CRT
Upgrade to biventricular pacing in patients with pacing-induced heart failure: can resynchronization do the trick?
A' University Department of Cardiology, Hippokration Hospital, Athens, Greece
Manuscript submitted 8 September 2005. Accepted after revision 15 January 2006.
* Corresponding author. Tel/fax: +30 210 6531377. E-mail address: hrodil{at}yahoo.com
 |
Abstract |
|---|
 Top Abstract IntroductionPathophysiology of pacing...Reversing the deleterious...Unresolved issues and future...References |
|---|
Dyssynchrony imposed on ventricular function by right ventricular (RV) apical pacing may lead in some cases to worsening or appearance of heart failure (HF) symptoms. This is a result of an altered pattern of activation, leading to several histological and functional adjustments of the left ventricle, including inhomogeneous thickening of the ventricular myocardium and myofibrillar disarray, fibrosis, disturbances in ion-handling protein expression, myocardial perfusion defects, alterations in sympathetic tone and mitral regurgitation. Studies of mid- and long-term effects of RV apical pacing on left ventricular (LV) function have demonstrated a progressive decline in ejection fraction and other indices of LV functional competence. Upgrading RV pacing systems to biventricular resynchronization modalities is a theoretically promising option for paced patients with worsening HF. The potentially favourable effect of upgrading on LV functional indices and patient clinical status has been demonstrated in few, non-randomized trials. Apart from the scantiness of existing clinical data, issues concerning technical aspects of the procedure and selection of eligible patients are raised. Is pacing-induced dyssynchrony equivalent to the indigenous dyssynchrony in unpaced patients with HF? What selection criteria should be applied in order to identify potential responders to cardiac resynchronization therapy in this patient population? Answers to these and more questions are still lacking.
Key Words: Dyssynchrony, Biventricular pacing, Heart failure, Upgrade, Pacemakers
|
Introduction |
|---|
|
TopAbstractIntroductionPathophysiology of pacing...Reversing the deleterious...Unresolved issues and future...References |
|---|
Pacing is a therapeutic intervention which, in most of its forms, imposes to some extent a hypo-physiological mode of function on the heart. This may lead, in some cases, to deterioration or appearance of heart failure (HF) symptoms, especially in patients chronically paced in the right ventricular (RV) apex.1
The mechanisms underlying the deleterious effect of pacing on ventricular function are complex. |
Pathophysiology of pacing-induced HF |
|---|
|
TopAbstractIntroductionPathophysiology of pacing...Reversing the deleterious...Unresolved issues and future...References |
|---|
Pacing-induced asynchrony
RV pacing results in interventricular asynchrony, leading to a 30–180 ms delay in left ventricular (LV) activation,2
as well as intraventricular asynchrony resulting from the complete reversion of ventricular activation sequence (apex to base instead of base to apex).3,4 RV apical pacing leads to a heterogeneous distribution of workload (lower strain, i.e. workload, in the early-activated region than in the late-activated regions5), which in turn results in regional heterogeneity of myocardial tissue mass.1,6,7 More specifically, it has been shown that early-activated regions tend to become thinner over time, as opposed to late-activated ones, which show a progressive increase in wall-thickness, with myocyte enlargement being the primary histological contributor to wall thickening.6 The regional heterogeneity of myocardial hypertrophy results in remodelling of the LV, which alters its contractile and haemodynamic conduct, reducing LV overall functional efficiency.8 The primary causative factor of this remodelling seems to be the alteration of force vectors,9 which entails an alteration of mechanical stress distribution in the ventricle; however, a role of a neuro-endocrine mechanism cannot be excluded.10
Haemodynamic effects
Haemodynamic parameters have been shown to deteriorate substantially when the physiological activation pattern is not respected. More specifically, right atrial pressure, pulmonary arterial pressure, and pulmonary capillary wedge pressure have been shown to be significantly different in AAI, DDD and VVI pacing modes, being lowest in the first case, where both atrioventricular and ventricular activation sequences are preserved, and highest in the third case, where dyssynchrony is complete.11 LV ejection fraction (EF) and peak filling velocity of the LV have been demonstrated to be lower with pacing modes that cause a higher degree of dyssynchrony (i.e. VVI vs. AAI).11 Studies comparing paced individuals with controls over long periods of time have shown a significant progressive deterioration of ventricular function, expressed as decreased LVEF12–15 and cardiac output1 as well as decreased LV fractional area change and myocardial performance index,16 with paced QRS duration being the major independent predictor of LV function deterioration.17 It has been demonstrated in humans that even as little as 2 h of RV pacing causes a significant and persistent LVEF reduction.18 Prolongation of pacing for 1 week further reduces LVEF and it is not restored before 32 h after cessation of pacing have elapsed.18 Another contributing factor to the unfavourable effect of RV pacing on LV haemodynamics is the diminution of LV relaxation and filling times, i.e. a diastolic dysfunction which further impairs LV haemodynamic efficiency.19–21
Effects on the tissue and cellular level
The effect of RV pacing on LV function may be primarily due to the dyssynchrony induced by pacing on LV activation and systole, but it appears that additional mechanisms, which tend to make pacing-induced changes more lasting and not immediately reversible following the cessation of RV pacing, are at work. Pacing-induced alterations in the transient outward current (Ito)22 and the L-type calcium channel23 have been implicated in the process of LVEF depression during RV pacing. Additionally, it has been shown that LV dyssynchrony induces a marked dysregulation of protein expression, leading to regional heterogeneity in ion channel-handling and gap-junction proteins, which most probably contributes to LV function impairment.24
On the tissue level, chronic RV apical pacing has been shown to cause significant histological alterations, mainly consisting of myofibrillar disarray, fibrosis, fat deposition, sclerosis, and mitochondrial morphological changes.25 In an interesting study, Hamdan et al.26 measured sympathetic nerve activity during acute RV, LV, and biventricular (BiV) pacing and were able to demonstrate significantly higher sympathetic nerve activity during RV when compared with LV and BiV pacing in patients with low EF. As increased sympathetic activity has been shown to be an important contributor to HF progression and a prognostic factor of cardiac mortality,27 if these findings are also true for long-term pacing, they are indicative of yet another association between RV pacing and LV functional deterioration. Alterations in the adrenergic innervation of the ventricular myocardium have been reported in patients with permanent DDD pacing, studied with I123-MIBG scintigraphy, mainly in the inferior and apical wall segments.28
Effects on myocardial perfusion
RV apical pacing has been shown to affect myocardial perfusion, both in animal models29 and humans.30 Several investigators31–34 have demonstrated a high incidence of perfusion defects with radionuclide scintigraphy in patients with long-term permanent RV pacing. These perfusion defects were most frequently located in an inferior or apical segment and were associated with significantly lower LVEF.31 Skalidis et al.33 further proceeded to assess coronary blood flow in the defect-related arteries, demonstrating that these perfusion defects are secondary to regional microvascular flow impairment. Nielsen et al.15 used positron emission tomography to assess myocardial blood flow in patients paced either in the AAI mode (which preserves physiological ventricular activation) or in the DDD mode (which preserves only atrioventricular synchrony) and reported a significant reduction in global as well as in regional myocardial blood flow in the inferior and septal regions (the early-activated regions) after 22±7 months of DDD pacing. It is worth noting that switch from DDD to AAI mode resulted in restoration of regional and global myocardial blood flow, indicating that the effects of long-term ventricular pacing on myocardial blood flow are reversible. It is obvious that AAI pacing is associated with better myocardial perfusion and haemodynamic characteristics than DDD pacing.35 Modern pacing algorithms in dual-chamber pacemakers attempt to increase the time in AAI pacing vs. the DDD pacing mode. This pacemaker function in combination with the better accommodation of the lower pacing rate to the activity status of the paced patient may decrease the time the patients receive RV apical pacing.
Mitral regurgitation
Mitral regurgitation (MR) of variable severity is another common result of RV pacing,36–38 which has a direct impact on patient functional status. RV pacing causes MR through a complex mechanism. It appears that the altered sequence of activation of the components of the mitral apparatus and the dyssynchronized conveyance of force from the papillary muscles through the chordae tendinae to the mitral leaflets lead to poor coaptation and thus to regurgitation during ventricular systole. The appearance or aggravation of pre-existing MR may contribute to the development or deterioration of HF in paced patients.
|
Reversing the deleterious effects of RV apical pacing |
|---|
|
TopAbstractIntroductionPathophysiology of pacing...Reversing the deleterious...Unresolved issues and future...References |
|---|
Alternative RV pacing sites
The differential effects of alternative RV pacing sites on QRS duration and ventricular systolic function have been studied in the past: Takagi et al.39
showed in a normal heart canine model that haemodynamics and interventricular conduction are less disturbed by proximal RV septal pacing than apical pacing. In contrast, Peschar et al.40 have demonstrated, also using a normal heart canine model, that although septal or apical LV pacing did not affect LV systolic function, RV septal pacing was not superior to RV apical pacing. In the human heart, despite reports of preservation of LV systolic function with RV septal pacing as opposed to RV apical pacing, in patients without HF,41 this was not re-iterated by studies in the failing heart.42 Interestingly, it has been demonstrated that finding the site of the RV septal surface causing the shortest QRS when paced and implanting the pacing lead there, may result in improved LV systolic performance.43,44 However, it was postulated that the latter finding is unlikely to have a significant clinical impact, as the effects on LVEF were relatively minor44 and the procedure is impractical for everyday clinical practice.45 The RV outflow tract was also proposed as an alternative site of RV pacing, associated with increased cardiac output when compared with RV apical pacing in acute pacing studies;46,47 however, this was not confirmed with long-term pacing.48 These data suggest that RV pacing at alternative sites has not demonstrated any unequivocally proven clinical benefit in terms of optimization of LV systolic function and, therefore, it is doubtful that it would be of use to consider alternative RV pacing sites for patients with pacemaker-related HF.
Biventricular pacing
LV or BiV pacing, or cardiac resynchronization therapy, has been proposed as an adjunctive treatment for patients with advanced HF complicated by discoordinate contraction due to intraventricular conduction delay. Both short-term and a growing number of long-term clinical trials have reported on the mechanisms and short- and mid-term efficacy of this approach, with encouraging results.49–51 A QRS duration >200 ms has been arbitrarily required to upgrade RV pacing in HF patients to BiV pacing because such a wide QRS has been suggested to correspond with notable inter- or intra-LV mechanical dyssynchrony.52–54 It should be noted, however, that improved mechanical synchrony and function do not necessarily require increased electrical synchrony,55 and more recent data56 dispute the correlation between electrical features (QRS duration) and the degree of electromechanical ventricular dyssynchrony in RV paced patients. It has also been shown that regardless of the presence of HF, the last activated LV wall is not always the free wall and the first one activated is not always the septal wall, as has already been shown in patients with spontaneous atrioventricular conduction. Pacing at mid-lateral LV sites has been demonstrated to achieve the greatest increase in systolic function when compared with any other region that could be accessed via the coronary sinus.57 Furthermore, more patients have RV pacing-induced intraventricular than interventricular dyssynchrony, suggesting that in these patients, the major cause of LV function impairment is likely to be the presence of intra-LV dyssynchrony. Echocardiographically documented and quantified dyssynchrony is a new approach to the issue of patient selection and also gives new insight into the possible mechanisms of improvement (Figure 1). As BiV pacing results in the improvement of intra-LV rather than of interventricular synchrony, RV-paced patients who present with an abnormally increased intra-LV dyssynchrony should benefit from BiV upgrading.58–60
|
Upgrading of previously implanted RV pacing systems has been attempted in the past by the use of different techniques, either using a variety of configurations of leads and connectors or by implanting additional pulse generators.61
–67 Current generator systems have three dedicated ports and truly independent output to both ventricles. Although most studies involved systems tying both ventricular leads to a common internal current source with the risk of an impedance mismatch that could result in only RV or only LV pacing, rather than both, new devices have two independent channels and further add programmability of the RV–LV stimulation delay.
Upgrading of an already implanted RV pacing system to BiV pacing in patients with HF and atrial fibrillation reversed dyssynchrony, improved ventricular performance and dimensions, quality of life and symptoms of HF in the same manner as described in patients with sinus rhythm and left bundle branch block who undergo BiV pacing.61,63 Improvement in functional class, increased EF, decrease in end-systolic and end-diastolic diameters, decrease in the number of hospitalizations and improved quality of life scores were demonstrated in this patient population.61 A 40% decrease in the MR area was reported in one of those two studies.63 However, in these first attempts to upgrade previously implanted RV pacing systems to BiV pacing, when a variety of configuration of leads and connectors was used, or implantation of additional pulse generators was required, several methodological problems were encountered.64–66 Nevertheless, although long-term benefits from upgrading to BiV pacing were reported in the AF subgroup of the MUSTIC study, they were less impressive when compared with the patients in sinus rhythm.67
By the use of more modern upgrading techniques to BiV pacing of previously implanted RV pacing systems, a greater degree of interventricular synchronization was achieved strictly through shortening of left pre-ejection intervals without increase in right pre-ejection intervals. In contrast, LV filling increased only from 45 to 50% of the cardiac cycle, probably because it was already optimized by the pre-existent pacing system. Intraventricular synchronization was also significantly enhanced.68 Finally, after upgrading to BiV pacing of previously implanted RV pacing systems, improvement in indices of systolic function, including LVEF, myocardial performance index, and LV ejection time, was demonstrated.69 LV end-diastolic and systolic volumes were similarly decreased with BiV pacing, whereas mitral valve deceleration time, an index of diastolic function, was not affected by BiV pacing.69
|
Unresolved issues and future perspectives |
|---|
|
TopAbstractIntroductionPathophysiology of pacing...Reversing the deleterious...Unresolved issues and future...References |
|---|
Given that dyssynchrony is the problem, or at least a prominent part of it, with pacing-induced or pacing-aggravated HF, resynchronization is a theoretically sound aim to pursue. The clinical settings and pre-conditions for conventional RV pacing to be upgraded to BiV resynchronization have not been clearly outlined because of the lack of clinical data, leading clinicians to treat paced patients with HF as equivalent to patients with indigenous conduction delay, using the same selection criteria for the prediction of responders in this patient population as in the general population of HF patients. There is a growing need to integrate new strategies of assessing the potential of an RV-paced patient with HF to respond to resynchronization treatment, such as the developing echocardiographic methods, namely tissue Doppler imaging, strain and strain-rate analysis and tissue tracking.70
,71 The few non-randomized, uncontrolled studies that have been reported have demonstrated that the ‘upgrading’ approach to the treatment of already paced HF patients is at least feasible and relatively safe.61–63,69 Future studies should define where LV leads should be placed when upgrading a previously implanted device and which are the potential complications that may arise from the upgrading approach beyond venous occlusive phenomena or the difficulties posed by the anatomic variability of the coronary sinus anatomy. Furthermore, more data are required concerning the application of resynchronization therapy in those previously paced HF patients in whom an ICD is also indicated. Conclusively, better powered and controlled trials with adequate follow-up time are clearly warranted in order to determine the mid- and long-term efficacy of upgrading from RV to BiV pacing, as well as its cost-effectiveness, which is a particularly relevant issue in the era of device therapy. |
References |
|---|
|
TopAbstractIntroductionPathophysiology of pacing...Reversing the deleterious...Unresolved issues and future...References |
|---|
[1] Thambo JB, Bordachar P, Garrigue S, et al. Detrimental ventricular remodeling in patients with congenital complete heart block and chronic right ventricular apical pacing. Circulation 2004; 110: 3766–72.
[2] Vassalo J, Cassidy D, Miller J, Buxton A, Marchlinsky F, Josephson M. Left ventricular endocardial activation during right ventricular pacing: effect of underlying heart disease. J Am Coll Cardiol 1986; 7: 1228–33.[Abstract]
[3] Lister JW, Klotz DH, Jomain SL, Stuckey JH, Hoffman BF. Effect of pacemaker site on cardiac output and ventricular activation in dogs with complete heart block. Am J Cardiol 1964; 14: 494–503.[CrossRef][Web of Science][Medline]
[4] Dagget W, Bianco J, Powell W, Austen W. Relative contributions of the atrial systole–ventricular systole and of patterns of ventricular activation to ventricular function during electrical pacing of the dog heart. Circ Res 1970; 27: 69–79.
[5] Prinzen FW, Hunter WC, Wyman BT, McVeigh ER. Mapping of regional myocardial strain and work during ventricular pacing: experimental study using magnetic resonance imaging tagging. J Am Coll Cardiol 1999; 33: 1735–42.
[6] Prinzen FW, Cheriex EC, Delhaas T, et al. Asymmetric thickness of the left ventricular wall resulting from asynchronous electric activation study in dogs with ventricular pacing and in patients with left bundle branch block. Am Heart J 1995; 130: 1045–53.[CrossRef][Web of Science][Medline]
[7] van Oosterhout MF, Prinzen FW, Arts T, et al. Asynchronous electrical activation induces asymmetrical hypertrophy of the left ventricular wall. Circulation 1998; 98: 588–95.
[8] 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: 1417–29.[CrossRef][Medline]
[9] Adomian GE and Beazell J. Myofibrillar disarray produced in normal hearts by chronic electrical pacing. Am Heart J 1986; 112: 79–83.[CrossRef][Web of Science][Medline]
[10] Kent RL and McDermott PJ. Passive load and angiotensin II evoke differential responses of gene expression and protein synthesis in cardiac myocytes. Circ Res 1996; 78: 829–38.
[11] 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: 1133–41.[CrossRef][Web of Science][Medline]
[12] Nielsen JC, Andersen HR, Thomsen PE, et al. Heart failure and echocardiographic changes during long-term follow-up of patients with sick sinus syndrome randomized to single chamber atrial or ventricular pacing. Circulation 1998; 97: 987–95.
[13] Rosenqvist M, Bergfeldt L, Haga Y, Ryden J, Ryden L, Owall A. The effect of ventricular activation sequence on cardiac performance during pacing. Pacing Clin Electrophysiol 1996; 19: 1279–86.[CrossRef][Medline]
[14] Paxinos G, Katritsis D, Kakouros S, Toutouzas P, Camm AJ. Long-term effect of VVI pacing on atrial and ventricular function in patients with sick sinus syndrome. Pacing Clin Electrophysiol 1998; 21: 728–34.[CrossRef][Medline]
[15] Nielsen JC, Bøttcher 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: 1453–61.
[16] Tei C, Dujardin KS, Hodge DO, Kyle RA, Tajik AJ, Seward JB. Doppler index combining systolic and diastolic myocardial performance: clinical value in cardiac amyloidosis. J Am Coll Cardiol 1996; 28: 658–64.[Abstract]
[17] Tantengco VT, Thomas RL, Karpawich PP. Left ventricular dysfunction after long-term right ventricular apical pacing in the young. J Am Coll Cardiol 2001; 37: 2093–100.
[18] Nahlawi M, Waligora M, Spies SM, Bonow RO, Kadish AH, Goldberger JJ. Left ventricular function during and after right ventricular pacing. J Am Coll Cardiol 2004; 44: 1883–8.
[19] Stojnic B, Stojanov P, Angelkov L, Pavlovic S, Radjen G, Velimirovic D. Evaluation of asynchronous left ventricular relaxation by Doppler echocardiography during ventricular pacing with AV synchrony (VDD): comparison with atrial pacing (AAI). Pacing Clin Electrophysiol 1996; 19: 940–4.[Medline]
[20] Zile MR, Blaustein AS, Shimizu G, Gaasch WH. Right ventricular pacing reduces the rate of left ventricular relaxation and filling. J Am Coll Cardiol 1987; 10: 702–9.[Abstract]
[21] Bedotto JB, Grayburn PB, Black WH, et al. Alterations in left ventricular relaxation during atrioventricular pacing in humans. J Am Coll Cardiol 1990; 15: 658–64.[Abstract]
[22] Yu H, McKinnon D, Dixon J, et al. Transient outward current, Ito1, is altered in cardiac memory. Circulation 1999; 99: 1898–905.
[23] Plotnikov A, Yu H, Geller J, et al. Role of L-type calcium channels in pacing-induced short-term and long-term cardiac memory in canine heart. Circulation 2003; 107: 2844–9.
[24] Spragg D, Leclercq C, Loghmani M, et al. Regional alterations in protein expression in the dyssynchronous failing heart. Circulation 2003; 108: 929–32.
[25] Karpawich PP, Rabah R, Haas JE. Altered cardiac histology following apical right ventricular pacing in patients with congenital atrioventricular block. Pacing Clin Electrophysiol 1999; 22: 1372–7.[CrossRef][Medline]
[26] Hamdan MH, Zagrodzky JD, Joglar JA, et al. Biventricular pacing decreases sympathetic activity compared with right ventricular pacing in patients with depressed ejection fraction. Circulation 2000; 102: 1027–32.
[27] Cleland JGF, Dargie HJ, Ford I. Mortality in heart failure: clinical variables of prognostic value. Br Heart J 1987; 58: 572–82.
[28] Simantirakis EN, Prassopoulos VK, Chrysostomakis SI, et al. Effects of asynchronous ventricular activation on myocardial adrenergic innervation in patients with permanent dual-chamber pacemakers; an I123-metaiodobenzylguanidine cardiac scintigraphic study. Eur Heart J 2001; 22: 323–32.
[29] Lee MA, Dae MW, Langberg JJ, et al. Effects of long-term right ventricular apical pacing on left ventricular perfusion, innervation, function and histology. J Am Coll Cardiol 1994; 24: 225–32.[Abstract]
[30] Kolettis TM, Kremastinos DT, Kyriakides ZS, Tsirakos A, Toutouzas PK. Effects of atrial, ventricular, and atrioventricular sequential pacing on coronary flow reserve. Pacing Clin Electrophysiol 1995; 18: 1628–35.[Medline]
[31] Tse HF and Lau CP. Long-term effect of right ventricular pacing on myocardial perfusion and function. J Am Coll Cardiol 1997; 29: 744–9.[Abstract]
[32] Lakkis NM, He ZX, Verani MS. Diagnosis of coronary artery disease by exercise thallium-201 tomography in patients with a right ventricular pacemaker. J Am Coll Cardiol 1997; 29: 1221–5.[Abstract]
[33] Skalidis EI, Kochiadakis GE, Koukouraki SI, et al. Myocardial perfusion in patients with permanent ventricular pacing and normal coronary arteries. J Am Coll Cardiol 2001; 37: 124–9.
[34] Tse HF, Yu C, Wong KK, et al. Functional abnormalities in patients with permanent right ventricular pacing. The effect of sites of electrical stimulation. J Am Coll Cardiol 2002; 40: 1451–8.
[35] Katritsis D and Camm AJ. AAI pacing mode: when is it indicated and how should it be achieved? Clin Cardiol 1993; 16: 339–43.[Web of Science][Medline]
[36] Vanderheyden M, Goethals M, Anguera I, et al. Hemodynamic deterioration following radiofrequency ablation of the atrioventricular conduction system. Pacing Clin Electrophysiol 1997; 20: 2422–8.[CrossRef][Medline]
[37] Twidale N, Manda V, Holliday R, et al. Mitral regurgitation after atrioventricular node catheter ablation for atrial fibrillation and heart failure: acute hemodynamic features. Am Heart J 1999; 138: 1166–75.[CrossRef][Web of Science][Medline]
[38] Núñez A, Alberca MT, Cosío FG, et al. Severe mitral regurgitation with right ventricular pacing successfully treated with left ventricular pacing. Pacing Clin Electrophysiol 2002; 25: 226–30.[CrossRef][Medline]
[39] Takagi Y, Dumpis Y, Usui A, Maseki T, Watanabe T, Yasuura K. Effects of proximal ventricular septal pacing on hemodynamics and ventricular activation. Pacing Clin Electrophysiol 1999; 22: 1777–81.[CrossRef][Medline]
[40] Peschar M, de Swart H, Michels KJ, Reneman RS, Prinzen FW. Left ventricular septal and apex pacing for optimal pump function in canine hearts. J Am Coll Cardiol 2003; 41: 1218–26.
[41] Karpawich PP and Mital S. Comparative left ventricular function following atrial, septal, and apical single chamber heart pacing in the young. Pacing Clin Electrophysiol 1997; 20: 1983–8.[CrossRef][Medline]
[42] Gold MR, Shorofsky SR, Metcalf MD, Feliciano Z, Fisher ML, Gottlieb SS. The acute hemodynamic effects of right ventricular septal pacing in patients with congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy. Am J Cardiol 1997; 79: 679–81.[CrossRef][Web of Science][Medline]
[43] Schwaab B, Frohlig G, Alexander C, et al. Influence of right ventricular stimulation site on left ventricular function in atrial synchronous ventricular pacing. J Am Coll Cardiol 1999; 33: 317–23.
[44] Schwaab B, Kindermann M, Frohlig G, Berg M, Kusch O, Schieffer H. Septal lead implantation for the reduction of paced QRS duration using passive-fixation leads. Pacing Clin Electrophysiol 2001; 24: 28–33.[CrossRef][Medline]
[45] Gold MR. Optimization of ventricular pacing: where should we implant the leads? J Am Coll Cardiol 1999; 33: 324–26.
[46] Giudici M, Thornburg GA, Buck DL, et al. Comparison of right ventricular outflow tract and apical lead permanent pacing on cardiac output. Am J Cardiol 1997; 79: 209–12.[CrossRef][Web of Science][Medline]
[47] De Cock CC, Meyer A, Kamp O, Visser CA. Hemodynamic benefits of right ventricular outflow tract pacing: Comparison with right ventricular apex pacing. Pacing Clin Electrophysiol 1998; 21: 536–41.[CrossRef][Medline]
[48] Victor F, Leclercq C, Mabo P, et al. Optimal right ventricular pacing site in chronically implanted patients: a prospective randomized crossover comparison of apical and outflow tract pacing. J Am Coll Cardiol 1999; 33: 311–6.
[49] Leclercq C and Kass DA. Retiming the failing heart: principles and current clinical status of cardiac resynchronization. J Am Coll Cardiol 2002; 39: 194–201.
[50] Bradley DJ, Bradley EA, Baughman KL. Cardiac resynchronization and death from progressive heart failure. A meta-analysis of randomized controlled trials. JAMA 2003; 289: 730–40.
[51] Mehra MR and Greenberg BH. Cardiac resynchronization therapy: caveat medicus!. J Am Coll Cardiol 2004; 43: 1145–8.
[52] Alonso C, Leclercq C, Victor F, et al. Electrocardiographic predictive factors of long-term clinical improvement with multisite biventricular pacing in advanced heart failure. Am J Cardiol 1999; 84: 1417–21.[CrossRef][Web of Science][Medline]
[53] Gras D, Mabo P, Tang T, et al. Multisite pacing as a supplemental treatment of congestive heart failure: preliminary results of the Medtronic Insync Study. Pacing Clin Electrophysiol 1998; 21: 2249–55.[CrossRef][Medline]
[54] Leclercq C, Cazeau S, Ritter P, et al. A pilot experience with permanent biventricular pacing to treat advanced heart failure. Am Heart J 2000; 140: 862–70.[CrossRef][Web of Science][Medline]
[55] Leclercq C, Faris O, Tunin R, et al. Systolic improvement and mechanical resynchronization does not require electrical synchrony in the dilated failing heart with left bundle-branch block. Circulation 2002; 106: 1760–3.
[56] Bordachar P, Garrigue S, Lafitte S, et al. Interventricular and intra-left ventricular electromechanical delays in right ventricular paced patients with heart failure: implications for upgrading to biventricular stimulation. Heart 2003; 89: 1401–5.
[57] 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.[Medline]
[58] 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: 438–45.
[59] Ansalone G, Giannantoni P, Ricci R, Trambaiolo P, Fedele F, Santini M. Doppler myocardial imaging to evaluate the effectiveness of pacing sites in patients receiving biventricular pacing. J Am Coll Cardiol 2002; 39: 489–99.
[60] Garrigue S, Jaïs P, Espil G, et al. Comparison of chronic biventricular pacing between epicardial and endocardial left ventricular stimulation using the Doppler tissue imaging in patients with heart failure. Am J Cardiol 2001; 88: 858–62.[CrossRef][Web of Science][Medline]
[61] Leon AR, Greenberg JM, Kanuru N, et al. Cardiac resynchronization in patients with congestive heart failure and chronic atrial fibrillation. Effect of upgrading to biventricular pacing after chronic right ventricular pacing. J Am Coll Cardiol 2002; 39: 1258–63.
[62] Erol-Yilmaz A, Tukkie R, Schrama TAM, Romkes HJ, Wilde AAM. Reversed remodeling of dilated left sided cardiomyopathy after upgrading from VVIR to VVIR biventricular pacing. Europace 2002; 4: 445–9.
[63] Valls-Bertault V, Fatemi M, Gilard M, Pennec PY, Etienne Y, Blanc JJ. Assessment of upgrading to biventricular pacing in patients with right ventricular pacing and congestive heart failure after atrioventricular junctional ablation for chronic atrial fibrillation. Europace 2004; 6: 438–43.
[64] Kranidis AI, Andrikopoulos GK, Kappos KG, Bouki TP, Dedehlias PN. Right ventricle bipolar pacing may prevent appropriate biventricular pacing from two pacemakers. J Electrocardiol 2004; 37: 321–4.[Medline]
[65] O'Cochlain B, Delurgio D, Leon A. Biventricular pacing using two pacemakers and the triggered VVT mode. Pacing Clin Electrophysiol 2003; 24: 1284–5.
[66] Chugh A, Scharf C, Hall B, et al. Prevalence and management of inappropriate detection and therapies in patients with first-generation biventricular pacemaker-defibrillators. Pacing Clin Electrophysiol 2005; 28: 44–50.[CrossRef][Medline]
[67] Linde C, Leclercq C, Rex S, et al. Long-term benefits of biventricular pacing in congestive heart failure: results from the Multisite Stimulation in Cardiomyopathy (MUSTIC) study. J Am Coll Cardiol 2002; 40: 111–8.
[68] Cazeau S, Bordachar P, Jauvert G, et al. Echocardiographic modeling of cardiac dyssynchrony before and during multisite stimulation: a prospective study. Pacing Clin Electrophysiol 2003; 26: 137–43.[CrossRef][Medline]
[69] Horwich T, Foster E, De Marco T, Tseng Z, Saxon L. Effects of resynchronization therapy on cardiac function in pacemaker patients upgraded to biventricular devices. J Cardiovasc Electrophysiol 2004; 15: 1284–9.[CrossRef][Web of Science][Medline]
[70] Bax JJ, Ansalone G, Breithardt OA, et al. Echocardiographic evaluation of cardiac resynchronization therapy: ready for routine clinical use? A critical appraisal. J Am Coll Cardiol 2004; 44: 1–9.
[71] Yu CM, Bax JJ, Monaghan M, Nihoyannopoulos P. Echocardiographic evaluation of cardiac dyssynchrony for predicting a favourable response to cardiac resynchronisation therapy. Heart 2004; 90:Suppl. 6, vi17–vi22.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  H. Ashrafian, M. J. Mason, and A. G. Mitchell Regression of dilated-hypokinetic hypertrophic cardiomyopathy by biventricular cardiac pacing Europace, January 1, 2007; 9(1): 50 - 54. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H.-F. Tse and C.-P. Lau Selection of Permanent Ventricular Pacing Site: How Far Should We Go? J. Am. Coll. Cardiol., October 17, 2006; 48(8): 1649 - 1651. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||