Prognostic implications of plasma volume status estimates in heart failure with preserved ejection fraction: insights from TOPCAT.
Pubmed ID: 30714658
Journal: European journal of heart failure
Publication Date: May 1, 2019
Link: https://onlinelibrary.wiley.com/doi/pdf/10.1002/ejhf.1407
MeSH Terms: Humans, Male, Female, Aged, Aged, 80 and over, Cardiovascular Diseases, Middle Aged, Proportional Hazards Models, Heart Failure, Hospitalization, Multivariate Analysis, Cause of Death, Prognosis, Kaplan-Meier Estimate, Stroke Volume, Mortality, Hematocrit, Body Weight, Mineralocorticoid Receptor Antagonists, Spironolactone, Plasma Volume
Authors: Grodin JL, Mullens W, Pandey A, Tang WHW, Drazner MH, Fang JC, Philips S, Nijst P, Martens P
Cite As: Grodin JL, Philips S, Mullens W, Nijst P, Martens P, Fang JC, Drazner MH, Tang WHW, Pandey A. Prognostic implications of plasma volume status estimates in heart failure with preserved ejection fraction: insights from TOPCAT. Eur J Heart Fail 2019 May;21(5):634-642. Epub 2019 Feb 4.
Studies:
Abstract
AIMS: Plasma volume expansion is clinically and prognostically relevant in individuals with heart failure. Prior cohorts either excluded or had limited representation of patients with heart failure with preserved ejection fraction (HFpEF). We aimed to examine the relationship between calculated plasma volume status (PVS) and outcomes in HFpEF. METHODS AND RESULTS: We included enrollees from the Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antagonist Trial (TOPCAT) with available haematocrit and weight data (n = 3414). Plasma volume was derived from the Hakim formula and compared to estimates of ideal plasma volume to generate a relative PVS. Multivariable Cox proportional hazards models tested the association of PVS with clinical outcomes. The median PVS was -11.9% (25th-75th percentile: -17.2% to -6.4%) and the majority (91.1%) had PVS consistent with relative volume contraction (PVS ≤ 0%) as opposed to volume expansion (8.9%, PVS > 0%). After multivariable adjustment, each 5% increment in PVS was associated with a ∼11%, 14%, and 12% higher risk for the primary composite endpoint, all-cause death, and heart failure hospitalization, respectively (P < 0.002 for all), but not cardiovascular death (P = 0.051). After additional adjustment for natriuretic peptides, PVS only remained associated with heart failure hospitalization (HR 1.10, 95% confidence interval 1.001-1.21, P = 0.047). There were no significant interactions between spironolactone use and the PVS-risk relationship for any endpoint (P > 0.1 for all). CONCLUSION: Higher calculated estimates of PVS were independently associated with a higher risk of long-term clinical outcomes in HFpEF, and particularly, heart failure hospitalization.