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Published on: July 20, 2022
Left Atrial Strain in Heart Failure With Reduced Ejection Fraction (HFrEF) and Angiotensin Receptor-Neprilysin
Zaran Butt1, Jonathan Shpigelman2, Robert Trueick1
1Department of Cardiology, Connolly Hospital Blanchardstown, Dublin, Ireland.
Insights
Left atrial strain (LAS) predicts treatment response in heart failure with reduced ejection fraction (HFrEF) patients receiving sacubitril-valsartan (SV). Specifically, left atrial reservoir strain (LASr) independently predicts changes in left ventricular end-systolic volume (LVESV).
Area of Science:
- Cardiology
- Cardiovascular Imaging
- Pharmacology
Background:
- Sacubitril-valsartan (SV) improves outcomes in heart failure with reduced ejection fraction (HFrEF) by promoting reverse remodeling.
- Predictors of SV response and the extent of reverse remodeling remain incompletely understood.
- Left atrial strain (LAS) may offer insights into cardiac remodeling processes.
Purpose of the Study:
- To investigate the association between baseline left atrial strain (LAS) parameters and subsequent changes in left ventricular function and volumes in HFrEF patients treated with SV.
- To determine if LAS can predict the degree of reverse remodeling induced by SV therapy.
Main Methods:
- Retrospective analysis of 127 HFrEF patients treated with SV from a heart failure registry.
- Assessment of correlations between baseline LAS phases (reservoir [LASr], conduit [LAScd], contractile [LASct]) and changes in left ventricular ejection fraction (LVEF) and end-systolic volume (LVESV).
- Multivariable linear regression models were employed to identify independent predictors of therapy-associated changes in LVEF and LVESV.
Main Results:
- SV therapy significantly improved LVEF and reduced LVESV.
- Baseline LASr and LAScd correlated with baseline LVEF and LVESV.
- Baseline LASr and LAScd were associated with subsequent improvements in LVEF and LVESV, with LASr showing independent association with LVESV changes after adjustment.
Conclusions:
- Left atrial strain, particularly LASr, is a significant predictor of reverse remodeling in HFrEF patients treated with SV.
- LASr independently tracks and predicts therapy-associated changes in left ventricular volumes, specifically LVESV.
- LAS assessment may enhance the prediction of treatment response to SV in HFrEF.
Background:
Sacubitril-valsartan (SV), an angiotensin receptor-neprilysin inhibitor, improves clinical outcomes in HFrEF patients through reverse remodeling; however, predictors of response remain uncertain. Left atrial strain (LAS) assessment may refine the definition and prediction of remodeling in this cohort.
Methods:
In our hospital's heart failure registry, HFrEF patients prescribed SV were retrospectively identified. Correlations were assessed between LAS phases (reservoir [LASr], conduit [LAScd], and contractile [LASct]) and both left ventricular ejection fraction (LVEF) and left ventricular end-systolic volume (LVESV), using baseline values and therapy-associated changes (Δ). Multivariable linear regression was used to investigate associations between baseline LAS phases and subsequent ΔLVEF and ΔLVESV.
Results:
Among 127 patients, SV therapy was associated with improvements in LVEF (+5.8 ± 12.8%; p < 0.001) and LVESV (-23.5 ± 53.5 mL; p < 0.001), as well as in left atrial and ventricular volumes. At baseline, LASr and LAScd correlated with both LVEF and LVESV, while only ΔLASr correlated with both ΔLVEF and ΔLVESV. On multivariable regression, baseline LASr, and LAScd were both associated with subsequent ΔLVEF (β per 5% increase: -1.69 [95% CI: -3.03 to -0.36] and -2.12 [95% CI: -4.12 to -0.13], respectively) and ΔLVESV (β per 5% increase: 11.01 [95% CI: 5.28 to 16.74], and 14.95 [95% CI: 6.39 to 23.51], respectively). When additionally adjusted for the baseline of the corresponding outcome measure, only LASr remained independently associated with ΔLVESV (β per 5% increase: 4.77 [95% CI: 0.01 to 9.53], p = 0.049).
Conclusion:
In HFrEF patients, LASr tracks SV-associated reverse remodeling and is independently associated with subsequent therapy-associated changes in LVESV.
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