Author + information
- Vincent Galand, MD,
- Brian Ghoshhajra, MD,
- Jackie Szymonifka, MA,
- Christophe Leclercq, MD, PhD,
- Quynh A. Truong, MD, MPH and
- Jagmeet P. Singh, MD, DPhil∗ ()
- ↵∗Cardiology Division, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, Boston, Massachusetts 02114
It has been well established that responders to cardiac resynchronization therapy (CRT) experience left ventricular (LV) reverse remodeling. However, data are scarce regarding the impact of CRT on LV wall thickness (WT). Computed tomography (CT) is an ideal modality that provides pertinent information to guide the CRT implantation procedure. Nevertheless, there is a paucity of data regarding the use of CT to assess the impact of CRT on LV wall remodeling. In this study, we evaluated the evolution of LV wall thickness (WT) between baseline and 6 months in a cohort of CRT recipients.
Fifty-four patients were prospectively enrolled in the DIRECT (Dual-Source Computed Tomography to Improve Prediction of Response to Cardiac Resynchronization Therapy) trial for CRT implantation (1). Each patient underwent CT before the CRT procedure. At the 6-month follow-up, echocardiography was performed to assess the response to CRT, and some patients underwent repeat CT. In this case series, we enrolled only those who underwent CT at baseline and 6 months.
Baseline and 6-month CT images were analyzed and compared using the ADAS-VT software (Galgo Medical, Barcelona, Spain) by an experienced observer who was blinded to the data. CT images were integrated in the software as previously described (2). A 3-dimensional visualization of the LV was created, and diastolic WT was defined using a color threshold (normal LVWT was defined as an end-diastolic WT >6 mm; WT <6 mm suggested reduced LVWT ). The extent of the total WT <6 mm burden was quantified as a proportion of total LV area. In addition, the LV was automatically segmented into 17 segments, and each segment was considered to have reduced WT in cases of WT of <6 mm area.
Positive response to CRT was determined using echocardiography at 6 months. Three parameters were used: 1) reduction in LV end-systolic volume by ≥15%; 2) reduction in LV end-diastolic volume by ≥10%; and 3) improvement in LV ejection fraction by ≥10%. Response to CRT was defined as greater than or equal to two-thirds of the positive response criteria, and nonresponse to CRT was fewer than or equal to one-third of the positive response criteria. LVWT change was compared between baseline and 6 months among patients who responded.
Among the 54 patients, 10 (18.5%) who underwent baseline and 6-month CT were analyzed. CT analysis at baseline showed a total LV area of 172.2 ± 50.1 cm2 per patient with 35.1 ± 24.6 cm2 of area with WT <6 mm (i.e., 17.6%; range 11.1% to 21.2% of the total LV area). In addition, each patient had a median of 3.0 (range 2.0 to 4.5) LV segments with WT <6 mm. At 6 months, 8 and 2 patients were classified as responders and nonresponders, respectively. Response to CRT was associated with a significant reduction in total LV area (183.5 ± 49.9 cm2 vs. 125.7 ± 44.4 cm2) and total LV area with WT <6 mm (35.2 ± 27.8 cm2 vs. 8.4 ± 9.3 cm2) between baseline and 6 months, respectively. Although for both reductions, the proportion of LVWT <6 mm area also decreased from 17.6% (range 11.1% to 21.2) at baseline to 3.6% (range 2.1% to 7.5%) at 6 months (average decrease of 11.6 ± 8.3% per patient). In other words, responders had 96.4% (range 92.5% to 97.9%) of normal LVWT at 6 months. In addition, responders had fewer LVWT segments of <6 mm at 6 months compared with baseline (1.0 [range 0.0 to 1.5] vs. 3.0 [range 2.0 to 4.5], respectively; p = 0.021). Basal and/or midsegments were sites of higher WT normalization compared with the apex (Table 1). Figure 1 illustrates the WT remodeling in a CRT responder.
This work is the first prospective CT-guided study that evaluated the impact of CRT on WT change in a responder. The primary finding was that response to CRT was associated with WT normalization (especially in basal and/or midsegments). The mechanism underlying this association remains elusive. Previous work showed that the correction of dyssynchrony led to regression in WT inhomogeneity (3). In addition, improvements in molecular function and calcium regulation, which lead to enhanced LV contraction, was seen in CRT responders. Notably, the apical WT remained unchanged after 6 months. This observation was supported by recent work that demonstrated that the apical region was thinner at baseline and even after resynchronization (3).
The limited sample size made our pilot study hypothesis-generating, which will require validation in larger studies. In addition, only 2 nonresponders had CT at 6 months and that limited our ability to compare change in WT between responders and nonresponders. Further CT-guided studies are needed to investigate the impact of CRT on WT normalization.
In summary, response to CRT is associated with WT normalization, as assessed by CT. This remodeling was particularly notable in the basal and/or midsegments.
Please note: This study was supported by the French Federation of Cardiology and Rennes University Hospital. The study was supported by National Institutes of Health (NIH)/National Heart, Lung, and Blood Institute (grant K23HL098370) and Abbott (formerly St. Jude Medical). Dr. Truong also received support from the NIH (grant L30HL093896). Dr. Ghoshhajra has received support from Siemens Healthcare; and owns stock in Apple. Dr. Leclercq has received honoraria from Abbott, Medtronic, Boston Scientific, Biotronik, and Livanova. Dr. Truong has received grant support from Ziosoft. Dr. Singh has received grant support from St. Jude Medical and Boston Scientific; and has served as a consultant to LivaNova, St. Jude Medical, Medtronic, Boston Scientific, Impulse Dynamics, Biotronik, and EBR. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
All authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Clinical Electrophysiology author instructions page.
- Truong Q.A.,
- Szymonifka J.,
- Picard M.H.,
- et al.
- Ustunkaya T.,
- Desjardins B.,
- Liu B.,
- et al.
- Cvijic M.,
- Duchenne J.,
- Ünlü S.,
- et al.