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Published on: December 11, 2017
Relation between heart rate, heart rhythm, and reverse left ventricular remodelling in response to carvedilol in
R H Arnold1, E Kotlyar, C Hayward
1Heart and Lung Transplant Unit, St Vincent's Hospital, and Victor Chang Cardiac Research Institute, Sydney, NSW, Australia.
Insights
Carvedilol improves heart function in heart failure patients regardless of their baseline heart rate or rhythm. The drug
Area of Science:
- Cardiology
- Pharmacology
- Heart Failure Management
Background:
- Chronic systolic heart failure impacts left ventricular dimensions and function.
- Carvedilol is a beta-blocker used to manage heart failure.
- Reverse left ventricular remodeling is a key indicator of treatment efficacy.
Purpose of the Study:
- To investigate if carvedilol-induced reverse left ventricular remodeling depends on baseline heart rate (BHR), heart rhythm, or heart rate reduction (HRR).
Main Methods:
- Retrospective analysis of 257 heart failure patients receiving carvedilol.
- Serial echocardiograms assessed changes in left ventricular end-diastolic dimension (LVEDD), end-systolic dimension (LVESD), and fractional shortening (LVFS).
- Statistical analysis explored relationships between BHR, HRR, heart rhythm, and remodeling outcomes.
Main Results:
- Carvedilol significantly improved LVEDD, LVESD, and LVFS (p < 0.0001).
- No significant correlation was found between BHR or HRR and the degree of reverse remodeling.
- No differences in remodeling were observed between patients with different baseline heart rhythms (sinus vs. atrial fibrillation).
Conclusions:
- Carvedilol's benefits for reverse left ventricular remodeling and symptom improvement are independent of baseline heart rate, heart rhythm, and heart rate reduction.
- These findings support the use of carvedilol across a spectrum of heart failure patients.
Objective:
To determine whether the process of reverse left ventricular remodelling in response to carvedilol is dependent on baseline heart rate (BHR), heart rhythm, or heart rate reduction (HRR) in response to carvedilol.
Design:
Retrospective analysis of serial echocardiograms in 257 patients with chronic systolic heart failure at baseline and at 12-18 months after starting carvedilol. Reverse left ventricular remodelling was determined by changes in left ventricular end diastolic dimension (LVEDD), end systolic dimension (LVESD), and fractional shortening (LVFS).
Setting:
Heart failure clinic within a university teaching hospital.
Main Outcome Measures:
Changes in LVEDD, LVESD, and LVFS.
Results:
LVEDD and LVESD decreased by 2.6 (0.4) mm and 4.9 (0.5) mm, respectively (mean (SEM)), and LVFS increased by 4.3 (0.5)% (all p < 0.0001 v baseline). Simple regression revealed no significant relation between BHR or HRR and the changes in LVEDD, LVESD, or LVFS. Stratification of patients into high and low BHR groups (above and below the mean) or according to the baseline heart rhythm (sinus rhythm v atrial fibrillation) showed no differences between groups in the extent of reverse left ventricular remodelling. Improvements in left ventricular function and dimensions were associated with significant improvements in New York Heart Association functional class.
Conclusions:
The benefits of carvedilol in terms of reverse left ventricular remodelling and symptomatic improvement in patients with chronic heart failure are independent of BHR, heart rhythm, and the HRR that occurs in response to carvedilol.
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