Prognostic implications of plasma volume status estimates in heart failure with preserved ejection fraction

insights from TOPCAT

Justin L Grodin, Steven Philips, Wilfried Mullens, Petra Nijst, Pieter Martens, James C. Fang, Mark H Drazner, W. H.Wilson Tang, Ambarish Pandey

Research output: Contribution to journalArticle

3 Citations (Scopus)

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.

Original languageEnglish (US)
JournalEuropean Journal of Heart Failure
DOIs
StatePublished - Jan 1 2019

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Plasma Volume
Heart Failure
Hospitalization
Mineralocorticoid Receptor Antagonists
Hematocrit
Proportional Hazards Models
Cause of Death

Keywords

  • Congestion
  • Heart failure with preserved ejection fraction
  • Plasma volume

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Prognostic implications of plasma volume status estimates in heart failure with preserved ejection fraction : insights from TOPCAT. / Grodin, Justin L; Philips, Steven; Mullens, Wilfried; Nijst, Petra; Martens, Pieter; Fang, James C.; Drazner, Mark H; Tang, W. H.Wilson; Pandey, Ambarish.

In: European Journal of Heart Failure, 01.01.2019.

Research output: Contribution to journalArticle

Grodin, Justin L ; Philips, Steven ; Mullens, Wilfried ; Nijst, Petra ; Martens, Pieter ; Fang, James C. ; Drazner, Mark H ; Tang, W. H.Wilson ; Pandey, Ambarish. / Prognostic implications of plasma volume status estimates in heart failure with preserved ejection fraction : insights from TOPCAT. In: European Journal of Heart Failure. 2019.
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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.",
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author = "Grodin, {Justin L} and Steven Philips and Wilfried Mullens and Petra Nijst and Pieter Martens and Fang, {James C.} and Drazner, {Mark H} and Tang, {W. H.Wilson} and Ambarish Pandey",
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T2 - insights from TOPCAT

AU - Grodin, Justin L

AU - Philips, Steven

AU - Mullens, Wilfried

AU - Nijst, Petra

AU - Martens, Pieter

AU - Fang, James C.

AU - Drazner, Mark H

AU - Tang, W. H.Wilson

AU - Pandey, Ambarish

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N2 - 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.

AB - 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.

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