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The optimal plasma volume status in heart failure in relation to clinical outcome

Session Patient management - From oral treatment to transplant

Speaker Pieter Martens

Congress : Heart Failure 2018

  • Topic : heart failure
  • Sub-topic : Chronic Heart Failure - Pathophysiology
  • Session type : Rapid Fire Abstracts
  • FP Number : 1540

Authors : P Martens (Genk,BE), P Nijst (Genk,BE), M Dupont (Genk,BE), W Mullens (Genk,BE)

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Authors:
P Martens1 , P Nijst1 , M Dupont1 , W Mullens1 , 1Hospital Oost-Limburg (ZOL), Cardiology - Genk - Belgium ,

Citation:

Background:
Progressive plasma volume (PV) expansion is a hallmark of chronic heart failure (HF), ultimately contributing to decompensated heart failure. Monitoring PV might offer prognostic information and might be a target for tailored therapy.

Methods:
The correlation between technetium-(99Tc)-labeled red blood cell measured PV and calculated PV was first determined in a validation cohort. The relationship between PV-status (PVS; a marker how much actual PV deviated from the ideal PV; for formula see figure) and outcome was analyzed using cox-proportional modeling in a prospective CHF-population (the outcome cohort).

Results:
Thirty-one HF-patients were included in the validation cohort. Calculated PV correlated well with technetium-(99Tc)-measured PV (r=0.714; p=0.001). A total of 1173-patients (HFrEF n=872, HFmrEF n=229, HFpEF n=72) were prospectively included in the outcome cohort. The mean PVS in the outcome cohort was -6.7±10%, indicating slight PV-contraction. Mean PVS was similar in HFrEF, HFmrEF and HFpEF (post-hoc ANOVA all p>0.05). A higher PVS was independently associated with an increased risk for heart failure hospitalization and all-cause mortality (HR=1.017; CI=1.007-1.028 per 1 % increase in PVS). ROC-curve analysis indicated that an PVS of -6.5% optimally predicted absence of adverse outcome (defined as optimal PVS). Hazard ratio analysis indicated that CHF-patients were less equipped in tolerating PV-expansion in comparison to PV-contraction (see figure). The use of ACE-I/ARBs and MRAs were independently associated with a higher odds for having an optimal PVS in HFrEF and HFmrEF (all p<0.05), but not in HFpEF.

Conclusions:
Calculated PV correlates well with measured PV in HF-patients. An increase in PV is independently associated with a higher risk for adverse outcome. The optimal PV in HF is lower than what would be expected based on an ideal prediction formula. Higher dosages of Renin-Angiotensin-Aldosterone blockers are associated with a higher odds for having an optimal PV-status in HFrEF, HFmrEF but not HFpEF.

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