Abstract 14358: Determinants of Diffuse Myocardial Fibrosis in Patients With Heart Failure With Preserved Ejection Fraction Compared to Age-Matched Volunteers.
Background: Several studies have shown that increased myocardial fibrosis may play a key role in HFpEF pathophysiology. The aim of this study was to evaluate the presence and the determinants of diffuse fibrosis in HFpEF patients compared to age-matched volunteers.
Methods: Between January 2015 and May 2016, we prospectively included 102 consecutive patients with HFpEF (78±9 years, 66% women) defined by LVEF≥ 50%, Framingham HF criteria, prior hospitalization for HF or NT-proBNP >350pg/ml. LV and RV functions were assessed by 2D echocardiography and cardiac magnetic resonance (cMR). Diffuse myocardial fibrosis was estimated by extra cellular volume (ECV) quantified by 3 Tesla cMR with the Modified Look-Locker Inversion Recovery sequence. We determined an ECV age-adjusted cutoff value (cutoff = 35%) corresponding to mean + 2 standard deviations in 27 age-matched volunteers (74±7years, 63% women) without previous cardiac history.
Results: Fibrosis estimated by ECV was significantly higher in HFpEF patients than in volunteers (32±5% vs. 28±3%, p<0.0001). Twenty-two percent of HFpEF patients (n=23) had significant fibrosis considering the ECV cutoff of 35%. Compared to those with ECV<35%, these patients had a lower BSA, more diabetes, a higher indexed left atrial volume (LAiV), a higher E/e’ ratio, a lower tricuspid annular plane systolic excursion (TAPSE) and higher indexed end diastolic and end systolic RV volumes (Table). In multivariate logistic regression, only LAiV (OR= 1.02 [1.00-1.05], p=0.041), TAPSE (OR=0.90 [0.82-0.99], p=0.036) and diabetes (OR= 3.59 [1.32-9.78], p=0.013) were significant determinants of fibrosis.
Conclusion: Among HFpEF patients, high levels of fibrosis were associated with LV diastolic function, decreased RV longitudinal systolic function and presence of diabetes. Yet, only 22% of HFpEF patients had high levels of fibrosis, suggesting that other mechanisms are involved in HFpEF pathophysiology.
Author Disclosures: C. Roy: None. A. Slimani: None. C. de Meester: None. M. Amzulescu: None. A. Pasquet: None. D. Vancraeynest: None. C. Beauloye: None. J. Vanoverschelde: None. B. Gerber: None. A. Pouleur: None.
- © 2016 by American Heart Association, Inc.