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Left ventricular lead position for cardiac resynchronization: a comprehensive cinegraphic, echocardiographic, clinical, and survival analysis

Ying-Xue Dong, Brian D. Powell, Samuel J. Asirvatham, Paul A. Friedman, Robert F. Rea, Tracy L. Webster, Kelly L. Brooke, David O. Hodge, Heather J. Wiste, Yan-Zong Yang, David L. Hayes, Yong-Mei Cha
DOI: http://dx.doi.org/10.1093/europace/eus045 1139-1147 First published online: 30 March 2012


Aims We sought to determine the clinical and survival outcomes of cardiac resynchronization therapy (CRT) associated with left ventricular (LV) lead location. The lateral left ventricle has been considered the optimal LV lead location for CRT.

Methods and results Left ventricular lead cinegrams taken in 30° right and left anterior oblique views were evaluated in 457 recipients of CRT with a pacemaker or a defibrillator from 1 January 2002 to 31 December 2008 in this retrospective study. Left ventricular lead placement was prioritized at implantation into posterolateral (PL), anterolateral (AL), middle cardiac, and anterointerventricular coronary veins. Using echocardiographic LV 16-segment analysis, we grouped the leads as anterior, AL, PL, and posterior locations. New York Heart Association (NYHA) class and echocardiography were assessed before and after CRT. Clinical and survival outcomes after CRT were compared among the four LV lead locations.  Patient baseline demographic characteristics were similar among these four groups. Improvement in NYHA class was significantly greater in the AL (P= 0.04) and PL (P= 0.03) locations than in the anterior location. There was a tendency for greater improvement in LV ejection fraction among the AL (P= 0.11) and PL (P= 0.08) locations than the anterior location. Kaplan–Meier survival estimate at 4 years varied for location: AL, 72%; anterior, 48%; PL, 62%; and posterior, 72% (P= 0.003).

Conclusion Cardiac resynchronization therapy recipients are profiting from all lead positions. However, LV lead placed in the AL and PL positions is more preferential for achieving optimal CRT benefit than leads placed in the anterior position.

  • Cardiac resynchronization therapy
  • Defibrillator
  • Ventricular ejection fraction
  • Survival


Cardiac resynchronization therapy (CRT) has been shown to improve outcomes in the majority of patients with early- or advanced-stage heart failure (HF) and a wide QRS complex.16 The location where transvenous left ventricular (LV) leads are placed via the coronary sinus has been considered an important element for an optimal outcome from CRT. A decade ago, an acute haemodynamic study of patients with advanced HF in the Pacing Therapies in Chronic Heart Failure trial found that LV pacing alone or biventricular pacing at the LV lateral wall yields greater improvement in LV dP/dtmax, than an anterior site.7 The findings of delayed LV free wall activation and mechanical contraction from subsequent studies corroborate this concept, given that the presence of left bundle branch block was found in the majority of CRT recipients.8,9

Despite the fact that CRT for advanced HF has been well implemented in the clinical practice for more than a decade, the long-term effect of LV lead position has not been fully assessed until lately. A few studies have yielded mixed results in supporting LV lateral wall pacing as the optimal location.1012 The investigators from the Comparison of Medical Therapy, Pacing, and Defibrillation in Chronic Heart Failure (COMPANION) study demonstrated equivalent HF and survival outcome from any LV lead location,13 while Multicenter Automatic Defibrillator Implantation Trial (MADI-CRT) showed an unfavourable outcome when LV leads positioned in the apical region.14 Given these inconsistent results, uncertainty continues about whether effort to place LV leads in the ideal destination should be made in the cardiac pacing laboratory, potentially at the cost of increased procedure time, increased radiation time, and complications. We sought to investigate the impact of LV lead position on clinical and survival outcomes of CRT in our study.


Study patients

We conducted a single-centre, retrospective study of 457 consecutive patients who underwent CRT with a defibrillator (90%) or a pacemaker (10%) at Mayo Clinic from 1 January 2002 to 31 December 2008. All patients were referred for device implantation according to current guidelines15 and had final cinegrams confirming the LV lead position. Only patients consenting to the use of their records for research were included. The Mayo Institutional Review Board approved this study.

Baseline evaluation

All patients underwent a baseline evaluation before CRT, including assessment of New York Heart Association (NYHA) functional class, HF aetiologic factors, concomitant cardiovascular conditions (e.g. hypertension, coronary artery disease, diabetes mellitus), plasma creatinine level, haemoglobin level, QRS duration and morphologic characteristics, and transthoracic echocardiography. Echocardiographic parameters included LV ejection fraction (derived from two-dimensional measurements of diastolic and systolic LV dimension analysis using the method of disks), pulmonary artery systolic pressure (estimated from the tricuspid regurgitant velocity and an estimate of right atrial pressure), mitral regurgitation severity (0, none/trivial; 1, mild; 2, moderate; 3, severe), right ventricular (RV) enlargement, and systolic dysfunction (scale for both: 0, normal; 1, mild; 2, moderate; and 3, severe).

Device implantation and left ventricular lead placement

During CRT implantation, venography of the coronary sinus commonly was performed to assess venous anatomy and to facilitate LV lead placement. The LV lead was prioritized to place at the lateral or posterolateral (PL) coronary vein. When a suboptimal pacing threshold (>4.0 V/0.5 ms) or diaphragmatic pacing became apparent, the middle cardiac vein or anterointerventricular (AI) vein was selected as the alternative vessel. At the end of the procedure, cardiac cinegram views were taken in the right anterior oblique (RAO) and the left anterior oblique (LAO), both at 30°, to confirm the LV lead position. All patients stayed in the hospital overnight and device reevaluation was performed before hospital dismissal, to confirm appropriate device and lead function and an absence of extracardiac pacing.

Device programming and follow-up

Standard CRT settings included atrioventricular delay of 100 ms (sensed) and 130 ms (paced) in DDD or DDDR mode and lower (50–60 b.p.m.) and upper (120–140 b.p.m.) pacing rates. V–V pacing interval was set at nominal, usually 0 ms. Patients received the recommendation to have a 3- to 6-month follow-up assessment after device implantation. The percentage of biventricular pacing was obtained through device interrogation at follow-up. Survival status as of 15 May 2011, was obtained with a national death and location database (Accruint).

Assessment of left ventricular lead position

The ostium of the coronary vein may be anterior, posterior, or lateral, but the tributaries of these veins interdigitate in such a way that a branch might get to the lateral wall from the anterior or posterior vein.16 As such, LV lead positions were categorized as (i) the tributaries of the coronary vein hosting the LV leads and (ii) the anatomical LV lead locations with echocardiographic 16-segment model.17 The coronary veins were grouped as PL (this group also included posterior and lateral), anterolateral (AL), AI, and middle cardiac (Figure 1). The anatomical lead locations in the 16-segment model were assessed exclusively through review of fluoroscopic cinegrams in RAO and LAO views. The longitudinal LV lead locations were categorized as basal, mid-, and apical left ventricle. The basal (segments 1–6) and mid- (segments 7–12) levels were divided further into 6 segments each: anteroseptum, anterior, AL, PL, posterior, and posteroseptum segments. The apex was divided into four segments: anterior, lateral, posterior, and septal walls (Figure 2). The 16-segment model was used for the analysis of final LV lead locations. The fluoroscopic cinegrams to assess lead position were reviewed by two observers together, who were blinded to the clinical outcome.

Figure 1

Coronary venous anatomy. Left anterior oblique indicates left anterior oblique.

Figure 2

The 16 segments of the left ventricle. Ant indicates anterior; Ant-lat, anterolateral; Post-lat, posterolateral, Post, posterior.

Statistical analysis

Continuous variables were expressed as mean (standard deviation) or median [interquartile range (IQR)]. Comparisons in continuous variables across multiple groups were performed with analysis of variance. Two-sample t-tests were used to assess the differences in continuous variables between the two groups. Paired t-tests were used to assess differences between pre-CRT and post-CRT continuous variables within the groups. Categorical variables were expressed as number (%) and differences across the groups were assessed with χ2 tests. Survival estimates were calculated by the Kaplan–Meier method. A log-rank test was used to compare survival between groups. Univariate predictors of survival were identified with Cox proportional hazards regression methods. All variables with univariate significance (P< 0.05) and missing for <5% of subjects were considered for a multivariate model. Stepwise selection was used to determine the final multivariate model, and then lead location was added to that model to determine whether it has an independent association with survival after controlling for other variables. Relative risks were expressed as hazard ratios with 95% confidence intervals. Analyses were performed with SAS version 9.2 (SAS Institute Inc., Cary, North Carolina). A two-sided P< 0.05 was considered significant.


Patient baseline characteristics

Overall baseline demographic characteristics in 457 patients [age, mean (SD), 68.8 (11.3) years; male, 76%] are shown in Table 1. The majority of the cohort (58%) had ischaemic cardiomyopathy. Nearly one-third of patients had atrial fibrillation.

View this table:
Table 1

Comparison of baseline characteristics in four left ventricular lead location groups defined with 16-segment data

VariableaOverall (N= 457)Anterior (n= 50)AL (n= 244)PL (n= 152)Posterior (n= 11)P value
Age, years68.8(11.3)70.3(11.6)68.2(11.7)68.9(10.7)72.9(11.6)0.39
Male sex, no. (%)346(76)41(82)173(71)122(80)10(91)0.06
DCM, no. (%)190(42)22(44)97(40)67(44)4(36)0.81
Chronic AF, no. (%)130(28)17(34)69(28)41(27)3(27)0.82
NYHA class3.0(0.5)3.0(0.6)3.0(0.5)3.0(0.4)3.0(0.6)0.89
QRS duration, ms164.1(32.5)164.3(35.1)167.0(31.9)158.8(31.4)172.0(43.3)0.09
LVEF, %23.6(7.3)22.6(7.7)23.6(7.3)23.8(7.2)24.9(10.1)0.72
LVEDD, mm65.7(8.7)66.1(8.5)65.4(9.3)65.9(7.8)70.3(10.1)0.33
LVESD, mm57.8(9.8)57.9(9.3)57.5(10.1)58.1(9.2)60.8(12.6)0.78
RV enlargement, grade0.9(0.9)0.9(0.9)0.9(0.9)0.9(0.9)0.6(0.8)0.57
RV dysfunction, grade1.1(0.9)1.1(0.9)1.0(0.9)1.2(0.9)0.9(1.1)0.45
LA size, mm61.5(9.6)61.2(9.7)61.2(9.5)62.2(9.6)62.2(11.2)0.82
MR, grade1.5(0.8)1.4(0.7)1.5(0.8)1.4(0.8)1.6(0.7)0.52
PASP, mmHg46.9(15.2)47.3(17.3)46.7(15.6)47.0(14.1)45.9(12.0)0.99
Creatinine, mg/dL1.4(0.6)1.5(0.6)1.4(0.7)1.4(0.4)1.5(0.5)0.49
Haemoglobin, g/dL13.0(1.7)13.0(1.5)13.0(1.7)13.0(1.9)12.9(1.4)>0.99
ACE inhibitor or ARB therapy, no. (%)365(81)44(90)193(81)118(78)10(91)0.26
Beta-blocker therapy, no. (%)398(88)46(94)208(87)134(89)10(91)0.58
Digoxin therapy, no. (%)251(56)28(57)138(58)79(52)6(55)0.72
  • ACE, angiotensin-converting enzyme; AF, atrial fibrillation; ARB, angiotensin receptor blocker; DCM, dilated cardiomyopathy; LA, left atrium; LVEDD, left ventricular end-diastolic dimension; LVEF, left ventricular ejection fraction; LVESD, left ventricular end-systolic dimension; MR, mitral regurgitation; NYHA, New York Heart Association; PASP, pulmonary artery systolic pressure; RV, right ventricular.

  • aValues are presented as mean (SD) unless indicated otherwise.

Left ventricular leads were placed in the AL vein in 156 patients (34.1%), the PL vein in 224 patients (49.0%), the AI vein in 50 patients (11.0%), and the middle cardiac vein in 27 patients (5.9%). A 16-segment analysis of LV lead location details that patients who received lead placement in the individual locations are as follows: anterior, 50 (11.0%); AL, 244 (53.4%); PL, 152 (33.3%); and posterior, 11 (2.4%). No significant differences among the four groups were seen in age, sex, NYHA class, QRS duration, echocardiographic findings, and medication use (Table 1). Of all patients, 52 (11.4%), 320 (70.0%), and 85 (18.6%) had LV leads located in the basal, mid, and apical left ventricle. Baseline characteristics were not significantly different among these three longitudinal lead locations (P> 0.05 for all). Routinely, RV leads were placed in the apex.

Coronary vein and left ventricular lead location

Of 224 LV leads placed in the tributary of the PL or lateral vein, 54% were located in the AL segment and 46% in the PL segment. Of 156 LV leads placed in the AL vein, 79% were in the AL segment and 21% were in the PL segment. Left ventricular leads placed in the AI vein (n= 50) were exclusively located in the anterior segment. Although 59% of LV leads placed in the middle cardiac vein were located in the PL segment, the other 41% were in the posterior segment.

Improvement in heart failure and left ventricular lead location

The patients received pacing in both ventricles 99% of the time (IQR, 94.0–99.9%).The median time between implantation and echocardiographic follow-up was 6.8 months (IQR, 4.4–10.5). Improvements in NYHA class and left ventricular ejection fraction (LVEF) were seen consistently in anterior, AL, and PL lead locations after CRT; these improvements were absent in the posterior group, but there were a small number of patients in this group (Table 2). Reduction in LVEDD, pulmonary systolic pressure, and mitral regurgitation was observed in AL and PL lead locations.

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Table 2

Pre-cardiac resynchronization therapy and post-cardiac resynchronization therapy comparison in four left ventricular lead location groups defined by 16-segment data

No.Pre-CRT, mean (SD)Post-CRT, mean (SD)Paired P valueNo.Pre-CRT, mean (SD)Post-CRT, mean (SD)Paired P value
NYHA class332.88 (0.48)2.59 (0.87)0.0521762.96 (0.50)2.34 (0.82)<0.001
LVEF, %3521.94 (8.01)25.53 (11.21)0.02417523.83 (7.10)30.21 (11.26)<0.001
LVEDD, mm3168.39 (8.42)67.35 (8.81)0.36016165.61 (9.65)63.57 (10.44)<0.001
LVESD, mm1661.81 (9.58)59.00 (12.26)0.0429057.53 (11.10)54.20 (12.24)<0.001
RV enlargement, mm310.73 (0.77)1.00 (0.93)0.0771490.82 (0.87)0.77 (0.82)0.417
RV dysfunction301.03 (0.94)1.10 (1.09)0.7261530.93 (0.89)0.88 (0.89)0.325
LA size, mm1962.16 (10.05)65.95 (10.10)0.19811061.85 (9.20)60.75 (8.78)0.171
MR, grade321.47 (0.77)1.27 (0.77)0.1251581.58 (0.78)1.33 (0.69)<0.001
PASP, mmHg2851.21 (18.16)47.21 (14.95)0.19514247.96 (16.45)41.94 (13.29)<0.001
NPre-CRT, mean (SD)Post-CRT, mean (SD)Paired P valueNPre-CRT, mean (SD)Post-CRT, mean (SD)Paired P value
NYHA class1233.06 (0.43)2.41 (0.83)<0.00183.06 (0.56)2.38 (0.88)0.130
LVEF, %12423.90 (7.42)31.00 (11.66)<0.001923.72 (10.81)26.83 (9.15)0.311
LVEDD, mm10565.68 (7.78)63.21 (8.70)<0.001971.11 (9.80)69.11 (10.20)0.115
LVESD, mm6357.17 (9.23)53.24 (11.44)<0.001762.14 (12.94)59.71 (13.56)0.377
RV enlargement, mm1050.98 (0.89)0.90 (0.89)0.28080.63 (0.92)1.06 (0.86)0.133
RV dysfunction1041.18 (0.93)1.00 (0.95)0.05470.93 (1.30)1.29 (1.11)0.535
LA size, mm7461.66 (8.34)62.47 (8.83)0.321864.25 (10.69)63.13 (8.11)0.794
MR, grade1141.43 (0.83)1.24 (0.71)<0.00181.50 (0.60)0.94 (0.73)0.038
PASP, mmHg9648.42 (13.61)43.98 (13.06)0.002743.00 (11.49)36.14 (13.16)0.255
  • CRT, cardiac resynchronization therapy; LA, left atrium; LVEDD, left ventricular end-diastolic dimension; LVEF, left ventricular ejection fraction; LVESD, left ventricular end-systolic dimension; MR, mitral regurgitation; PASP, pulmonary artery systolic pressure; RV, right ventricular.

The AL and PL groups achieved similar changes in NYHA class and LVEF. The anterior group had less improvement in these variables than both the AL and PL groups (Figure 3), although the differences were not significant for LVEF. When we combined the AL and PL lead locations as a lateral group compared with a non-lateral group (anterior and posterior locations), the change in NYHA was −0.6 (0.8) vs. −0.4 (0.9) (P= 0.06); LVEF, 6.7% (10.1) vs. 3.5% (8.8) (P= 0.05); and LVEDD, −2.2 mm (6.0) vs. −1.3 mm (5.6) (P= 0.34).  The incremental improvement in NYHA class, LVEF, and LVEDD comparing basal, mid, and apical LV lead locations was not significant (Figure 4).

Figure 3

Comparison of changes after cardiac resynchronization therapy (CRT) for anterior, anterolateral, posterolateral, and posterior lead locations. (A) New York Heart Association (NYHA) class. (B) Left ventricular ejection fraction (LVEF). (C) Left ventricular end-diastolic dimension (LVEDD). The improvement in NYHA class was greater in anterolateral and posterolateral locations than in the anterior location, and this was the case marginally for LVEF.

Figure 4

Comparison of changes after cardiac resynchronization therapy (CRT) for left ventricular base, mid, and apex lead locations. (A) New York Heart Association (NYHA) class. (B) Left ventricular ejection fraction (LVEF). (C) Left ventricular end-diastolic dimension (LVEDD). The improvements in NYHA class, LVEF, and LVEDD were similar across all groups.

Survival outcomes

There were 191 deaths over a median follow-up period of 4.8 (IQR, 3.5–6.6) years. Kaplan–Meier survival was significantly different when the LV lead were grouped as anterior, AL, PL, and posterior locations (P= 0.003) (Figure 5A). The 4-year survival estimates were 48, 72, 62, and 72% in anterior, AL, PL, and posterior locations, respectively. Survival was worse in the anterior (P< 0.001) and PL (P= 0.03) locations than in the AL location. With only 11 patients (three events) with LV leads located in the posterior region, we were unable to detect a statistically significant difference in survival from any other groups. Survival was not significantly different when LV lead was grouped as basal, mid, and apical (P= 0.57) (Figure 5B).

Figure 5

Kaplan–Meier survival curves. (A) Anterior, anterolateral, posterolateral, and posterior left ventricular lead locations (P= 0.003). (B) Basal, mid, and apical left ventricular locations (P= 0.57).

Mortality predictors

Table 3 shows the mortality predictors identified in all patients in the univariate and the multivariate models. Univariate predictors of death included older age, male sex, ischaemic cardiomyopathy vs. dilated cardiomyopathy, higher baseline NYHA class, and BIV pacing <99%. The use of angiotensin-converting enzyme/ angiotensin receptor blocker (ACE/ARB) was associated with reduced risk of death univariately. Left ventricular lead location also was a significant predictor of death when defined as four groups with use of 16-segment data but not when defined in accordance with basal, mid-, or apical locations. The multivariate model includes lead location, defined by the 16-segment data, and is adjusted for age, sex, ischaemic cardiomyopathy vs. dilated cardiomyopathy, and baseline NYHA class. The LV lead location defined by the 16-segment data was an independent predictor of survival (P= 0.003), with decreased risk in the AL segment compared with the anterior segment (P= 0.001).

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Table 3

Univariate and multivariate mortality predictors after cardiac resynchronization therapy

Clinical and laboratory variablesUnivariateMultivariate
Patient no.Hazard Ratio (95% CI)P valueHazard ratio (95% CI)P value
Age at implantation (per 10 years)4571.43 (1.23–1.66)<0.0011.28 (1.09–1.49)0.002
Male sex4571.93 (1.30–2.87)0.0011.46 (0.97–2.21)0.068
Ischaemic cardiomyopathy4571.99 (1.45–2.75)<0.0011.60 (1.14–2.25)0.006
Chronic atrial fibrillation4571.32 (0.98–1.78)0.070
Baseline NYHA class4572.06 (1.53–2.77)<0.0012.01 (1.49–2.72)<0.001
QRS duration (per 30 ms)4490.94 (0.82–1.08)0.386
Biventricular pacing (99–100% paced vs. <99% paced)3350.60 (0.42–0.85)0.005
Pharmacologic therapy
 ACE inhibitor or ARB4480.68 (0.48–0.97)0.031
 Beta-blocker4500.80 (0.53–1.23)0.310
 Digoxin4481.23 (0.91–1.65)0.174
Lead location by vein4570.003
 AI1.00 (reference)
 AL0.54 (0.35–0.85)0.007
 PL0.49 (0.32–0.75)0.001
 Middle cardiac0.93 (0.49–1.78)0.835
Lead location by 16-segment data4570.0030.003
 LV anterior1.00 (reference)1.00 (reference)
 LV AL0.47 (0.30–0.71)<0.0010.49 (0.32–0.75)0.001
 LV PL0.66 (0.42–1.02)0.0630.73 (0.47–1.15)0.172
 LV posterior0.44 (0.13–1.45)0.1770.32 (0.09–1.09)0.068
Lead location by long axis4570.569
 LV basal1.00 (reference)
 LV mid0.85 (0.55–1.31)0.450
 LV apical1.00 (0.59–1.67)0.990
  • ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; LV, left ventricular; LVEF: left ventricular ejection fraction; NYHA: New York Heart Association; PASP, pulmonary artery systolic pressure; RV, right ventricular.


Main findings

This large, single-centre study determined the effect of LV lead location on CRT outcome through comprehensive analysis of cinegrams, with clinical and mortality follow-up. We found three main outcomes in this clinical practice population. First, most LV leads (83%) were placed in the AL and PL wall of the left ventricle. Second, improvement in NYHA class and LVEF was seen across all LV lead locations. However, the magnitude of improvement in NYHA class and LVEF was better in lateral LV lead locations than in the anterior LV lead location. Third, consistent with improvement in HF symptoms and haemodynamics, the survival outcome favours in the order of AL, PL, and non-lateral LV lead locations.

Coronary vein tributary and segmental left ventricular lead location

The number of coronary veins and the site of where these veins drain into the coronary sinus differ individually. These coronary venous trees serve as the vehicle and host for LV lead placement. Despite multiple factors that may impact lead placement, >80% of LV leads in this study were successfully placed in the lateral, PL, and AL veins, because we prioritized the locations at the procedure. One finding, that has not be examined in detail previously and is added to the literature from this study, is most coronary veins do not exclusively collect venous return from the LV region for which they are named. We found that half of the LV leads located in the AL segment were coming from a PL or lateral vein; another half located in the PL segment were originating in the region for which each segment is named. Approximately 60% of LV leads placed in the middle cardiac vein were able to be navigated to the PL wall of the left ventricle. Leads placed in the anterior left ventricle were solely from an AI venous tributary. Overall, lateral lead position can be accomplished through multiple venous distribution, including AL, lateral, PL, and middle cardiac veins.

Lateral lead position is preferential for response to cardiac resynchronization therapy

The lateral lead location has been considered an ideal or best site for CRT. This conclusion derived from an acute haemodynamic study when CRT was initially introduced.7 In that study, pacing mid-LV free wall achieved the greatest improvement in LV dp/dtmax. This notion is supported by the fact that electrical and mechanical delays in the LV lateral wall often occur in patients with left bundle branch block, often accompanied by HF.1823

Reestablishing biventricular mechanical concordance improves HF. However, the critical role of LV lead location in long-term CRT outcome has been controversial. A few single-centre cohort studies agree that a lateral lead location achieves greater improvement in relieving HF symptoms and reversing LV remodelling than non-lateral locations,1012 yet, Gasparini et al.24 reported that they found no difference between lateral and non-lateral lead positions in short-term clinical and echocardiographic outcomes. Becker et al.22 and Ypenburg et al.20 have proposed the optimal lead position being the latest LV contraction determined through advanced echocardiographic imaging. In the present study, we found improvement in NYHA class and LV systolic function across all lead position segments except for a small group of leads in the posterior location. Still, greater haemodynamic and NYHA functional class benefits were seen in both AL and PL lead positions than in the anterior lead position. Although placement of the LV lead to the PL position has been proposed as the first priority, AL lead location results in HF improvement comparable with that in PL lead location in our study. We found similar HF improvement regardless of whether LV leads were placed in the basal, mid, or apical left ventricle.

Lateral left ventricular lead location favours survival outcome

Kaplan–Meyer analysis of survival showed survival was lower when leads were positioned in the anterior wall and higher in the AL wall of the left ventricle. The differential survival outcome coincides with the clinical and haemodynamic improvements. It is plausible that the greater magnitude in response to CRT derived from lateral lead location may translate into a greater survival outcome in contrast to non-lateral location. The finding of unfavourable anterior lead location agrees with data from a previous study that showed an increase in mortality rate of more than five-fold when comparing anterior with lateral lead location.25 Our result was in agreement with the report from the COMPANION trial:13 CRT improved HF functional outcomes across all lead locations. However, in disagreement with that trial, we observed a more favourable lateral lead location in improving both HF function and survival. Most recently published MADI-CRT sub-analysis of LV lead position and clinical outcome and another large cohort study14,26 did not observe a survival difference with regard to the circumferential LV lead position. This discrimination may attribute to the methods used for lead location assessment. The COMPANION trial reported lead location using anteroposterior and LAO projections and categorized into three segments, the MADIT-CRT trial divided LV wall into five equal parts in the short-axis view and analysed in anterior, lateral, and posterior three segments,13,14 while RAO and LAO in 30° and four-segment assessment were performed in our study. The intuitive explanation for the best survival benefit in AL lead location might be the larger separation between LV and RV leads that were placed in the RV apex in the majority of patients.

After controlling for age, sex, ischaemic cardiomyopathy, and NYHA class, the multivariate analysis identified LV lead position as a predictor of survival. Specifically, the AL lead location had the most favourable impact on survival, with a 51% mortality reduction compared with the anterior lead location. The most recently published study from Delgado et al.27 found larger baseline LV dyssynchrony favoured – while discordant LV lead position not located at a delayed contractile segment (32%) and myocardial scar burden disfavoured – long-term survival after CRT. The study addressed the interlink effect of LV radial dyssynchrony and myocardial scar region on CRT outcome in addition to the LV lead anatomical location. Of note, after controlling for LV lead location and other confounding factors, patients with ischaemic cardiomyopathy had a 1.6-fold risk of mortality compared with those subjects with non-ischaemic aetiology. It has been appreciated that non-ischaemic cardiomyopathy favours a greater response to CRT.28,29


The present study is retrospective in nature; hence, the clinical follow-up duration varied. However, all patients included in this study had cinegrams for LV lead position, and survival information was complete for the cohort except nine patients that were not found when we pulled data from the death registry. The coronary vein selection for LV lead destination was at the implanter's discretion; nevertheless, we have consistently prioritized the lateral lead position in the clinical practice. The cinegrams were taken in standard RAO and LAO views at 30° and were not individualized on the basis of each patient's anatomy. This approach may affect the precise assessment of longitudinal lead location. Other important factors that may impact CRT outcome and interact with LV lead location, such as LV scar burden and location, were not in the scope of this study. We had small sample sizes for some of the lead groups which may reduce the power we have to detect differences in the groups.

Conclusions and clinical implication

Our study comprehensively addressed the association of LV lead location with CRT outcomes, a clinical area that has been controversial. The AL lead location that has not been emphasized previously achieved an equivalent effect in improving HF symptoms, functional status, and a greater survival benefit compared with the PL location. Left ventricular lateral wall pacing could be accessed through multiple venous tributary, including the AL, lateral, PL, and middle cardiac vein. The AI vein, exclusively distributing in the anterior or anteroseptal left ventricle, might be considered as an unfavourable LV lead destination for CRT.

Conflict of interest: D.L.H. is an educational speaker for Medtronic, Boston Scientific, Sorin Medical Group, and St Jude Medical; serves on the advisory board for Boston Scientific, Sorin Medical Group, and St Jude Medical; and is a member of the steering committee for St Jude Medical. S.J.A. receives honoraria and is on the speaker's board for St Jude Medical, Boston Scientific, and Medtronic. In addition, he is a co-patent holder for an alternative resynchronization therapy technique (application #12131756, 6/2/08). T.L.W. is on an advisory board for Boston Scientific. Y.-M.C. received a research grant from St Jude Medical and Medtronic. B.D.P. received consulting fees from Boston Scientific.


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