To date, all major clinical trials for anemia correction using erythrocyte stimulating agents (ESAs) failed to show improved outcomes for cardiovascular disease (CVD), stroke, and vascular thrombosis. Even moderate elevations in hemoglobin (e.g., to 13 g/dL) using erythropoietin have been associated with significantly increased risk of thrombotic cardiovascular events and heart failure. This review presents a biophysical rationale for increased risk of CVD among certain patients treated with ESAs and suggests a risk management approach based on blood viscosity. Whole blood viscosity is a key determinant of the work of the heart, and elevated blood viscosity appears to be both a strong predictor of cardiovascular disease and an important pathophysiological factor in the development of atherothrombosis. Blood donation has been shown to reduce viscosity. Reflecting these findings, studies in male blood donors and in women of premenopausal age with regular menstruation have shown reduced incidence of cardiovascular events such as myocardial infarction, angina, stroke, and the requirement for procedures such as percutaneous transluminal coronary angioplasty and coronary artery bypass graft compared with non-donors and postmenopausal women, respectively. We propose that blood viscosity monitoring should be considered as part of a cardiovascular risk assessment, whenever an increased cardiovascular risk is detected and particularly in the context of anemia correction.
Increased whole blood viscosity (WBV) can be injurious to the vascular endothelium and increase the risk of atherothrombotic events. This study examined the effect of hemodialysis ultrafiltration (UF) on WBV, with a focus on high vs. low-volume UF patients. In stable hemodialysis patients, blood was drawn for hematocrit (Hct) and WBV at the start, midpoint, and at the end of dialysis. For analysis, patients were divided into high UF (≥2700 mL) or low UF (<2700 mL) groups. A total of 59 patients completed the study. Mean Hct increased during dialysis in both groups. The intradialytic increase in Hct was significantly greater in the high vs. the low UF group (3.2% vs. 1.28%, P = 0.01), with a significantly higher end-dialysis Hct in the high UF group (40.5% vs. 38%, P = 0.02). At the end of dialysis, both high shear rate WBV (P < 0.01) and low shear rate WBV (P < 0.01) were significantly higher in the high UF compared with the low UF group. There was an approximately two-fold greater increase in high shear rate (P < 0.01) and low shear rate (P = 0.01) WBV during dialysis in high vs. low UF groups. The increase in high shear rate WBV during dialysis was significantly correlated with an increase in Hct (R(2) = 0.63, P < 0.01). We found that hemodialysis UF causes a surge in WBV. The surge was of greater magnitude in high than in low UF patients.
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