
- Bailin SJ, Adler S, Giudici M. Prevention of chronic atrial fibrillation by pacing in the region of Bachmann’s bundleresults of a multicenter randomized trial. J Cardiovasc Electrophysiol 2001;12:912-917.[CrossRef][ISI][Medline]
- Knight BP, Desai A, Coman J, et al. Long-term retention of cardiac resynchronization therapy J Am Coll Cardiol 2004;44:72-77.[Abstract/Free Full Text]
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Pacing for atrioventricular block.
N. Engl. J. Med.,
October 20, 2005;
353(16):
1742 - 1744.
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Abstract
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