European Journal of Echocardiography Advance Access published online on September 10, 2007
European Journal of Echocardiography, doi:10.1016/j.euje.2007.07.002
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The influence of myocardial scar and dyssynchrony on reverse remodeling in cardiac resynchronization therapy
1 Department of Cardiology, Catharina Hospital, Michelangelolaan 2, P.O. Box 1350, 5602 ZA Eindhoven, The Netherlands
2 Department of Radiology, Catharina Hospital, Eindhoven, The Netherlands
3 Technical University of Eindhoven, Eindhoven, The Netherlands
4 Department of Psychology and Health, Medical Psychology, Tilburg University, Tilburg, The Netherlands
5 Utrecht University, Utrecht, The Netherlands
Received 18 April 2007; accepted after revision 22 July 2007.
* Corresponding author. Tel: +31 40 239 7004; fax: +31 40 244 7885. E-mail address: annemieke.jansen{at}cze.nl (A.H.M. Jansen).
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Abstract |
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Aim: The influence of location and extent of transmural scar and its relation with dyssynchrony in cardiac resynchronization therapy (CRT) was investigated as posterolateral scar tissue has been invoked as a cause of non-response to CRT.
Methods and results: Fifty-seven patients eligible for CRT were assessed for transmural scar with gadolinium-enhanced MRI and for left ventricular (LV) dyssynchrony with tissue Doppler. After implant, both atrioventricular and interventricular pacing intervals were optimized. LV reverse remodeling was defined as 
10% decrease in LV end-systolic volume after 3 months. Sixteen patients had transmural scar in the posterolateral (PL) area (LV lead location), 14 at a remote site (non-PL) and 27 patients had no scar. LV reverse remodeling was observed in respectively 25%, 64% and 89% (P = 0.0001). Univariate analyses showed a relation with LV dyssynchrony (P = 0.004) and with absence of PL scar (P = 0.04) but not with QRS duration and the extent of LV scar tissue. In multivariate analysis, only LV dyssynchrony (OR: 19.62; 95% CI: 2.5–151.9; P = 0.004) independently predicted LV reverse remodeling.
Conclusion: In this study LV dyssynchrony remains the most important determinant of response to CRT, even in the presence of posterolateral scar provided atrioventricular and interventricular pacing intervals are optimized.
Keywords: Cardiac resynchronization therapy; Heart failure; Magnetic resonance imaging; Echocardiography; Myocardial infarction
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Introduction |
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Cardiac resynchronization therapy (CRT) improves symptoms, functional capacity, left ventricular (LV) function and survival in patients with congestive heart failure and left bundle branch block.1–3 Although there is a tendency for greater benefit in patients with dilated than ischemic cardiomyopathy, the relation between etiology and effectiveness of CRT is equivocal. In previous reports, classification between ischemic vs. idiopathic dilated etiology was inferred by clinical history and an abnormal coronary angiogram but location and size of actual myocardial scar were not considered.1–7 Recently, Bleeker et al. described the negative influence of posterolateral scar independently from the presence of LV dyssynchrony on the response to CRT.8 However, the influence of scar tissue remote from the LV lead and the influence of the extent of LV scar tissue is still not elucidated.9,10 Since myocardial scar may influence the effects of CRT regardless of its location or etiology of the cardiomyopathy, we assessed extent and location of scar tissue with contrast-enhanced cardiac magnetic resonance imaging (MRI) in patients scheduled for CRT. The relation of scar tissue to both the acute hemodynamic effect and LV reverse remodeling after CRT were investigated.
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Methods |
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Patients
MRI was available in 57 out of 69 consecutive patients eligible for CRT according to standard criteria. Patients with mitral valve replacement or severe valvular disease other than mitral regurgitation were excluded. All patients had heart failure New York Heart Association class (NYHA) III or IV despite optimal medication, a LV ejection fraction below 35%, sinus rhythm and left bundle branch block with QRS >120 ms. Although LV dyssynchrony was assessed by tissue Doppler this was not used as a selection criterion. Diuretics were used by 92% of patients, angiotensin-converting enzyme inhibitors by 80%, β-blocker by 67%, spironolactone by 53%, and digoxin by 20%. Changes in medication during the study were avoided unless clinically indicated.
Based on cardiovascular history (CABG, PCI or myocardial infarction) and coronary angiography (available in all patients), 30 patients were categorized as ischemic cardiomyopathy. The remaining 27 patients were classified as dilated cardiomyopathy. None of the patients with ischemic cardiomyopathy were considered candidates for coronary revascularization.
Functional status (NYHA class) and a 6-min walk test (MWT) were obtained before and 3 months after the start of CRT. Ten patients were unable to perform the MWT due to intermittent claudication or gout.
The local ethics committee approved the study protocol and informed consent was obtained in all patients.
Cardiac magnetic resonance imaging
Gadolinium-enhanced MRI was performed within 2 weeks prior to biventricular pacemaker implantation. Images were acquired on a 1.5-T Philips Intera CV system using a phased-array coil during repeated breath-holds of circa 8 s (Philips Medical Systems, Best, the Netherlands). Steady-state free precession cine images were acquired in multiple short axes (every 1 cm throughout the entire LV) and two to three long-axis planes. Gadolinium (gadoteridol, 0.1 to 0.15 mmol/kg) was administered intravenously, and contrast-enhanced images were acquired after 10 min with a three-dimensional segmented inversion-recovery technique in the identical planes.11
The MRI scans were evaluated by two observers unaware of the patient's clinical condition or results of other imaging modalities in a 17-segment model according to the American Heart Association.12 Hyperenhanced tissue on the gadolinium-enhanced images was assumed to represent scarred myocardium.13–16 Transmural extent of hyperenhancement within each segment was graded on a 4-point scale: (0) indicated no hyperenhancement, (1) less then 25% of wall thickness, (2) 26% to 50%; (3) 51% to 75% and (4) more than 76%.13–16 As both grade 3 and 4 hyperenhancement showed lack of improved contractility after revascularization in the study by Kim et al., we hypothesized that no significant contribution to contraction of these segments could be expected after CRT. Therefore, for the purpose of this study both grade 3 and 4 hyperenhancement were considered transmural scar tissue.15
The infarct size was quantified as the sum of the scores of all segments divided by 68 (this represents all 17 segments multiplied by the maximal hyperenhancement score of 4).13–15 The result indicates the scarred fraction of the total left ventricular mass. To accommodate the different LV segment nomenclature in MRI and echocardiography, inferolateral and anterolateral segments on MRI were considered to correspond to echocardiographic posterolateral (PL) segments (Figure 3). Since the left ventricular leads were positioned in the basal and mid PL segments in all patients, presence of PL scar was compared to non-PL (remote) scar, while a third group was comprised of patients without scar. Subgroup analysis of scar patients was performed to analyze the influence of location and extent of scar tissue on the response to cardiac resynchronization therapy.
Biventricular pacemaker implant
The coronary sinus lead (Medtronic 4193) was positioned in a posterior or posterolateral branch of the coronary sinus in all patients. The position of the coronary sinus lead was assessed fluoroscopically using different orthogonal views, using the basal and mid-segments of the 17 LV-segment MRI model. The right ventricular lead was placed in the apical or mid septal region and the right atrial lead in the atrial appendage. All leads were connected to a Medtronic InSync 8042 pulse generator.
The atrioventricular (A-V) delay and interventricular (V-V) pacing interval were optimized within 1 day after implant using invasive LV dP/dtmax measurements with a sensor-tipped pressure guide wire (PW-4, RADI Medical Systems, Uppsala, Sweden) as previously described.17 In the remaining five patients, optimization was not performed invasively due to logistical and technical reasons but by echo Doppler using the velocity time integral of the transmitral flow and of the left ventricular outflow tract.18 Acute hemodynamic benefit was defined as the difference in LV dP/dtmax between atrial pacing and biventricular pacing with optimized A-V and V-V delay at identical heart rates.
Echocardiography
Echo-Doppler was performed with a Philips Sonos 7500 and S3 transducer (Philips Medical Systems, Andover, MA) less than 1 week before and 3 months after pacemaker implant. Recordings were stored in digital format for off-line analysis. Nomenclature of LV segments and measurements of LV dimensions were according the recommendations of the American Society of Echocardiography.19 LV volumes and ejection fraction were obtained in apical four- and two-chamber views. Severity of mitral regurgitation (grade I–IV) was assessed both by absolute color jet area as well as by mid-systolic jet area relative to left atrial size in the apical 4-chamber view. Cardiac index was assessed by pulsed wave Doppler of the LV-outflow tract. Measurements were averaged for at least three consecutive beats. LV reverse remodeling was defined as a decrease of LV end-systolic volume of 10% or more after 3 months of CRT.
To determine intraventricular dyssynchrony, pulsed wave tissue Doppler was obtained by placing the sample volume (length 0.38 cm) in the middle of the six basal LV segments in the four-, three- and two-chamber apical views respectively. Gain and filter settings were adjusted to eliminate background noises and allow for a clear spectral display. Recordings were made at a sweep speed of 100 mm/s and digitally stored for offline analysis. The interval from the onset of QRS to onset of systolic velocity (TsO) was measured in four end-expiratory beats and averaged. Previously, we demonstrated that LV reverse remodeling can be well predicted by the standard deviation of TsO of six basal LV segments (SDTsO-6): a SD-TsO-6 of more than 20 ms had a sensitivity of 96%, a specificity of 92%, a positive and negative predictive value of respectively 96% and 92% to predict LV reverse remodeling.5
Statistical analysis
Numerical values are expressed as mean ± SD. Differences between groups at baseline and follow-up were examined using multivariate analysis. ANOVA repeated measures were performed to examine changes over time. Differences between two groups were analyzed using a Student t-test or Chi-square test when appropriate. Univariate and multivariate logistic regression analysis (backward Wald method) was used to examine which parameters predict LV reverse remodeling.
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Results |
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The study population (43 male, age 69 ± 8 years) had a baseline QRS and PR interval of respectively 169 ± 28 ms and 189 ± 27 ms. Further baseline patient characteristics of the study population are summarized in Table 1.
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Hyperenhancement was observed in 219 of 969 segments (22.6%), of which 90 (41%) were considered grade 1–2 and 129 segments (59%) grade 3–4. The distribution of transmural scar (grade 3–4) over the left ventricle is provided in Figure 1. Scar tissue was present in six patients without coronary artery disease defined as having dilated cardiomyopathy. Four of these patients had grade 3 or 4 scar tissue of one or more LV-segments (mean total infarct size 12 ± 7%): two were added to the PL group and two to the non-PL group. The remaining two patients had non-transmural grade 2 hyperenhancement in small LV areas (infarct size 3 ± 0%) and were not reclassified. On the other hand, five patients with a clinical and angiographic diagnosis of ischemic cardiomyopathy had only grade 1 or 2 scar tissue (infarct size 8 ± 4%) and were included in the no-scar group. Thus finally 16 patients were assigned to the PL group, 14 to the non-PL group, and 27 to the no-scar group. The relative distribution of hyperenhancement for all three groups is depicted in Figure 2
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Baseline QRS duration did not significantly differ between PL, non-PL and no-scar groups (respectively, 164 ± 27, 167 ± 29, 174 ± 28 ms; P not significant).
Baseline clinical and echocardiographic characteristics were also not significantly different between the three groups (Table 2). Only LV dyssynchrony, measured by SD-TsO-6, was significantly different between groups, respectively 16 ± 12 ms, 28 ± 16 ms and 37 ± 17 ms (P < 0.001). LV dyssynchrony (TsO-SD-6 >20 ms) was present in 25% of patients in the PL scar group, 71% in the non-PL scar group and 81% in the no-scar group (P < 0.0001). Mean infarct size was not significantly different between PL and non-PL group (33 ± 18% versus 26 ± 15%, P not significant).
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The changes following CRT are summarized in Table 2. Immediately after start of CRT, LV dP/dtmax showed a significant smaller increase in the PL scar group than in the non-PL and the no-scar group (respectively +15 ± 10%, +28 ± 16% and +28 ± 18%; P = 0.0025). The optimal A-V delays for the PL, non-PL and no-scar group were respectively 117 ± 23 ms, 115 ± 26 ms and 119 ± 20 ms (P not significant) and the optimal V-V interval respectively 49 ± 28 ms, 52 ± 22 ms and 36 ± 30 ms (P not significant). Clinical benefit, as assessed by NYHA class and MWT, improved in all groups after 3 months (Table 2). In contrast, improvement in echocardiographic indices only occurred in the non-PL and no-scar groups, whereas no significant change was found in the PL group.
Echocardiographic LV reverse remodeling was observed in 37 patients (65%): in only four patients (25%) of the PL group compared to 9 patients (64%) in the non-PL group and 24 patients (89%) in the no-scar group (P = 0.0001). The absolute changes in LV end-systolic volume after 3 months of CRT for the three groups were –1.2 ± 9%, –12 ± 8%, and –25 ± 17%, respectively. LV ejection fraction and mitral regurgitation improvement was significantly more in the non-PL scar and no-scar group than in the PL scar group. Univariate analyses related only LV dyssynchrony (OR 127.2; 95% CI 4.6–3550.1; P = 0.004) and absence of PL scar (OR 5.4; 95% CI 1.1–26.0; P = 0.036) to LV reverse remodeling while QRS duration and extent of LV scar tissue showed no relation (Table 3). However, multivariate analysis revealed that only LV dyssynchrony (OR: 19.62; 95% CI 2.5–151.9; P = 0.004) independently predicted LV reverse remodeling (Table 3).
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Discussion |
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This study investigated the influence of the location and extent of transmural myocardial scar as assessed by gadolinium enhanced MRI on both the acute hemodynamic effect and LV reverse remodeling after CRT. In search for an explanation for non-responders to CRT, attention has been given to the etiology of heart failure. Although in the MIRACLE study the ejection fraction increased more in patients with idiopathic dilated than ischemic left ventricular dysfunction,2 other studies observed no difference in response between the two groups.1,6,20 The cause of heart failure in all these studies was determined by documented history or coronary angiography and did not consider the presence and the influence of myocardial scar tissue. Kim et al. have demonstrated the importance of scar tissue for ventricular performance.15 They found that 90% of regions with more than 50% hyperenhancement (considered transmural scar) did not regain contractility after revascularization. Therefore, also in CRT the presence of transmural scar tissue would presumably influence the effect of CRT especially if scar tissue is present in the posterolateral wall, which is often the last activated and hence a desired site for LV stimulation. Our study population was therefore divided according to the presence of transmural scar in the posterolateral wall, in a remote area or no scar on the basis of gadolinium enhanced MRI. As a result, 15% of patients classified initially as idiopathic cardiomyopathy had transmural scar by MRI, whereas in 19% of patients presumed to have an ischemic etiology no transmural scar tissue could be documented.
We found that LV dyssynchrony was only present in 25% of the PL scar group. These patients showed a smaller increase in acute LV dP/dtmax and only 25% showed LV reverse remodeling. If scar tissue occurred in a remote area there were no significant differences with patients without scar. Although this suggests a pivotal role for scar in the latest activated region and in this study the location of the LV lead, in the response to CRT, multivariate analysis revealed that only the presence of LV dyssynchrony was independently related to LV reverse remodeling. As a result, if dyssynchrony is proven, no further investigation into the presence of scar tissue would be necessary to proceed with CRT.
These findings are in contrast to a recent study in 50 patients by Bleeker et al. who showed that in their patients the influence of posterolateral scar tissue was more important than LV dyssynchrony to predict clinical and echocardiographic response to CRT.8 Nevertheless, both studies concur in showing the importance of dyssynchrony on the response to CRT, which is in line with published reports.5–7,21,22 However, there are some important notes regarding the difference between the two studies. The criteria used for the measurement of LV dyssynchrony may influence prediction of responders. We previously demonstrated that a 20 ms standard deviation of the time from the beginning of the QRS complex to the onset of systolic movement of six basal LV segments obtained by tissue Doppler optimally predicted LV reverse remodeling and is superior compared to the use of septal to lateral delay.5 In the posterolateral scar group, the mean SD-TsO-6 of 16 ± 12 ms was well below this value and LV reverse remodeling would thus be less probable.
Moreover, it has been recognized that optimizing the interventricular stimulation interval contributes significantly to the hemodynamic effect of CRT.17 In a previous study of 53 patients we demonstrated that although simultaneous biventricular pacing increased LV dP/dtmax by 17% and 18% respectively in ischemic and idiopathic cardiomyopathy, further adjustment of the V-V interval resulted in a further increase of LV dP/dtmax to 25% in both groups.17 The mean optimal interventricular pacing interval (left ventricle first) was 28 ms in the dilated cardiomyopathy group and 52 ms in the ischemic cardiomyopathy group. In the current study, the mean optimal interventricular pacing interval in patients with posterolateral scar, remote scar and no scar was 49 ± 28 ms, 52 ± 22 ms and 36 ± 30 ms respectively. (P not significant). Although this is not as major a difference as previously reported, this may nevertheless correct for the slower myocardial conduction velocity in patients with ischemic versus dilated cardiomyopathy as has been demonstrated by Rodriguez et al.23 Furthermore, pacing in a scar area will take a longer time to reach myocardium that can contribute to ventricular performance and correct for dyssynchrony.22
In the present study we found no relation between the extent of LV scar and LV reverse remodeling after CRT. Recently, Ypenburg et al. described the impact of scar extent, obtained by gated SPECT, to be negatively related to LV reverse remodeling in 51 patients. However, most scar areas were located posterolaterally and showed significantly less LV dyssynchrony.10 In a recent study by White et al. in 23 patients, a correlation was suggested between total scar and clinical response to CRT. However, scar tissue (n = 10) was almost exclusively observed in the septal and anterior region compared to patients without scar.9 Therefore, the diversity of location of scar tissue and the relatively small study populations might explain some of the differences with our study. In this study, no differentiation for infarct size in the posterolateral area was made given the small number of patients.
Ideally, the location of the coronary sinus lead should be determined by the same technique as the infarct location. Although the best estimate comparing orthogonal fluoroscopic images with the standard 17 segments CMR model was used, a suboptimal match cannot be ruled out. Further, all patients with posterolateral scar had the LV pacing lead positioned within this area. It remains to be investigated if a pacing position outside this area would improve the results of CRT in these patients. Also the relatively low number of patients limits the study.
In conclusion, this study observed that the presence of scar tissue in the posterolateral area does not preclude a positive effect on LV remodeling in the presence of significant LV dyssynchrony and optimization of the interventricular pacing interval.
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