Abstract 15776: Longitudinal to Circumferential Diastolic Dyssynchrony in Heart Failure With Preserved Ejection Fraction and its Relationship to Myocardial Fibrosis
Background: Diastolic dysfunction is a prominent feature of Heart Failure with Preserved Ejection Fraction (HFpEF). The basis of abnormal diastolic function in HFpEF is incompletely understood. We hypothesized that dyssynchronous relaxation of longitudinal (Lx) and circumferential (Cx) fibers is present in HFpEF.
Methods: We studied 60 subjects with HFpEF, 81 subjects with heart failure with reduced ejection fraction and 406 control subjects without HF. Systolic Lx and Cx strain were measured with SSFP MRI, using tissue tracking. Extracellular volume fraction (ECV) was measured with myocardial T1 mapping before and after gadolinium administration.
Results: Despite being associated with a shorter ejection duration, HFrEF was associated with prolongation of both longitudinal and circumferential contraction. In contrast, among subjects with HFpEF, ejection duration and time to peak circumferential contraction was similar to that of controls. However, a selective prolongation of longitudinal contraction was seen. Thus, the difference in the timing of peak longitudinal vs. circumferential strain (delta-Lx-Cx-time) was increased in HFpEF, but not in HFrEF. In a multivariable model that adjusted for age, sex, race, diabetes mellitus, body mass index, blood pressure, medication use, and glomerular filtration rate, HFpEF remained an independent predictor of a greater delta-Lx-Cx-time (β=-0.43; P=0.013). ECV, but not focal subendocardial delayed enhancement (i.e., myocardial infarction) was independently predictive of a greater delta-Lx-Cx-time (β=0.28; P=0.004).
Conclusions: Diastolic dyssynchrony, with prolonged contraction of longitudinal fibers, is present in HFpEF, likely contributing to abnormalities in early diastolic relaxation. Diastolic dyssynchrony is related to the presence of diffuse interstitial myocardial fibrosis, but not to a focal scarring from myocardial infarction.
Author Disclosures: J.A. Chirinos: Research Grant; Significant; NIH, American College of Radiology Network, Fukuda Denshi, Bristol Myers Squibb, Microsoft and CVRx Inc. Other Research Support; Modest; Fukuda Denshi, Withings, Atcor Medical. Consultant/Advisory Board; Modest; Fukuda Denshi, Microsoft Research, Merck and Vital Labs. Consultant/Advisory Board; Significant; Bristol Myers Squibb, OPKO Healthcare. H. Soto-Calderon: None. S. Varakantam: None. A. Syed: None. T.S. Phan: None. M.R. Koppula: None. U. Kewan: None. E. Shah: None. S.R. Akers: None.
- © 2016 by American Heart Association, Inc.