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The optimal plasma volume status in heart failure in relation to clinical outcome.
Journal of Cardiac Failure 2018 December 5
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-(99 Tc)-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) 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-(99 Tc)-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. A higher PVS was independently associated with an increased risk for heart failure hospitalization and all-cause mortality (HR=1.016; CI=1.006-1.027 per 1 % increase in PVS; p=0.002). ROC-curve analysis indicated that an PVS of -6.5% optimally predicted absence of adverse outcome. Hazard ratio analysis indicated that CHF-patients were less equipped in tolerating PV-expansion in comparison to PV-contraction. 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 and a slight contraction of the predicted PV seems to be related to less adverse events. Higher dosages of Renin-Angiotensin-Aldosterone blockers are associated with a higher odds for having an optimal PV-status.
METHODS: The correlation between technetium-(99 Tc)-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) 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-(99 Tc)-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. A higher PVS was independently associated with an increased risk for heart failure hospitalization and all-cause mortality (HR=1.016; CI=1.006-1.027 per 1 % increase in PVS; p=0.002). ROC-curve analysis indicated that an PVS of -6.5% optimally predicted absence of adverse outcome. Hazard ratio analysis indicated that CHF-patients were less equipped in tolerating PV-expansion in comparison to PV-contraction. 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 and a slight contraction of the predicted PV seems to be related to less adverse events. Higher dosages of Renin-Angiotensin-Aldosterone blockers are associated with a higher odds for having an optimal PV-status.
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