Methods

A total of 292 patients with heart failure treated with CRT and who completed a 6-month follow-up period were selected from an ongoing registry. Optimally treated patients with heart failure (New York Heart Association functional class III or IV) with an LV ejection fraction (LVEF) ≤35%, who showed a wide QRS complex (>120 ms), were selected for CRT. Patients with recent myocardial infarction (≤3 months), decompensated heart failure requiring continuous intravenous therapy, or patients in atrial fibrillation and high beat-to-beat variability that would preclude 2D speckle-tracking radial strain analysis were excluded. Heart failure etiology was considered ischemic if previous myocardial infarction or revascularization or significant angiographic coronary disease was documented. According to the institutional protocol, clinical evaluation was performed before CRT implantation and included New York Heart Association functional class, exercise capacity using the 6-minute walk test, and quality of life assessment using the Minnesota Living with Heart Failure Questionnaire. In addition, all patients underwent 2D echocardiography at baseline to evaluate LV volumes and LVEF. In addition, LV dyssynchrony, the sequence of activation, and site of latest activation were evaluated with 2D radial strain speckle-tracking. At 6-month follow-up the clinical status was reevaluated and echocardiography was repeated to evaluate LV volumes, LVEF, LV dyssynchrony, and sequence of LV mechanical activation. Response to CRT was defined as a ≥15% decrease in LV end-systolic volume 6 months after CRT implantation. The changes in sequence of LV mechanical activation after CRT were related to the echocardiographic response. All clinical and echocardiographic data were prospectively entered into the departmental Cardiology Information System (EPD-Vision; Leiden University Medical Center, Leiden, the Netherlands) and retrospectively analyzed.

All echocardiographic data were obtained at rest in the left lateral decubitus position using a commercially available system (Vingmed System 7 and E9; GE-Vingmed Ultrasound AS, Horten, Norway) with a 3.5-MHz transducer. Apical 2- and 4-chamber views were used to calculate LV end-diastolic and end-systolic volumes and to derive LVEF according to Simpson’s method. LV volumes and ejection fraction were assessed before and 6 months after CRT. In addition, LV dyssynchrony, sequence of LV mechanical activation, and identification of the site of latest mechanical activation were assessed with 2D radial strain speckle-tracking. These parameters were evaluated using commercially available software (EchoPAC 111.0.00, GE-Vingmed, Horten, Norway) as previously described. The mid LV short-axis view was divided into 6 segments and the time-strain tracings are provided for each segment. The time difference between the peak radial strain of the anteroseptal and the posterior segments is calculated to define LV dyssynchrony ( Figure 1 ). An established cut-off value of ≥130 ms indicates significant LV dyssynchrony, as previously described. Furthermore, the time-to-peak radial strain of the 6 LV segments was recorded creating the sequence of mechanical activation of the LV. The latest activated segment was identified. A distinct sequence of activation was defined as <94 ms absolute timing of mechanical activation difference between a preactivated posterior wall and a delayed anteroseptal wall 6 months after CRT.

Two-dimensional radial strain speckle-tracking for the assessment of LV sequence of activation. (A) The evaluation of LV dyssynchrony, sequence of mechanical activation, and site of latest activation by 2D radial strain speckle-tracking in a patient with heart failure before CRT is shown. LV dyssynchrony, defined as the absolute time difference between peak systolic radial strain in the posterior wall (pink curve) and the anteroseptum (yellow curve) , was assessed. This patient exhibited significant LV dyssynchrony (183 ms). Furthermore, there was a delayed mechanical activation of the posterior wall compared with the anteroseptum. The site of latest activation was the posterior wall (pink arrow) . (B) The evaluation of LV dyssynchrony, site of latest activation, and sequence of activation with 2D radial strain speckle-tracking were repeated 6 months after CRT. Of interest, a decrease in the value of LV dyssynchrony was noted (52 ms), by earlier mechanical activation of the lateral wall (pink curve and arrow) that is synchronized to the timing of mechanical activation of the anteroseptum (yellow curve) . t = time.

All CRT devices were implanted in the pectoral region and during implantation, pacing, sensing, and defibrillation thresholds were tested. CRT leads were implanted by way of the subclavian vein. First, a coronary sinus venogram was obtained. Thereafter, with the help of an 8-Fr guiding catheter, the LV lead was positioned (Easytrak, Guidant Corporation, St. Paul, Minnesota; Attain, Medtronic Inc., Minneapolis, Minnesota; or Corox, Biotronik, Berlin, Germany) by way of the coronary sinus, preferably in the posterolateral vein at the midventricular level. The right atrial and ventricular leads were positioned conventionally. A defibrillator was combined to CRT in all patients. Finally, all leads were connected to a dual-chamber biventricular CRT device (Contak Renewal, Guidant Corporation; Consulta, InSync III, or InSync Sentry, Medtronic Inc; or Lumax, Biotronik). The cardiologist performing the procedure was unaware of the site of latest mechanical activation identified on 2D speckle-tracking echocardiography.

According to protocol, all patients underwent a conventional chest x-ray before discharge to confirm the position of the LV lead. Using the lateral views, LV lead position was recorded as anterior, lateral, posterior, or inferior. Using the frontal views, the LV lead position was scored as basal, mid, or apical. Concordant LV lead position was defined by the present of an LV lead targeting the site of latest activation identified with speckle-tracking echocardiography.

Continuous variables are presented as mean ± SD, unless otherwise specified, and were compared between responders and nonresponders to CRT using the Student t test for unpaired data. In addition, the comparison between the timings of mechanical activation at baseline and at 6-month follow-up was performed using the Student t test for paired data. Categorical variables are presented as number and percentage and were compared with chi-square test. A multivariate logistic regression model was created introducing the significant univariate variables as covariates with the stepwise enter method to identify independent predictors of a distinct sequence of activation (<94 ms absolute timing of mechanical activation difference between a preactivated posterior wall and a delayed anteroseptal wall 6 months after CRT). For each variable, the odds ratio and the 95% confidence intervals were calculated. A p value <0.05 was considered statistically significant. Data were analyzed with SPSS 21.0 (IBM, Chicago, Illinois).

Results

The baseline characteristics of the population are listed in Table 1 . In most patients the LV lead was implanted at the midventricular level (91%). Concordant LV lead position was observed in 164 patients (60%). According to the prespecified definition of response (≥15% decrease in LV end-systolic volume at 6-month follow-up), 61% of patients were responders to CRT (n = 177) and 39% were nonresponders (n = 115). Comparisons between baseline characteristics in responders and nonresponders to CRT are outlined in Table 2 .

The sequence of activation in responders and nonresponders to CRT at baseline and after 6 months of CRT is illustrated in Figure 2 . Of interest, responders and nonresponders showed a comparable sequence of mechanical activation at baseline. The mechanical activation of the posterior wall was delayed compared with the anteroseptum in both responders and in nonresponders. However, different sequences of mechanical activation were observed after 6 months of CRT in responders and in nonresponders. In particular, responders experienced LV resynchronization at 6-month follow-up (LV dyssynchrony from 200 ± 127 to 85 ± 86 ms; p <0.001) by earlier activation of the posterior segment (438 ± 141 to 394 ± 132 ms; p = 0.001) and delayed activation of the anteroseptal segment (295 ± 155 to 407 ± 138 ms; p <0.001). In contrast, nonresponders showed worsening of LV dyssynchrony (from 106 ± 86 ms before CRT to 155 ± 112 ms 6 months after CRT; p = 0.001) with an earlier mechanical activation of posterior wall (391 ± 139 to 355 ± 136 ms; p = 0.039) that did not match the delayed anteroseptal wall (360 ± 148 to 415 ± 122 ms; p = 0.001).

LV sequence of activation at baseline and at 6-month follow-up in responders and in nonresponders to CRT. Upper panel , the LV sequence of mechanical activation in responders to CRT is shown. Of interest, at baseline, marked LV dyssynchrony was present. Moreover, responders show a delayed mechanical activation of the posterior segment compared with the anteroseptum timing of mechanical activation. At 6-month follow-up, responders to CRT show resynchronization of the sequence of mechanical activation within the LV. In particular, the mechanical activations of anteroseptum and the inferoseptum occur significantly later compared with baseline, whereas the activation of the posterior and lateral segments occurs significantly earlier than at baseline. Lower panel , the LV sequence of mechanical activation in nonresponders to CRT is shown. Of interest, at baseline, nonresponders exhibit a lesser degree of LV dyssynchrony than responders. The posterior wall’s mechanical activation is delayed compared with the mechanical activation of the septum. However, at 6-month follow-up, nonresponders to CRT show increased LV dyssynchrony and absence of resynchronization by reversion of the sequence of activation within the LV. Precisely, although the activations of anteroseptum and the inferoseptum occur significantly later compared with baseline, the earlier activation of the posterior segment does not equate the later activation of the anteroseptum, creating an unbalanced sequence of mechanical activation within the LV. Mean values of timing of systolic mechanical activation ± standard error of the mean are displayed. A = anterior; AS = anteroseptum; I = inferior; L = lateral; P = posterior; S = inferoseptum. *p <0.05 between baseline and 6-month follow-up.

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