Abstract
Expansion in blood volume (BV) is a well-recognized response to arterial underfilling secondary to impaired cardiac output in heart failure (HF). However, the effectiveness of this response in terms of outcomes remains inadequately understood. Prospective analysis was undertaken in 110 patients with HF hospitalized and treated for fluid overload. BVs were measured in a compensated state at the hospital discharge using the indicator-dilution methodology. Data were analyzed for composite 1-year HF-related mortality/first rehospitalization. Despite uniform standard of care, marked heterogeneity in BVs was identified across the cohort. The cohort was stratified by BV expansion greater than or equal to +25% above normal (51% of cohort), mild-moderate expansion (22%), and normal BV (27%). Kaplan–Meier (K-M) survival estimates and regression analyses revealed BV expansion (greater than or equal to +25%) to be associated with better event-free survival relative to normal BV (P = 0.038). Increased red blood cell mass (RBCm; RBC polycythemia) was identified in 43% of the overall cohort and 70% in BV expansion greater than or equal to +25%. K-M analysis demonstrated polycythemia to be associated with better outcomes compared with normal RBCm (P < 0.002). Persistent BV expansion to include RBC polycythemia is common and, importantly, associated with better clinical outcomes compared with normal total BV or normal RBCm in patients with chronic HF. However, compensatory BV expansion is not a uniform physiological response to the insult of HF with marked variability in BV profiles despite uniform standard of care diuretic therapy. Therefore, recognizing the variability in volume regulation pathophysiology has implications not only for impact on clinical outcomes and risk stratification but also potential for informing individualized volume management strategies.NEW & NOTEWORTHY The novel findings of this study demonstrate that intravascular volume profiles among the patients with chronic heart failure (HF) vary substantially even with similar clinical compensation. Importantly, a profile of blood volume (BV) expansion (compared with a normal BV) is associated with lower HF mortality/morbidity. Furthermore, RBC polycythemia is common and independently associated with improved outcomes. These observations support BV expansion with RBC polycythemia as a compensatory mechanism in chronic HF.
Highlights
The importance of an effective blood volume (BV) to maintain integrity of the circulatory system in health and disease is well recognized
Blood volume quantitation and clinical data were available on 110 patients who were prospectively followed for the composite end point over 1 year after the index hospitalization; 53 composite outcome events (33 deaths) occurred over the 1 year follow-up period
More males than females across the subgroups participated in the study, and patients with the greater BV expansion had lower fasting glucose level than patients with less blood volume expansion
Summary
The importance of an effective blood volume (BV) to maintain integrity of the circulatory system in health and disease is well recognized. The circulation will fail if intravascular volume is insufficient to fill the capacity of the vascular system. With the onset of heart failure (HF) and associated impaired cardiac output, arterial underfilling develops and, as a result, compensatory mechanisms are activated to maintain intravascular volume and critical perfusion pressure despite hemodynamic perturbations. Sympathetic-mediated arterial and venous constriction provide early responses to maintain organ perfusion; longer-term mechanisms come into play that include an expansion in intravascular volume. The concept of BV expansion in patients with chronic HF is not new and has a background in earlier human physiology investigations demonstrating that both intravascular and interstitial compartment fluid volumes increase in HF and that fluid volume distributions can be highly variable [1,2,3,4,5]. We and others have shown, by quantitative volume analyses, persistence in intravascular volume expansion despite aggressive diuretic therapy and, and importantly, significant variability in intravascular volume profiles (normal BV to marked expansion) despite similar clinical presentations and
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