Intravascular Volume Profiles in Patients With Class I and II Systolic Heart Failure: Heterogeneity and Volume Overload Are Common Even in Mild Heart Failure

• Published in: Journal of cardiac failure 2018-07, Vol.24 (7), p.417-424
• Main Authors: Miller, Wayne L., Albers, Diana P., Gansen, Denise N., Mullan, Brian P.
• Format: Article
• Language: English
• Subjects: change over time; Class I-II heart failure; serial intravascular volume assessment; Total blood volume quantitation
• ISSN: 1071-9164; 1532-8414
• DOI: 10.1016/j.cardfail.2017.09.010

•Marked heterogeneity in intravascular volume is present even in class I and II chronic heart failure (HF) patients.•Persistent plasma volume expansion is common despite good function status and optimal medical therapy.•Red cell mass deficit (true anemia) and excess (polycythemia) contribute to volume heterogeneity.•These findings have implications for patient management in early HF to limit progression of HF.•Intravascular volume should be considered a modifiable risk marker in chronic HF. Although volume overload is a commonly described clinical feature of advanced heart failure (HF), less is known regarding volume profiles of patients with less severe class I and II HF. Intravascular volume was quantitated by radiolabeled-albumin indicator-dilution technique in clinic outpatients. Forty-six patients (age 61 ± 13years, left ventricular ejection fraction 30 ± 8%) were prospectively evaluated with 28 undergoing repeat evaluations at 1 year. There was no difference in averaged total blood volume (TBV) at baseline between class I (N = 26) and II (N = 20) patients (5.6 ± 1.6vs 6.0 ± 1.3 L, P = .368) and at 1-year of follow-up. However, there was marked heterogeneity in plasma volume (–13% to +69% of normal) and red cell mass (RBCM –31% to +50%) profiles with TBV expansion identified in 46% of the cohort, whereas only 48% had a normal TBV. RBCM deficit (true anemia) was common (39%), but a low hemoglobin concentration was accurate in identifying anemia in only 11% of the cohort. RBCM excess (polycythemia) also was identified in 20% of the cohort. Marked heterogeneity in plasma volume and RBCM volume profiles is present even in mild HF, and identifying volume overload, which was common in early HF, has the potential to help guide therapy in the reduction of HF progression. Intravascular volume as a modifiable risk factor in early HF warrants further study.