CLINICAL RESEARCH: LEFT VENTRICULAR DEFORMATION
Effects of Cardiac Resynchronization Therapy on Left Ventricular Twist
Matteo Bertini, MD*, ,
Nina Ajmone Marsan, MD*,
Victoria Delgado, MD*,
Rutger J. van Bommel, MD*,
Gaetano Nucifora, MD*,
C. Jan Willem Borleffs, MD*,
Giuseppe Boriani, MD, PhD,
Mauro Biffi, MD,
Eduard R. Holman, MD, PhD*,
Ernst E. van der Wall, MD, PhD*, ,
Martin J. Schalij, MD, PhD* and
Jeroen J. Bax, MD, PhD*,*
* Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands
Department of Cardiology, University of Bologna, Bologna, Italy
Department of Cardiology, Interuniversity Cardiology Institute of the Netherlands Utrecht, Utrecht, the Netherlands
Manuscript received November 25, 2008;
revised manuscript received April 17, 2009,
accepted May 4, 2009.
* Reprint requests and correspondence: Dr. Jeroen J. Bax, Department of Cardiology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, the Netherlands (Email: j.j.bax{at}lumc.nl).
 |
Abstract
|
|---|
Objectives: This study explored the effects of cardiac resynchronization therapy (CRT) on left ventricular (LV) twist, particularly in relation to LV lead position.
Background: LV twist is emerging as a comprehensive index of LV function.
Methods: Eighty heart failure patients were included. Two-dimensional echocardiography was performed at baseline, immediately after CRT, and at 6-month follow-up. Speckle-tracking analysis was applied to assess LV twist. The LV lead was placed preferably in a (postero)lateral vein, and at fluoroscopy, the position was classified as basal, midventricular, or apical. Response to CRT was defined as reduction of LV end-systolic volume  15% at 6-month follow-up. A control group comprised 30 normal subjects.
Results: Peak LV twist in heart failure patients was 4.8 ± 2.6° compared with 15.0 ± 3.6° in the control subjects (p < 0.001). At 6-month follow-up, peak LV twist significantly improved only in responders (56%), from 4.3 ± 2.4° to 8.5 ± 3.2° (p < 0.001). The strongest predictor of response to CRT was the improvement of peak LV twist immediately after CRT (odds ratio: 1.899, 95% confidence interval: 1.334 to 2.703, p < 0.001). Furthermore, LV twist significantly improved in patients with an apical (from 4.3 ± 3.1° to 8.6 ± 3.0°, p = 0.001) and midventricular (from 4.8 ± 2.2° to 6.4 ± 3.9°, p = 0.038) but not with a basal (5.0 ± 3.3° vs. 4.1 ± 3.2°, p = 0.28) LV lead position. Similarly, LV ejection fraction significantly increased in patients with an apical (from 26 ± 7% to 37 ± 7%, p < 0.001) and midventricular (from 26 ± 6% to 33 ± 8%, p < 0.001) but not with a basal (26 ± 5% vs. 28 ± 8%, p = 0.30) LV lead position.
Conclusions: An immediate improvement of LV twist after CRT predicts LV reverse remodeling at 6-month follow-up.
Key Words: heart failure • cardiac resynchronization therapy • left ventricular twist • left ventricular reverse remodeling • left ventricular lead position
|
Abbreviations and Acronyms
| | ANOVA = analysis of variance | | CRT = cardiac resynchronization therapy | | HF = heart failure | | LV = left ventricle/ventricular | | LVEDV = left ventricular end-diastolic volume | | LVEF = left ventricular ejection fraction | | LVESV = left ventricular end-systolic volume | | NYHA = New York Heart Association |
|
The human heart has a specific helical arrangement of the myofibers with a right-hand orientation from the base toward the apex in the endocardial layers and a left-hand orientation in the epicardial layers. This spiral architecture of the myofibers leads to a left ventricular (LV) systolic wringing motion as a result of an opposite rotation of LV apex and base (1,2). The gradient between apex and base in the rotation angle along LV longitudinal axis is called twist and contributes significantly to LV systolic function, in addition to myocardial shortening and thickening (3–5).
In heart failure (HF) patients, LV twist is significantly reduced (6). Cardiac resynchronization therapy (CRT) is considered a major therapeutic breakthrough for HF patients, and recent large randomized trials have shown that CRT has beneficial effects on HF symptoms, LV systolic function, and survival (7,8). At present, minimal data are available about the effect of CRT on LV twist (9,10).
In the current study, the effect of CRT on LV twist was assessed using speckle-tracking echocardiography. Furthermore, the relationship between the change in LV twist and LV reverse remodeling at 6-month follow-up was investigated. Finally, the influence of the LV lead position on the improvement in LV twist and response to CRT was explored.
|
Methods
|
|---|
Study population and protocol.
A total of 87 consecutive HF patients scheduled for CRT were prospectively included. According to current guidelines, the inclusion criteria were New York Heart Association (NYHA) functional class III to IV, sinus rhythm, left ventricular ejection fraction (LVEF)  35%, and QRS duration 120 ms (11). Etiology of HF was considered ischemic in the presence of significant coronary artery disease (>50% stenosis in 1 major epicardial coronary artery) on coronary angiography and/or a history of myocardial infarction or revascularization.
The clinical evaluation consisted of: 1) assessment of clinical status: NYHA functional class, quality of life (using the Minnesota Living With Heart Failure questionnaire) (12), and 6-min walk distance (13) at baseline and 6-month follow-up; and 2) assessment of LV volumes, function, dyssynchrony, and twist, using standard echocardiography and speckle-tracking analysis at baseline, within 48 h (immediately after CRT) and at 6-month follow-up.
In addition, 30 subjects without evidence of structural heart disease, frequency matched for age, sex, and body surface area, were included as a normal control group, selected from an echocardiographic database. These subjects were referred for the echocardiographic evaluation because of atypical chest pain, palpitations, or syncope without murmur.
Standard echocardiography.
All patients were imaged in the left lateral decubitus position using a commercially available system (Vingmed Vivid 7, General Electric-Vingmed, Milwaukee, Wisconsin). Standard 2-dimensional images were obtained using a 3.5-MHz transducer and digitally stored in cine-loop format; the analysis was performed offline using EchoPAC version 6.0.1 (General Electric-Vingmed).
From the standard apical views (4- and 2-chamber), LV volumes and LVEF were calculated according to the American Society of Echocardiography guidelines (14). At 6-month follow-up, patients were classified as echocardiographic responders based on a reduction 15% of left ventricular end-systolic volume (LVESV) (15).
Segmental wall motion was assessed according to the American Society of Echocardiography in order to evaluate the presence of scarred segments within ischemic HF patients (14). Akinetic and diskinetic segments (wall motion score 3 and 4) were classified as scarred segments (16).
Speckle-tracking analysis.
The speckle-tracking software tracks frame-to-frame the movement of natural myocardial acoustic markers, or speckles, on standard gray-scale images. Speckles are randomly distributed and each region of the myocardium has a distinguishing pattern, a fingerprint. Furthermore, speckle-tracking analysis is angle independent and allows the evaluation of myocardial contraction/relaxation along the circumferential, longitudinal, and radial direction (17,18).
In the current study, speckle-tracking analysis was applied to evaluate LV dyssynchrony (based on radial strain analysis) and LV twist. Parasternal short-axis images were acquired at 3 distinct levels: 1) basal level, identified by the mitral valve; 2) papillary muscle level; and 3) apical level (the smallest cavity achievable distally to the papillary muscles, moving the probe down and slightly laterally, if needed). Frame rate ranged from 45 to 100 frame/s, and 3 cardiac cycles for each parasternal short-axis level were stored in cine-loop format for the offline analysis (EchoPAC, General Electric-Vingmed). The endocardial border was traced at an end-systolic frame, and the region of interest was chosen to fit the whole myocardium. The software allows the operator to check and validate the tracking quality and to adjust the endocardial border or modify the width of the region of interest, if needed. Furthermore, each short-axis image was automatically divided into 6 standard segments: septal, anteroseptal, anterior, lateral, posterior, and inferior. Aortic valve opening and closure were identified on pulsed-wave Doppler tracings obtained from the LV outflow tract.
LV Dyssynchrony Analysis
LV dyssynchrony was derived from the radial strain curves obtained from the papillary muscle short-axis view. As previously described, LV dyssynchrony was defined as the time difference of peak radial strain between the anteroseptal and posterior segments (19).
LV Twist Analysis
The speckle-tracking software calculates LV rotation from the apical and basal short-axis images as the average angular displacement of the 6 standard segments referring to the ventricular centroid, frame by frame. Counterclockwise rotation was marked as positive value and clockwise rotation as negative value when viewed from the LV apex. LV twist was defined as the net difference (in degrees) of apical and basal rotation at isochronal time points. For the calculation of LV twist, averaged apical and basal rotation data were exported to a spreadsheet program (Excel 2003, Microsoft Corp., Redmond, Washington) (Fig. 1) (20,21). The following measurements were derived: peak apical and basal rotation and peak LV twist.
View larger version (55K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 1 Assessment of LV Twist
Examples of left ventricular (LV) twist in a normal control patient (A) and in a heart failure patient (B). The top 2 panels in A and B represent apical and basal rotations and the bottom panels represent LV twist calculation after exporting the data to a spreadsheet program (Excel 2003, Microsoft Corp., Redmond, Washington). AVC = aortic valve closure; AVO = aortic valve opening.
|
|
Reproducibility.
Reproducibility of left ventricular end-diastolic volume (LVEDV), LVESV, LVEF, and peak LV twist was assessed on 20 randomly selected HF patients. Bland-Altman analysis was performed to evaluate the intraobserver and interobserver agreement repeating the analysis a few days later by the same observer and by a second independent observer. The results were expressed as absolute mean difference ± 2 SDs.
The intraobserver agreement for LVEDV, LVESV, LVEF, and peak LV twist were 7.4 ± 11.2 ml, 7.0 ± 10.1 ml, 1.9 ± 4.4%, and 0.2 ± 0.3°, respectively. The interobserver agreement for LVEDV, LVESV, LVEF, and peak LV twist were 12.9 ± 14.7 ml, 11.3 ± 13.9 ml, 2.5 ± 4.9%, and 0.7 ± 0.8°, respectively.
CRT implantation.
All patients received a biventricular pacemaker with cardioverter-defibrillator function (Contak Renewal 4RF, Boston Scientific, St. Paul, Minnesota; or InSync Sentry, Medtronic Inc., Minneapolis, Minnesota; Lumax 340 HF-T, Biotronik, Berlin, Germany). The right atrial and ventricular leads were positioned conventionally. All LV leads were implanted transvenously, and positioned preferably in a (postero)lateral vein. A coronary sinus venogram was obtained using a balloon catheter, followed by the insertion of the LV pacing lead. An 8-F guiding catheter was used to place the LV lead (Easytrak, Boston Scientific, or Attain-SD, Medtronic, or Corox OTW Biotronik) in the coronary sinus.
LV lead position.
Target veins were lateral or postero-lateral veins. The LV lead position was determined using biplane fluoroscopy classification (22). In the right anterior oblique view and/or in the postero-anterior view, the distance between the coronary sinus/mitral plane and the cardiac apex was divided in 3 parts and the LV lead position was classified in 3 groups: basal, midventricular, and apical.
Statistical analysis.
All continuous variables had a normal distribution (as evaluated with Kolmogorov-Smirnov tests). Summary statistics for these data are therefore presented as mean ± SD. Categorical data are presented as numbers and percentages. The paired t test was used for the comparison between continuous variables at baseline and immediately after CRT and between baseline and at 6-month follow-up. The unpaired t test was performed to compare continuous variables between normal control subjects and HF patients and between CRT responders and nonresponders. Chi-square/Fisher exact tests were computed to test for differences in categorical variables. Linear regression analysis was performed to determine the relations between LV twist, LVEF, and LV dyssynchrony. In order to identify independent determinants of LV twist, a multivariable linear regression analysis using the enter model was performed including as covariates LVEF and LV dyssynchrony. Linear regression analysis was used to assess the relation between the  (difference between immediately after CRT and baseline) peak LV twist and LVEF. The differences in peak LV twist during follow-up in responders and nonresponders were assessed using analysis of variance (ANOVA) for repeated measurements. In order to identify variables related to a positive response to CRT, univariable and multivariable logistic regression analyses were performed including clinical (age, sex, etiology, QRS duration at baseline, and 6-min walk distance at baseline) and echocardiographic (LVESV at baseline, LVESV, LV dyssynchrony at baseline, LV dyssynchrony, peak LV twist at baseline, peak LV twist) characteristics of the patients. Only significant (p < 0.05) univariable predictors were entered as covariates in the multivariable logistic regression analysis, which was performed using the entire model. Odds ratio and 95% confidence intervals were calculated. Model discrimination was assessed using c-statistic, and model calibration was assessed using Hosmer-Lemeshow statistic. The differences in peak LV twist and LVEF between the groups of patients with different LV lead position were assessed by 1-way ANOVA. All statistical tests were 2-sided, and a p value <0.05 was considered significant. The statistical software program SPSS version 14.0 (SPSS Inc., Chicago, Illinois) was used for statistical analysis.
|
Results
|
|---|
Study population.
Reliable speckle-tracking for rotation analysis was obtained in all normal control subjects and in 80 (92%) HF patients. Consequently, 7 (8%) patients were excluded from the study. Of the 80 HF patients enrolled, 9 did not complete the 6-month follow-up; 3 patients died of worsening HF, 1 had LV pacing switched off due to intolerable phrenic stimulation, 1 had CRT device explantation secondary to infection, and 4 were lost to follow-up. Therefore, data at baseline and immediately after CRT were collected for 80 patients and data at 6-month follow-up were collected for 71 patients. Baseline characteristics of normal control subjects and the HF patients are listed in Table 1.
LV twist baseline.
As shown in Table 1, peak apical rotation, peak basal rotation, and peak LV twist were severely reduced in HF patients compared with normal control subjects: 2.4 ± 1.8° versus 9.4 ± 3.2° (p < 0.001), –3.3 ± 2.0° versus –6.1 ± 2.4° (p < 0.001), and 4.8 ± 2.6° versus 15.0 ± 3.6° (p < 0.001), respectively.
A significant relation (r = 0.53, p < 0.001) was observed between peak LV twist and LVEF in HF patients. This relation was stronger in nonischemic (r = 0.60, p < 0.001) than in ischemic HF patients (r = 0.34, p = 0.020) (Fig. 2A). Moreover, a modest relation (r = –0.33, p = 0.003) was observed between peak LV twist and LV dyssynchrony in HF patients. At multivariable linear regression analysis, LVEF (beta = 0.47, p < 0.001) and LV dyssynchrony (beta = –0.21, p = 0.032) were independent determinants of LV twist.
View larger version (25K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 2 LV Twist and LV Systolic Function
(A) Correlation between baseline peak left ventricular (LV) twist and left ventricular ejection fraction (LVEF) in heart failure (HF) patients (ischemic: open circles, and nonischemic: solid circles). (B) Correlation between peak LV twist and LVEF immediately after cardiac resynchronization therapy in HF patients (ischemic: open circles, and nonischemic: solid circles).
|
|
LV twist after CRT.
Immediately After CRT
Immediately after CRT, peak LV twist increased from 4.8 ± 2.6° to 5.9 ± 3.2° (p = 0.007). In particular, peak LV twist was strongly related to LVEF (r = 0.83, p < 0 .001), and this relation was good in both nonischemic (r = 0.85, p < 0.001) and ischemic HF patients (r = 0.82, p < 0.001) (Fig. 2B). Furthermore, the relations between peak LV twist and LV dyssynchrony (r = –0.57, p < 0.001) and between LV dyssynchrony and LVEF (r = –0.63, p < 0.001) were good but less strong than the previous relation between peak LV twist and LVEF.
Six-Month Follow-Up
At 6-month follow-up, 40 of 71 (56%) patients were classified as echocardiographic responders to CRT (defined as a decrease in LVESV 15%). No significant differences in the baseline clinical characteristics were found between responders and nonresponders (Table 2). At 6-month follow-up, significant improvement in NYHA functional class (from 3.0 ± 0.5 to 2.0 ± 0.7, p < 0.001), quality of life (from 35 ± 23 to 20 ± 20, p < 0.001), and 6-min walk distance (from 306 ± 106 m to 363 ± 109 m, p < 0.001) were observed in CRT responders only (Table 2).
Baseline echocardiographic characteristics were also similar between the 2 groups, except for LV dyssynchrony (Table 3), which was larger in responders compared with nonresponders (182 ± 71 ms vs. 116 ± 83 ms, p = 0.003). A trend toward lower values of peak LV twist were noted in responders as compared with nonresponders (4.3 ± 2.4° vs. 5.4 ± 2.9°, p = 0.072). At 6-month follow-up, LV dyssynchrony improved in CRT responders (from 182 ± 71 ms to 60 ± 45 ms, p < 0.001), whereas in nonresponders LV dyssynchrony did not change (116 ± 83 ms vs. 136 ± 89 ms, p = 0.30) (Table 3). Importantly, within ischemic HF patients, CRT responders presented a significantly lower number of scarred segments at 2-dimensional echocardiography as compared with nonresponders (2.7 ± 0.9 vs. 4.2 ± 2.2, p = 0.016).
View this table:
[in this window]
[in a new window]
|
Table 3 Standard Echocardiographic Variables and Rotational Parameters in Responders Versus Nonresponders at Baseline and 6-Month Follow-Up
|
|
Concerning the rotational parameters, in responders peak LV twist progressively improved during follow-up (ANOVA p < 0.001), whereas in nonresponders a progressive deterioration of peak LV twist was noted (ANOVA p < 0.001) (Fig. 3). Particularly, both apical and basal rotation significantly improved in responders (from 2.3 ± 1.7° to 5.0 ± 3.0°, p < 0.001 and from –3.2 ± 2.2° to –4.3 ± 1.9°, p = 0.006), whereas only basal rotation significantly deteriorated in nonresponders (from –3.5 ± 1.7 to –2.1 ± 2.2, p = 0.001) (Table 3).
View larger version (28K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 3 LV Twist in Responders and Nonresponders
Peak left ventricular (LV) twist in responders and nonresponders at baseline, immediately after cardiac resynchronization therapy (CRT), and at 6-month follow-up. ANOVA = analysis of variance.
|
|
Prediction of LV reverse remodeling.
At univariable logistic regression, LV dyssynchrony at baseline, LV dyssynchrony, LVESV, and peak LV twist were significantly related to LV reverse remodeling at 6-month follow-up (Table 4). At multivariable logistic regression analysis, peak LV twist was the strongest predictor of response to CRT at 6-month follow-up (odds ratio: 1.899, 95% confidence interval: 1.334 to 2.703, p < 0.001) (Table 4).
LV twist in relation to LV lead position.
Considering the 71 patients with 6-month follow-up, 68 patients had the LV lead placed in a (postero)lateral vein and 3 in an anterior vein. The 3 patients with the LV lead positioned in an anterior vein were nonresponders at 6-month follow-up. Of the remaining 68 patients, the LV lead position was classified (from the right anterior oblique/postero-anterior view on fluoroscopy) as basal in 17 (25%), midventricular in 34 (50%), and apical in 17 (25%) patients. At baseline, peak LV twist was not significantly different between patients with apical, midventricular, and basal LV lead position (ANOVA p = 0.68). However, at 6-month follow-up, peak LV twist showed a significant improvement in patients with apical (from 4.3 ± 3.1° to 8.6 ± 3.0°, p = 0.001) and midventricular (from 4.8 ± 2.2° to 6.4 ± 3.9°, p = 0.038) LV lead position, whereas in patients with a basal LV lead position, peak LV twist did not change significantly (5.0 ± 3.3° vs. 4.1 ± 3.2°, p = 0.28) (Fig. 4A). Similarly, LVEF increased significantly in patients with an apical (from 26 ± 7% to 37 ± 7%, p < 0.001) and midventricular (from 26 ± 6% to 33 ± 8%, p < 0.001) but not with a basal (26 ± 5% vs. 28 ± 8%, p = 0.30) LV lead position (Fig. 4B).
View larger version (25K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 4 LV Twist and LVEF in Relation to LV Lead Position
(A) Peak LV twist at baseline and 6-month follow-up in patients with basal, midventricular, and apical LV lead position. Significant improvement was observed in patients with an apical or midventricular LV lead position but not in patients with basal LV lead position. (B) LVEF at baseline and 6-month follow-up in patients with basal, midventricular, and apical LV lead position. Significant improvement was observed in patients with an apical or midventricular LV lead position but not in patients with basal LV lead position. Abbreviations as in Figure 2.
|
|
Figure 5
shows an example of a responder with the LV lead placed in an apical position of a postero-lateral vein and significant improvement in peak LV twist and LVEF after CRT (both immediately after CRT implantation and at 6-month follow-up).
View larger version (50K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 5 Example of a CRT Responder With LV Lead in an Apical Position
(A) Peak LV twist improved from 3.9° at baseline to 9.7° immediately after cardiac resynchronization therapy (CRT) implantation. Peak LV twist further improved at 6-month follow-up (peak LV twist 10.9°). (B) Biplane fluoroscopy: the left anterior oblique (LAO) view shows the LV lead in a posterolateral cardiac vein; in the postero-anterior (PA) view, the distance between the coronary sinus/mitral plane and the cardiac apex was divided (dotted lines) into 3 parts (basal, midventricular, and apical). LVEF = left ventricular ejection fraction; other abbreviations as in Figure 1.
|
|
|
Discussion
|
|---|
The current study evaluated the effects of CRT on LV twist and provides new insights on the relationship between LV rotational mechanics, CRT response, and LV lead position. The main findings can be summarized as follows: 1) LV twist was significantly reduced in HF patients; 2) LV twist improved in responders and worsened in nonresponders to CRT; 3) the strongest predictor of LV reverse remodeling at 6-month follow-up was peak LV twist (immediate change in LV twist after CRT); and 4) an LV lead placed in a (postero-)lateral vein with apical or midventricular position was associated with the greatest improvement of LV twist after CRT and with the highest response rate to CRT.
Relationship between LV twist and LV function.
Several techniques have been applied for the assessment and quantification of LV twist. For this purpose, tagged cardiac magnetic resonance imaging and sonomicrometry are considered the gold standard, but the most recent speckle-tracking echocardiographic technique, used in the present study, demonstrated a good agreement with these imaging modalities (20,21). Previous studies, using both tagged cardiac magnetic resonance imaging and speckle-tracking analysis, suggested an important relation between LV twist and LVEF (4,9). Similarly, in the current study, the relation between LV twist and LV systolic function was good (r = 0.53, p < 0 .001), illustrating the potential role of LV twist as a comprehensive index of LV systolic function. Furthermore, the results of the present study highlight that the relation between LV systolic function and LV twist was stronger in nonischemic patients as compared with ischemic patients. A possible reason may be the presence of regional myocardial damage in ischemic patients, involving specifically the apex or the base with a different effect on LV twist (23).
Finally, LV twist was modestly related to LV dyssynchrony (r = –0.33, p < 0 .001), but at multivariable linear regression analysis, LV dyssynchrony was still independently related to LV twist. This finding points out that LV twist not only is a sensitive and thorough parameter of LV function, but also it may reflect the extent of LV (dys)synchrony.
Relationship between LV twist and CRT response.
The effects of CRT on torsional mechanics were different in responders and nonresponders. A trend toward more reduced LV twist at baseline in responders as compared with nonresponders was observed. In the present study, a significant improvement of LV twist was observed in CRT responders and a significant worsening in nonresponders. In contrast, a previous study by Zhang et al. (10) did not show any significant increase of LV twist in responders to CRT. The different results may be related to sample size and population characteristics.
In the multivariable model, baseline LV dyssynchrony and an immediate improvement in LV twist after CRT were the only predictors of LV reverse remodeling at 6-month follow-up. The predictive value of LV dyssynchrony has been shown already in previous studies (19,24). The novelty of the present study is that CRT may (partially) restore LV twist, possibly by providing a more physiological electrical depolarization and mechanical contraction of the myofibers. Specifically, CRT partially restored LV torsional behavior in responders, by not only improving apical rotation but also basal rotation. In nonresponders, the deterioration of LV twist was mainly due to worsening of the basal rotation underscoring the influence of the basal level on LV twist (25).
Relationship between LV twist and LV lead position.
Previous studies showed that HF patients treated with CRT showed the best hemodynamic improvement when the LV pacing lead was positioned in (postero)lateral veins (26). In the current study, 3 patients had the LV lead placed in an anterior vein, and none of them responded to CRT. The remaining 68 patients had the LV lead positioned in the (postero)lateral vein. In these patients, the optimal position of LV lead inside the target vein was explored. Patients with a midventricular or apical position had the largest systolic improvement, and showed a significant increase in LV twist, whereas patients with a basal LV lead position did not show improved systolic function and decreased in LV twist, confirming that the pacing site may influence torsional behavior of the LV (27). Similarly, a recent study by Helm et al. (28) reported that the optimal site of stimulation (although in a canine model of HF) was the LV free wall centered over the midapical part. This finding may be related to the fact that normal cardiac depolarization is directed from the apex toward the base (29), and an earlier activation of the LV basal region, altering the normal contraction pattern of the myofibers, may lead to a significant deterioration of LV twist. Another explanation for the findings may be related to the fact that the myocardial wall is thinner toward the apex (30,31); therefore, the epicardial LV lead in this position is closer to the Purkinje network. Consequently, pacing from this position may generate a cardiac pulse that spreads faster to the entire myocardium with a more physiological activation (32–34).
|
Conclusions
|
|---|
LV twist is reduced in HF patients and improves in patients who respond to CRT. Particularly, the change in LV twist immediately after CRT predicts LV reverse remodeling at 6-month follow-up.
|
Footnotes
|
|---|
Drs. Ajmone Marsan and Delgado are supported by a research grant from the European Society of Cardiology. Dr. Nucifora is supported by a research grant from the European Association of Percutaneous Cardiovascular Interventions. Dr. Schalij has received grants from Biotronik, Medtronic, and Boston Scientific. Dr. Bax has received grants from Medtronic, Boston Scientific, Biotronik, St. Jude Medical, Bristol-Myers Squibb Medical Imaging, Edwards Lifesciences, and GE Healthcare. Richard A. Grimm, DO, served as Guest Editor for this article.
|
References
|
|---|
1. Greenbaum RA, Ho SY, Gibson DG, Becker AE, Anderson RH. Left ventricular fibre architecture in man Br Heart J 1981;45:248-263.[Abstract/Free Full Text]2. Torrent-Guasp F, Kocica MJ, Corno AF, et al. Towards new understanding of the heart structure and function Eur J Cardiothorac Surg 2005;27:191-201.[Abstract/Free Full Text] 3. Buchalter MB, Weiss JL, Rogers WJ, et al. Noninvasive quantification of left ventricular rotational deformation in normal humans using magnetic resonance imaging myocardial tagging Circulation 1990;81:1236-1244.[Abstract/Free Full Text] 4. Kanzaki H, Nakatani S, Yamada N, Urayama S, Miyatake K, Kitakaze M. Impaired systolic torsion in dilated cardiomyopathy: reversal of apical rotation at mid-systole characterized with magnetic resonance tagging method Basic Res Cardiol 2006;101:465-470.[CrossRef][Web of Science][Medline] 5. Notomi Y, Martin-Miklovic MG, Oryszak SJ, et al. Enhanced ventricular untwisting during exercise: a mechanistic manifestation of elastic recoil described by Doppler tissue imaging Circulation 2006;113:2524-2533.[Abstract/Free Full Text] 6. Fuchs E, Muller MF, Oswald H, Thony H, Mohacsi P, Hess OM. Cardiac rotation and relaxation in patients with chronic heart failure Eur J Heart Fail 2004;6:715-722.[Abstract/Free Full Text] 7. Abraham WT, Fisher WG, Smith AL, et al. Cardiac resynchronization in chronic heart failure N Engl J Med 2002;346:1845-1853.[CrossRef][Web of Science][Medline] 8. Cleland JG, Daubert JC, Erdmann E, et al. The effect of cardiac resynchronization on morbidity and mortality in heart failure N Engl J Med 2005;352:1539-1549.[CrossRef][Web of Science][Medline] 9. Sade LE, Demir O, Atar I, Muderrisoglu H, Ozin B. Effect of mechanical dyssynchrony and cardiac resynchronization therapy on left ventricular rotational mechanics Am J Cardiol 2008;101:1163-1169.[CrossRef][Web of Science][Medline] 10. Zhang Q, Fung JW, Yip GW, et al. Improvement of left ventricular myocardial short-axis, but not long-axis function or torsion after cardiac resynchronisation therapy: an assessment by two-dimensional speckle tracking Heart 2008;94:1464-1471.[Abstract/Free Full Text] 11. Hunt SA. ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure) J Am Coll Cardiol 2005;46:e1-e82.[Free Full Text] 12. Rector TS, Kubo SH, Cohn JN. Validity of the Minnesota Living with Heart Failure questionnaire as a measure of therapeutic response to enalapril or placebo Am J Cardiol 1993;71:1106-1107.[CrossRef][Web of Science][Medline] 13. Lipkin DP, Scriven AJ, Crake T, Poole-Wilson PA. Six minute walking test for assessing exercise capacity in chronic heart failure Br Med J (Clin Res Ed) 1986;292:653-655.[CrossRef][Medline] 14. Lang RM, Bierig M, Devereux RB, et al. Recommendations for chamber quantification: a report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology J Am Soc Echocardiogr 2005;18:1440-1463.[CrossRef][Web of Science][Medline] 15. Chung ES, Leon AR, Tavazzi L, et al. Results of the Predictors of Response to CRT (PROSPECT) trial Circulation 2008;117:2608-2616.[Abstract/Free Full Text] 16. Schuijf JD, Kaandorp TA, Lamb HJ, et al. Quantification of myocardial infarct size and transmurality by contrast-enhanced magnetic resonance imaging in men Am J Cardiol 2004;94:284-288.[CrossRef][Web of Science][Medline] 17. Leitman M, Lysyansky P, Sidenko S, et al. Two-dimensional strain—a novel software for real-time quantitative echocardiographic assessment of myocardial function J Am Soc Echocardiogr 2004;17:1021-1029.[CrossRef][Web of Science][Medline] 18. Reisner SA, Lysyansky P, Agmon Y, Mutlak D, Lessick J, Friedman Z. Global longitudinal strain: a novel index of left ventricular systolic function J Am Soc Echocardiogr 2004;17:630-633.[CrossRef][Web of Science][Medline] 19. Suffoletto MS, Dohi K, Cannesson M, Saba S, Gorcsan III J. Novel speckle-tracking radial strain from routine black-and-white echocardiographic images to quantify dyssynchrony and predict response to cardiac resynchronization therapy Circulation 2006;113:960-968.[Abstract/Free Full Text] 20. Helle-Valle T, Crosby J, Edvardsen T, et al. New noninvasive method for assessment of left ventricular rotation: speckle tracking echocardiography Circulation 2005;112:3149-3156.[Abstract/Free Full Text] 21. Notomi Y, Lysyansky P, Setser RM, et al. Measurement of ventricular torsion by two-dimensional ultrasound speckle tracking imaging J Am Coll Cardiol 2005;45:2034-2041.[Abstract/Free Full Text] 22. Albertsen AE, Nielsen JC, Pedersen AK, Hansen PS, Jensen HK, Mortensen PT. Left ventricular lead performance in cardiac resynchronization therapy: impact of lead localization and complications Pacing Clin Electrophysiol 2005;28:483-488.[CrossRef][Medline] 23. Opdahl A, Helle-Valle T, Remme EW, et al. Apical rotation by speckle tracking echocardiography: a simplified bedside index of left ventricular twist J Am Soc Echocardiogr 2008;21:1121-1128.[CrossRef][Web of Science][Medline] 24. Delgado V, Ypenburg C, van Bommel RJ, et al. Assessment of left ventricular dyssynchrony by speckle tracking strain imaging comparison between longitudinal, circumferential, and radial strain in cardiac resynchronization therapy J Am Coll Cardiol 2008;51:1944-1952.[Abstract/Free Full Text] 25. Notomi Y, Srinath G, Shiota T, et al. Maturational and adaptive modulation of left ventricular torsional biomechanics: Doppler tissue imaging observation from infancy to adulthood Circulation 2006;113:2534-2541.[Abstract/Free Full Text] 26. Butter C, Auricchio A, Stellbrink C, et al. Effect of resynchronization therapy stimulation site on the systolic function of heart failure patients Circulation 2001;104:3026-3029.[Abstract/Free Full Text] 27. Notomi Y, Popovic ZB, Yamada H, et al. Ventricular untwisting: a temporal link between left ventricular relaxation and suction Am J Physiol Heart Circ Physiol 2008;294:H505-H513.[Abstract/Free Full Text] 28. Helm RH, Byrne M, Helm PA, et al. Three-dimensional mapping of optimal left ventricular pacing site for cardiac resynchronization Circulation 2007;115:953-961.[Abstract/Free Full Text] 29. Sengupta PP, Khandheria BK, Korinek J, et al. Apex-to-base dispersion in regional timing of left ventricular shortening and lengthening J Am Coll Cardiol 2006;47:163-172.[Abstract/Free Full Text] 30. Bogaert J, Rademakers FE. Regional nonuniformity of normal adult human left ventricle Am J Physiol Heart Circ Physiol 2001;280:H610-H620.[Abstract/Free Full Text] 31. Sengupta PP, Korinek J, Belohlavek M, et al. Left ventricular structure and function: basic science for cardiac imaging J Am Coll Cardiol 2006;48:1988-2001.[Abstract/Free Full Text] 32. 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;41:1218-1226.[Abstract/Free Full Text] 33. Vanagt WY, Prinzen FW, Delhaas T. Reversal of pacing-induced heart failure by left ventricular apical pacing N Engl J Med 2007;357:2637-2638.[CrossRef][Web of Science][Medline] 34. Vanagt WY, Prinzen FW, Delhaas T. Physiology of cardiac pacing in children: the importance of the ventricular pacing site Pacing Clin Electrophysiol 2008;31(Suppl 1):S24-S27.[CrossRef][Medline]
Related Article
-
Inside This Issue
J. Am. Coll. Cardiol. 2009 54: A26.
[Full Text]
[PDF]
This article has been cited by other articles:
|
|
|
|
 
D. Auger, G. B. Bleeker, M. Bertini, S. H. Ewe, R. J. van Bommel, T. G. Witkowski, A. C. T. Ng, L. van Erven, M. J. Schalij, J. J. Bax, et al.
Effect of cardiac resynchronization therapy in patients without left intraventricular dyssynchrony
Eur. Heart J.,
January 24, 2012;
(2012)
ehr468v1.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Iwasaki, K. Masuda, T. Asanuma, and S. Nakatani
Effects of mechanical limitation of apical rotation on left ventricular relaxation and end-diastolic pressure
Am J Physiol Heart Circ Physiol,
October 1, 2011;
301(4):
H1456 - H1460.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Adabag, H. Roukoz, I. S. Anand, and A. J. Moss
Cardiac Resynchronization Therapy in Patients With Minimal Heart Failure: A Systematic Review and Meta-Analysis
J. Am. Coll. Cardiol.,
August 23, 2011;
58(9):
935 - 941.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M.-K. Seo, S.-A. Chang, H.-K. Kim, D.-H. Shin, E.-K. Choi, Y.-J. Kim, S. Oh, G.-Y. Cho, D.-W. Sohn, B.-H. Oh, et al.
Synchronicity of LV Contraction as a Determinant of LV Twist Mechanics: Serial Speckle-Tracking Analyses in WPW Syndrome Before and After Radiofrequency Catheter Ablation
J. Am. Coll. Cardiol. Img.,
April 1, 2011;
4(4):
338 - 347.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. P.-W. Lee, Q. Zhang, G. Yip, F. Fang, Y.-J. Liang, J.-M. Xie, Y.-Y. Lam, and C.-M. Yu
LV Mechanical Dyssynchrony in Heart Failure With Preserved Ejection Fraction Complicating Acute Coronary Syndrome
J. Am. Coll. Cardiol. Img.,
April 1, 2011;
4(4):
348 - 357.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
V. Mor-Avi, R. M. Lang, L. P. Badano, M. Belohlavek, N. M. Cardim, G. Derumeaux, M. Galderisi, T. Marwick, S. F. Nagueh, P. P. Sengupta, et al.
Current and Evolving Echocardiographic Techniques for the Quantitative Evaluation of Cardiac Mechanics: ASE/EAE Consensus Statement on Methodology and Indications Endorsed by the Japanese Society of Echocardiography
Eur Heart J Cardiovasc Imaging,
March 1, 2011;
12(3):
167 - 205.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. K. Ho and A. Mahajan
Review Article: Cardiac Resynchronization Therapy for Treatment of Heart Failure
Anesth. Analg.,
December 1, 2010;
111(6):
1353 - 1361.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Shanks, M. Bertini, V. Delgado, A. C. T. Ng, G. Nucifora, R. J. van Bommel, C. J. W. Borleffs, E. R. Holman, N. R. L. van de Veire, M. J. Schalij, et al.
Effect of Biventricular Pacing on Diastolic Dyssynchrony
J. Am. Coll. Cardiol.,
November 2, 2010;
56(19):
1567 - 1575.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. Ashikaga, C. Leclercq, J. Wang, D. A. Kass, and E. R. McVeigh
Hemodynamic Improvement in Cardiac Resynchronization Does Not Require Improvement in Left Ventricular Rotation Mechanics: Three-Dimensional Tagged MRI Analysis
Circ Cardiovasc Imaging,
July 1, 2010;
3(4):
456 - 463.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Bertini, P. P. Sengupta, G. Nucifora, V. Delgado, A. C.T. Ng, N. A. Marsan, M. Shanks, R. R.J. van Bommel, M. J. Schalij, J. Narula, et al.
Role of Left Ventricular Twist Mechanics in the Assessment of Cardiac Dyssynchrony in Heart Failure
J. Am. Coll. Cardiol. Img.,
December 1, 2009;
2(12):
1425 - 1435.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
Top
Abstract
Methods