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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
Effect of biventricular pacing on diastolic dyssynchrony
Miriam Shanks1, Matteo Bertini, Victoria Delgado
1Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
Insights
Cardiac resynchronization therapy (CRT) improves diastolic dyssynchrony in heart failure patients who respond to treatment. Non-responders showed less baseline diastolic dyssynchrony, and it did not improve after CRT.
Area of Science:
- Cardiology
- Heart Failure Research
- Medical Imaging
Background:
- Diastolic dyssynchrony in heart failure (HF) is not well understood.
- The impact of cardiac resynchronization therapy (CRT) on diastolic dyssynchrony requires further investigation.
Purpose of the Study:
- To investigate the changes in diastolic dyssynchrony in heart failure patients undergoing CRT.
- To compare diastolic dyssynchrony between CRT responders and non-responders.
Main Methods:
- 266 heart failure patients were assessed using color-coded tissue Doppler imaging at baseline, 48 hours, and 6 months post-CRT.
- Diastolic dyssynchrony was defined as the maximal time delay in early diastolic velocities in basal left ventricular segments.
- CRT responders were identified by a ≥15% decrease in left ventricular end-systolic volume at 6 months.
Main Results:
- At baseline, diastolic dyssynchrony (51.9%) was more prevalent than systolic dyssynchrony (46.2%).
- CRT responders exhibited significantly longer baseline systolic and diastolic delays compared to non-responders.
- Both systolic and diastolic delays significantly improved in responders at 48 hours and 6 months post-CRT, but not in non-responders.
Conclusions:
- Diastolic dyssynchrony is common in heart failure patients and is more pronounced in CRT responders.
- CRT effectively improves diastolic dyssynchrony, but only in patients who respond to the therapy.
- Understanding the pathophysiology of diastolic dyssynchrony and its response to CRT can inform personalized patient treatments.
Objectives:
This study sought to examine the changes in diastolic dyssynchrony with cardiac resynchronization therapy (CRT).
Background:
Little is known about the effect of CRT on diastolic dyssynchrony.
Methods:
Consecutive heart failure patients (n = 266, age 65.7 ± 10.0 years) underwent color-coded tissue Doppler imaging at baseline, 48 h, and 6 months after CRT. Systolic and diastolic dyssynchrony were defined as maximal time delay in peak systolic and early diastolic velocities, respectively, in 4 basal LV segments. CRT responders were defined as those with ≥15% decrease in LV end-systolic volume at 6 months.
Results:
Baseline LVEF was 25.2 ± 8.1%; 63.5% patients were CRT responders. Baseline incidence of systolic and diastolic dyssynchrony, and a combination of both was 46.2%, 51.9%, and 28.6%, respectively. Compared to nonresponders, responders had longer baseline systolic (79.2 ± 43.4 ms vs. 45.4 ± 30.4 ms; p < 0.001) and diastolic (78.5 ± 52.0 ms vs. 50.1 ± 38.2 ms; p < 0.001) delays. In follow-up, systolic delays (45.4 ± 31.6 ms at 48 h; 38.9 ± 26.2 ms at 6 months; p < 0.001) and diastolic delays (49.4 ± 36.3 ms at 48 h; 37.7 ± 26.0 ms at 6 months; p < 0.001) improved only in responders.
Conclusions:
At baseline: 1) diastolic dyssynchrony was more common than systolic dyssynchrony in HF patients; 2) nonresponders had less baseline diastolic dyssynchrony compared to responders. After CRT: 1) diastolic dyssynchrony improved only in responders. Further insight into the pathophysiology of diastolic dyssynchrony and its changes with CRT may provide incremental information on patient-specific treatments.
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