Serum Albumin Is a Marker of Myocardial Fibrosis, Adverse Pulsatile Aortic Hemodynamics, and Prognosis in Heart Failure With Preserved Ejection Fraction.

Background Data regarding the phenotypic correlates and prognostic value of albumin in heart failure with preserved ejection fraction (HFpEF) are scarce. The goal of the current study is to determine phenotypic correlates (myocardial hypertrophy, myocardial fibrosis, detailed pulsatile hemodynamics, and skeletal muscle mass) and prognostic implications of serum albumin in HFpEF. Methods and Results We studied 118 adults with HFpEF. All-cause death or heart-failure-related hospitalization was ascertained over a median follow-up of 57.6 months. We measured left ventricular mass, myocardial extracellular volume, and axial muscle areas using magnetic resonance imaging. Pulsatile arterial hemodynamics were assessed with a combination of arterial tonometry and phase-contrast magnetic resonance imaging. Subjects with lower serum albumin exhibited a higher body mass index, and a greater proportion of black ethnicity and diabetes mellitus. A low serum albumin was associated with higher myocardial extracellular volume (52.3 versus 57.4 versus 39.3 mL in lowest to highest albumin tertile, respectively; =0.0023) and greater N-terminal pro B-type natriuretic peptide levels, but not with a higher myocardial cellular volume (123 versus 114 versus 102 mL; =0.13). Lower serum albumin was also associated with an increased forward wave amplitude and markedly increased pulsatile power in the aorta. Serum albumin was a strong predictor of death or heart failure hospitalization even after adjustment for N-terminal pro B-type natriuretic peptide levels and the Meta-Analysis Global Group in Chronic Heart Failure (MAGGIC) risk score (adjusted standardized hazard ratio=0.56; 95% CI=0.37-0.83; <0.0001). Conclusions Serum albumin is associated with myocardial fibrosis, adverse pulsatile aortic hemodynamics, and prognosis in HFpEF. This readily available clinical biomarker can enhance risk stratification in HFpEF and identifies a subgroup with specific pathophysiological abnormalities.