© 2008 European Society of Cardiology
Left ventricular pacing site in cardiac resynchronization therapy: Clinical follow-up and predictors of failed lateral implant
Department of Cardiology and Cardiovascular Surgery, University Clinic, School of Medicine, University of Navarra Pamplona, Spain
* Corresponding author. Department of Cardiology and Cardiovascular Surgery, University Clinic, C/ Pío XII, s/n. 31008 Pamplona, Spain. Tel.: +34 948 2554000; fax: +34 948 296500. E-mail address: igarciab{at}unav.es (I. García-Bolao).
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Abstract |
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 Top Abstract 1. Introduction2. Methods3. Results4. DiscussionReferences |
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The effects of the left ventricular (LV) pacing site on the clinical results of resynchronization therapy (CRT) are not well characterized. The aim of this study was to define the effect of LV lead location on clinical response and LV remodelling, and to identify predictors of failure to implant the LV lead in a lateral location.
One hundred and seventy two consecutive patients were evaluated at baseline and 6 months after CRT. In 128 patients, the LV lead was implanted in the lateral region (Group 1), while 44 received an anterior implant due to anatomical or electrical factors (Group 2). Group 1 was associated with a significantly better functional outcome assessed both by NYHA class (p < 0.001) and by the six-minute-walk test (p = 0.01) compared with group 2. LV ejection fraction and volumes, and inter- and intraventricular dyssynchrony only improved significantly (p < 0.01) in group 1. The only independent predictor of a failed lateral implant was the presence of ischaemic cardiomyopathy (OR 3.29, 95% CI 2.2–13.7; p = 0.02).
In conclusion, a lateral lead location results in a better functional outcome and greater reverse LV remodelling compared with anterior locations. The presence of ischaemic cardiomyopathy is a risk factor for a failed lateral LV implant.
Key Words: Cardiac resynchronization therapy • Heart failure • Coronary sinus • Left ventricular pacing site
Received August 13, 2007; Revised December 22, 2007; Accepted February 28, 2008
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1. Introduction |
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TopAbstract1. Introduction2. Methods3. Results4. DiscussionReferences |
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Although cardiac resynchronization therapy (CRT) is a well established treatment for patients with advanced systolic heart failure (HF) and ventricular dyssynchrony, up to 30% of patients do not respond to this therapy [1]. Besides clinical and electromechanical factors [2-4], the implantation procedure with regard to the optimal left ventricular (LV) pacing site has also been advocated as one of the potential causes of non-response [1,5,6]. However, the choice of the LV pacing site for best resynchronization is often challenging because of the inherent characteristics of the coronary venous anatomy, the presence of unacceptable electrical parameters in the targeted area, or the existence of phrenic nerve stimulation [7]. In fact, it has been reported from a large study, that up to 22% of patients receive LV pacing from anterior sites [8]. Although some authors advocate an individualized approach based on tailoring the LV lead position to the exact area of maximal mechanical delay [9,10], this strategy can be impeded by the technical limitations inherent in the transvenous implantation procedure and by scarce clinical long-term validation. For these reasons, in most centres standard current practice includes the systematic implantation of the LV lead in the lateral region whenever possible. In the general CRT population, the lateral or posterolateral region of the LV has been identified as the site that provides not only the greatest acute haemodynamic benefit, particularly for dp/dt [11-13], but also the most efficient resynchronization capability assessed by echocardiography [14]. However, the long-term clinical benefit of lateral vs. other pacing sites remains controversial and is the subject of much debate [15,16].
The aim of this study was to compare the clinical and echocardiographic response to CRT among different LV pacing sites at six months follow-up and to identify predictive risk factors for an unsuccessful LV implant in the lateral region.
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2. Methods |
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TopAbstract1. Introduction2. Methods3. Results4. DiscussionReferences |
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2.1. Patient population
From a population of 181 consecutive patients referred for CRT implantation between December 2000 and June 2005, 172 were successfully implanted and were included in this prospective, non-randomised study. All patients had refractory HF of any aetiology, NYHA functional class III or IV, LV dysfunction with LV ejection fraction (EF) below 0.35 and left bundle branch block (LBBB) with a QRS width >130 ms. An ischaemic aetiology of HF was defined as the presence of any history of myocardial infarction or coronary revascularization or the presence of any epicardial coronary vessels with
70% stenosis at coronary angiography. Prior to the implant procedure, patients underwent a complete clinical and echocardiographic evaluation and gave written informed consent to participate in the study. The study conformed with the principles of the Declaration of Helsinki.
2.2. Implantation procedure
Implantation was performed transvenously in an electrophysiology laboratory equipped with a Hicor digital angiography system (Siemens). Patients received either a pacemaker or an implantable cardioverter defibrillator according to current clinical indications.
All patients received an over-the-wire LV lead (Easytrak, Guidant, St. Paul, Minnesota). The LV lead was implanted preferably in the lateral region and, if possible, midway between base and apex. An anterior site was chosen only as the last resort if a lateral implantation was not possible due to anatomical reasons (inability to deliver the LV lead or absence of lateral access), unacceptable pacing thresholds (defined as 6 V at 0.5 ms), or significative phrenic nerve stimulation with diaphragmatic pacing (defined as <2 V at 0.5 ms or less than twice the LV threshold). From 2003 onwards, a telescopic catheter system (Rapido Advance, Guidant, St. Paul, Minnesota) was routinely used to help the selective catheterization of the target vein. Additional techniques namely double guide technique and venous angioplasty were used when necessary.
Patients were divided into two groups depending on the site of LV pacing. The lateral region (Group 1) was defined as lying between 2 and 5 o'clock while the anterior region (Group 2) was defined as lying between 11 and 2 o'clock in the 45° left anterior oblique projection (Fig. 1). This categorization was made on the basis of the final anatomic location of the LV lead tip rather than on the entry venous branch.
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Prior to discharge, the atrioventricular delay was optimized at rest by echo-Doppler. All patients received simultaneous biventricular pacing.
2.3. Follow-up
Patients were evaluated at baseline (pre-implant) and at the 6-month follow-up visit. Evaluation included NYHA functional class, quality of life (using the Minnesota Living with Heart Failure Questionnaire), 6-minute walk test and echocardiography. The 6-minute walk tests were performed in a standardized manner (according to Guyatt's recommendations) [17]. Patients were instructed before the test and assisted by the same control physician (S.C.), who was blinded to their clinical status. The tests were performed in an uncrowded area.
Non-response to CRT was prospectively predefined as those patients that 1) did not increase the distance walked in 6 min by >10%, 2) were scheduled for heart transplantation, or 3) died of HF. Categorization of the response to CRT was made at the 6-month follow-up.
2.4. Echocardiographic evaluation
Transthoracic two-dimensional echocardiograms, M-mode recordings, and Doppler ultrasound measurements were performed in each patient at baseline and at 6 months using a Sonos 5500 or 7500 ultrasound system (Phillips). All echocardiographic studies were performed by a cardiologist who was blinded to the patient's clinical status. LV end-diastolic diameter (LVEDD) and end-systolic diameter (LVESD) were measured from M-mode recordings using leading edge methodology according to the American Society of Echocardiography criteria [18]. LVEF was determined with the Simpson rule. The Tei index was calculated by assessing isovolumic contraction time and isovolumic relaxation time divided by ejection time [19].
Interventricular dyssynchrony was defined as the difference in electromechanical delay between the right ventricle (time in milliseconds from onset of the QRS complex until onset of pulmonary flow) and LV (time in milliseconds from onset of the QRS complex until onset of aortic flow). Intraventricular dyssynchrony was assessed with the following parameters: 1) septal-to-posterior-wall motion delay (SPWMD) and 2) septal-to-lateral-wall motion delay (SLWMD) as the difference (in milliseconds), assessed by tissue echo-Doppler evaluation, between the onset of the QRS complex and the maximum systolic velocity of each ventricular region along the 4-chamber apical axis.
2.5. Statistical analysis
Differences in baseline parameters between responders and nonresponders were tested by Student's t test for unpaired data once normality was demonstrated (Shapiro-Wilks test); otherwise, a nonparametric test (Mann-Whitney U test) was used. Differences in parameters before and after treatment within each group of patients were tested by the Student's t test for paired data once normality was demonstrated (Shapiro-Wilks test); otherwise, a nonparametric test (Wilcoxon test) was used. Dichotomous or categorical variables were analyzed by the 
2 test or Fischer's exact test when necessary. Only variables significant at the 0.25 level in the univariate analysis were included in the logistic regression analysis to determine independent predictors of failed lateral implant. The accuracy of the model was verified with the Hosmer-Lemeshow goodness-of-fit test.
Data are presented as the mean value±standard deviation (SD). A p value below 0.05 was considered statistically significant. Statistical tests were performed with the SPSS 12.0 statistical package (SPSS Inc., Chicago, IL, USA).
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3. Results |
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TopAbstract1. Introduction2. Methods3. Results4. DiscussionReferences |
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3.1. Patient groups
All devices were pacing correctly when patients were discharged from hospital and after 3 and 6 months.
Of the 172 patients included in the study, 128 (74%) (53 ischaemic cardiomyopathy, 75 non-ischaemic cardiomyopathy) were implanted in a lateral or posterolateral position (Group 1), while 44 (26%) (29 ischaemic cardiomyopathy, 15 non-ischaemic cardiomyopathy) were implanted in the anterior or anterolateral region of the LV (Group 2). The reasons for a failed lateral implant were: inability to deliver the LV lead into the target vein in 11 patients (25%), absence of a lateral vein or collateral access in 20 cases (45%), 7 patients (16%) had unacceptable pacing thresholds, while phrenic nerve stimulation or diaphragmatic stimulation was encountered in 6 patients (14%). The most frequent reason for a failed lateral implant in patients with ischaemic cardiomyopathy was the absence of a lateral vein or collateral access to the lateral region (14/29; 48%), in patients with non-ischaemic cardiomyopathy, the most prevalent cause that explained an anterior implant was the inability to deliver the LV lead into the target vein (8/15; 53%).
As expected, total procedure time and radioscopic time were higher in group 2 when compared to group 1, while electrical performance of the LV lead and the number of complications was similar between the two groups (Table 1).
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There were 22 significant complications. Nine patients (5.2%) had lead dislodgement, with five involving the LV lead. Four patients (2.3%) has coronary sinus (CS) dissection and three (1.7%) had phrenic nerve stimulation requiring lead repositioning. Other complications included: pneumothorax in two patients (1.1%), severe haematoma in two patients (1.1%), infection in one patient (0.6%) and transient ischaemic attack in another patient (0.6%).
3.2. Clinical characteristics
Baseline clinical characteristics of the patients in each group are shown in Table 2. The cause of HF was ischaemic cardiomyopathy in 82 patients (47.6%) and idiopathic dilated cardiomyopathy in 90 (52.4%).
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At baseline, there were no significant differences in the majority of the clinical characteristics between both groups. However, there was a greater prevalence (p=0.04) of ischaemic aetiology in group 2 (29 patients, 66%) when compared to group 1 (53 patients, 41%). At the end of follow-up, 130 patients (75.5%) were considered responders to CRT according to the previously defined criteria. There were 42 nonresponder patients (24.5%), of whom 32 did not increase the distance walked in 6 min by >10%, 5 underwent heart transplantation and 5 died. By lead location, there were 104 responders (82%) and 24 nonresponders (18%) in group 1 and 26 responders (59%) and 18 nonresponders (41%) in group 2.
For the distance walked in 6 min the cut-off value used to separate responders and nonresponders was 10%, however, the mean distance walked by responders increased by 101±67 m (39±11%), compared with an increase of only 9±17 m (2±6%) in the nonresponders, this difference was significant (p<0.001). Whereas LVESD and LVEDD decreased in responders at 6 months (55.8±11.3 vs. 48.1±9.6, p=0.001; and 69.3±10.8 vs. 63.1±8.3; p=0.002, respectively), they did not change in nonresponders (55.5±10.2 vs. 53.8±9.3; p=0.317) and 68.0±7.7 vs. 66.7±9.8; p=0.08, respectively). Similarly, whereas mean LVEF increased in responders (25.0±6.3 vs. 35.1±10.7; p<0.01) it was unchanged in the nonresponders at follow-up (24.1±9.6 vs. 25.0±8.2; p=0.295).
Clinical evolution according to the LV lead location is shown in Table 3. Group 1 exhibited a higher proportion of responder patients when compared to Group 2 (81.2% vs. 59.0%; p=0.027). At 6 months, NYHA functional class improved significantly only in group 1 (3.09±0.7 to 2.20±0.9; p<0.001), while it was unchanged in group 2 (3.17±0.6 to 2.75±1.3; p=0.344). Similarly, the distance walked in 6 min increased only in group 1 at follow-up (297.1±49.5 to 378.8±69.3; p=0.01). The improvement in quality of life seen after CRT was also limited to patients in group 1.
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The rate of response to CRT according to different HF aetiologies is shown in Table 4. There were no statistically significant differences in the rate of positive response between ischaemic and non-ischaemic cardiomyopathy in both groups.
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3.3. Echocardiographic parameters
The results of the echocardiographic evaluation are shown in Table 5. At baseline, patients in group 2 had a lower baseline anteroposterior left atrial diameter than group 1 (43.8±6.3 vs. 49.7±7.2.; p<0.05). At follow-up, whereas mean LVEF, LVESD, LVEDD and Tei index improved significantly in group 1 when compared to their respective baseline values, they remained unchanged in group 2. Among the 44 patients with LV leads positioned in the anterior or anterolateral region, 14 patients experienced improvement in LVEF, while 30 patients experienced no change or worsening of LVEF. The mean percentage improvement from baseline LVEF was 40.4% in group 1 vs. 3.7% in group 2. The degree of mitral regurgitation improved significantly only in group 1.
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Similarly, a significant reduction in echocardiographic parameters of inter- and intraventricular dyssynchrony compared to baseline values was only observed in group 1 at the end of follow-up. Although the values of SLWMD also tended to decrease in group 2 at 6 months, the difference did not reach statistical significance (p=0.06).
3.4. Predictors of a failed lateral implant
Logistic regression analysis showed that the only independent predictor of a failed lateral LV lead implant was the presence of ischaemic cardiomyopathy (OR 3.29, 95% CI 2.2-13.7; p=0.02). The accuracy of the model was confirmed by the non-significant Hosmer-Lemeshow goodness-of-fit test (p=0.714).
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4. Discussion |
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TopAbstract1. Introduction2. Methods3. Results4. DiscussionReferences |
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The major findings of the current study are as follows: 1) in the general CRT population, LV pacing from the lateral or posterolateral region results in a significantly better clinical improvement, reverse LV remodelling and correction of dyssynchrony when compared to pacing from anterior sites and 2) a prior history of ischaemic cardiomyopathy is a predictive factor for a failed lateral implantation.
The original concept upon which CRT was conceived and developed was based on the premise that in patients with HF and disturbed electrical activation (particularly those with LBBB pattern and prolongation of the PR interval), depolarization of the LV free wall is significantly delayed compared to that of the right ventricle (interventricular dyssynchrony) and the interventricular septum (intraventricular dyssynchrony). These electrical disturbances result in discoordinate contraction with paradoxical septal wall motion and reduction of LV contractility, which further impairs the pumping ability of an already damaged myocardium. Although the different activation patterns of QRS prolongation with LBBB morphology in the setting of HF constitute a heterogeneous spectrum which depends on the different degree of integrity of the distal conduction system and the presence of large ischaemic scars, the site of the latest LV activation is often located laterally, especially in the setting of dilated cardiomyopathy [20,21]. For all these reasons, one of the rationales of CRT was to preexcite the most delayed LV region in order to improve intraventricular mechanical synchrony. Nevertheless, this rationale has demonstrated several pitfalls, particularly in ischaemic patients, in whom the most delayed LV activation is usually located around the scar area. Pacing the LV in scarred myocardium, where the most delayed LV activation is usually located, may result in non-response to CRT [3].
Even though it seems clear that the site with maximal electrical delay may not be reflective of the site with maximal mechanical dyssynchrony, many acute or short-term haemodynamic data suggest that a lateral position yields greater benefit compared with an anterior position. This holds true for benefits in dp/dt, aortic pulse pressure and echocardiographic parameters of resynchronization [11-14]. However, the impact of stimulation site on clinical end-points over a long-term follow-up remains controversial. Although some authors have shown that implantation of the LV lead at lateral sites is associated with a greater improvement in clinical functional capacity and LV function compared to anterior locations [6,22], others have shown no differences [15].
Our results show not only that lateral locations are more effective than anterior sites, but also that the benefit of LV anterior pacing is almost negligible when we consider the general CRT population. However, according to our data, 41% of the patients that received an anterior implant showed some degree of clinical improvement. Although we cannot rule out a placebo effect, it has been shown that a significant minority of patients (10-25%) may have the anterior wall as the site of greatest contractile delay. In this specific subgroup of patients, an anterior lead placement might be reasonable [23]. Nevertheless, this approach has not yet been prospectively validated in a large population and the methods for identifying such a population are not clear.
Taken together, our data strongly suggest that although the anterior location is technically the easiest region to access during the implantation procedure, it should be avoided whenever possible. However, it is not clear whether a primary surgical approach would be preferable when a lateral coronary vein position cannot be achieved with the standard percutaneous approach. From a practical standpoint, the fact that the majority of patients are implanted with a CRT-D device, and hence a percutaneous approach is mandatory for the right ventricular defibrillator leads, must be taken into account. Thus, in the absence of randomised data, if an optimal lateral vein is not accessible for LV pacing, it seems reasonable to implant the LV lead in a suboptimal site. If the patient does not respond adequately, a surgical approach should be performed in a subsequent procedure.
Although ischaemic cardiomyopathy is not a predictive factor for unsuccessful LV lead implantation [24], our work also shows that an ischaemic aetiology is a predictive factor for a failed lateral implant. This finding probably reflects the distorted coronary venous anatomy commonly seen around the scar area (Fig. 2). In fact, in our study the most frequent reason for a failed lateral implant in patients with ischaemic cardiomyopathy was the absence of a lateral vein or collateral access to the lateral region. In accordance with our data, a recent study has nicely demonstrated that patients with a history of myocardial infarction were less likely to have a left marginal vein. Using 64-slice computed tomography, the authors showed that a left marginal vein was present in only 27% of patients with a history of infarction, compared with 71% of the control patients [25]. The absence of CS tributaries may be related to scar formation secondary to previous myocardial infarction. In these cases, the absence of at least one marginal vein implies that the only way to reach the lateral region with a percutaneous approach is via collaterals arising from more posterior or anterior branches, rendering a lateral implantation more difficult. An alternative explanation for the higher rate of anterior implants in patients with ischaemic cardiomyopathy may include increased scar formation which could prevent appropriate pacing in the lateral site.
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In our group, there were no statistically significant differences in the rate of positive response between those patients with ischaemic and those with non-ischaemic cardiomyopathy in both groups (anterior and lateral), which suggests that an anterior location (independently of the aetiology) is associated per se with a worse response to CRT. It has recently been suggested that ischaemic heart disease is a risk factor for lack of response to CRT [2,26]. In accordance with our data, and taking into account other electrical or mechanical factors which could explain this finding, such as the presence of transmural scar tissue [27], a higher prevalence of anterior implants should be considered as an additional explanation for the relatively worse CRT response seen in patients with ischaemic cardiomyopathy.
4.1. Study limitations
In our study, the pacing site was not randomly assigned but rather chosen according to anatomical and electrical factors. We therefore cannot separate the effects of the LV pacing site from other factors (whether anatomical or of some other kind) that prevented implantation in the lateral region.
4.2. Conclusions
Implantation of the LV lead in the lateral or posterolateral LV is associated with a greater improvement in functional capacity, LV function and dyssynchrony parameters compared to anterior locations. Prior history of ischaemic cardiomyopathy is a predictive risk factor for a failed lateral implantation.
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