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Updated: Jun 25, 2026

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing
Published on: December 11, 2017
Patients with non-ischaemic dilated cardiomyopathy and hyper-responders to cardiac resynchronization therapy:
Philippe Castellant1, Marjaneh Fatemi, Erwann Orhan
1Département of Cardiology, Hôpital de la Cavale Blanche, Brest University Hospital, Bd Tanguy Prigent, 29609 Brest Cedex, France.
Insights
Cardiac resynchronization therapy (CRT) can significantly improve left ventricular (LV) function in some patients with non-ischaemic dilated cardiomyopathy (NIDCM) and left bundle branch block (LBBB). Approximately 21.5% of NIDCM patients achieve
Area of Science:
- Cardiology
- Electrophysiology
- Heart Failure Management
Background:
- Cardiac resynchronization therapy (CRT) can reverse left ventricular (LV) dysfunction in select patients with non-ischaemic dilated cardiomyopathy (NIDCM), left bundle branch block (LBBB), and severe heart failure.
- Patients achieving substantial functional recovery are termed 'hyper-responders' and have been exclusively identified in NIDCM cohorts.
Purpose of the Study:
- To determine the proportion of 'hyper-responders' among patients with NIDCM receiving CRT.
- To identify potential baseline clinical profiles that predict CRT 'hyper-response' in NIDCM patients.
Main Methods:
- Prospective follow-up of consecutive NIDCM patients (LV ejection fraction <35%, LV end-diastolic diameter >60 mm, LBBB, NYHA class III-IV) who received CRT.
- 'Hyper-responders' were defined as achieving NYHA class I-II and LVEF ≥50% after at least 6 months of CRT.
- Baseline clinical parameters were compared between 'hyper-responders' and non-hyper-responders.
Main Results:
- Out of 51 NIDCM patients, 11 (21.5%) were identified as 'hyper-responders' post-CRT, showing a significant increase in LVEF (26% to 59%, P < 0.01).
- The remaining 40 patients (78.5%) exhibited minimal functional improvement with a modest LVEF increase (21% to 26%, P = 0.03).
- Baseline parameters in 'hyper-responders' were less severely deteriorated compared to non-responders, although no single discriminating factor was identified.
Conclusions:
- A significant subset of NIDCM patients with LBBB experience complete functional recovery and normalized LV function after CRT.
- The findings suggest LBBB might be a causative factor for DCM in these 'hyper-responder' patients.
- No unique baseline predictor distinguished 'hyper-responders' from other patients, highlighting the need for further research into predictive markers.
Aims:
In some patients with non-ischaemic dilated cardiomyopathy (NIDCM), left bundle branch block (LBBB), and severe cardiac failure, cardiac resynchronization therapy (CRT) has been shown to reverse almost completely left ventricular (LV) function. These patients thus eligible to be qualified 'hyper-responders' are exclusively recruited in patients with NIDCM. Evaluate proportion of 'hyper-responders' among patients with NIDCM and try to determine their profile before implantation of CRT.
Methods And Results:
Consecutive patients with DCM [LV ejection fraction (LVEF) <35%, LV end-diastolic diameter >60 mm], sinus rhythm, LBBB, and New York Heart Association (NYHA) class III and IV implanted with a CRT were prospectively followed. Patients were considered 'hyper-responders' if they fulfilled after a minimum period of 6 months the following criteria: functional recovery (NYHA class I or II) and LVEF >or=50%. Among the 51 NIDCM patients, 11 (21.5%) were 'hyper-responders' following CRT (LVEF increased from 26 +/- 9 to 59 +/- 6%, P < 0.01). In the 40 (78.5%) remaining patients, there was no or minimal functional improvement and only a modest increase in LVEF from 21 +/- 9 to 26 +/- 12% (P = 0.03). Comparison between 'hyper-responders' and remaining patients showed that baseline parameters of 'hyper-responders' were less severely deteriorated.
Conclusion:
In a significant subset of patients with CRT for NIDCM, a 'complete' functional recovery associated with normalization of LV function was observed. This observation suggests that LBBB could be the causative factor of DCM in this subgroup of patients. There was not a unique discriminating factor at baseline between 'hyper-responders' and remaining patients.
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