Abstract 14838: Regional Contributions to Impaired Myocardial Mechanical Function in Heart Failure With Preserved Ejection Fraction
Background: The pathophysiology underlying the transition from hypertensive heart disease (HHD) to heart failure with preserved ejection fraction (HFpEF) remains unclear. Regional differences in impaired myocardial function may contribute to the more pronounced overall mechanical dysfunction seen in HFpEF compared to HHD.
Methods: We assessed regional myocardial deformation in 129 HFpEF patients, 158 hypertensive patients with HHD and no heart failure, and 40 healthy controls. Peak systolic strain was assessed in the apical 4 and 2 chamber views and the average was calculated for the 4 apical (ALS), 4 mid ventricular (MLS) and 4 basal (BLS) regions.
Results: All 3 groups had preserved left ventricular ejection fraction (LVEF ≥50%). Whereas BLS and MLS were more impaired in HHD than in controls, ALS was significantly more impaired in HFPEF than HHD (Figure). In area under the receiver operating curve (AUC) analyses, ALS was the best diagnostic marker for differentiating HFpEF from HHD (AUC: ALS=0.67; MLS=0.59; BLS=0.60). After adjusting for the main characteristics that differed between HFpEF and HHD (age, e’, systolic blood pressure, NT-pro BNP, LV end-diastolic volume, and LVEF), ALS remained independently associated with HFpEF vs. HHD status (OR 1.18 [1.02-1.37], P=0.030 per 1% decrease). By contrast, global longitudinal strain was not significantly associated with HFpEF vs. HHD status in multivariable analyses (P=0.09).
Conclusion: We observed that whereas basal and mid-level longitudinal strain is more impaired in HHD than in controls, apical longitudinal strain is substantially more impaired in HFPEF than HHD. These findings suggest that preservation of apical mechanical function may play an important role in the transition from HHD to HFPEF.
- Regional Myocardial Mechanical Function
- Heart Failure with Preserved Ejection Fraction
- Strain imaging
Author Disclosures: T. Biering-Sørensen: None. M. Cikes: None. E. Kraigher-Krainer: None. A.M. Shah: Other Research Support; Modest; research support from Novartis, Gilead, Actelion. S.D. Solomon: None. S. Cheng: None.
- © 2015 by American Heart Association, Inc.