Hemorrheologic abnormalities in defined primary dyslipoproteinemias with both high and low atherosclerotic risks

Dyslipoproteinemias are associated with hemorrheologic abnormalities (eleva ted fibrinogen concentration, higher viscosity of plasma and blood). Epidem iologic data suggest that not only elevated lipoprotein concentrations (eg. low-density lipoprotein [LDL] cholesterol), but also hemorrheologic abnorm alities could causally be involved in the atherosclerotic process. To eluci date potential effects of hemorrheological disturbances, we investigated pa tients suffering from primary hyperlipoproteinemias with both low (familial hypertriglyceridemia, n = 25) and high (type III hyperlipoproteinemia. n = 21; familial hypercholesterolemia. n = 19; mixed hyperlipoproteinemia. n = 19) atherosclerotic risk, as well as healthy controls (n = 49) in a cross- sectional design. Dyslipoproteinemias were classified by lipoprotein measur ements (using ultracentrifugation), family history, and apolipoprotein E ph enotype. Hemorrheology was characterized by the measurement of fibrinogen c oncentration, viscosity of plasma and blood at different shear rates, and r ed cell aggregation (RCA) at stasis and low shear. Fibrinogen concentration was lower in controls (2.38 +/- 0.09 g/L) compared with familial hyperchol esterolemia (3.19 +/- 0.19 g/L), to type III hyperlipoproteinemia (3.02 +/- 0.12 g/L), to familial hypertriglyceridemia (2.95 +/- 0.21 g/L) and to mix ed hyperlipoproteinemia (3.01 +/- 0.12 g/L) (P < .05, respectively) without differences between dyslipoproteinemia groups. Plasma viscosity was higher in patients with type III hyperlipoproteinemia (1.42 +/- 0.03 mPas), with familial hypertriglyceridemia (1.47 +/- 0.04 mPas), and with mixed hyperlip oproteinemia (1.43 +/- 0.02 mPas) compared with controls (1.29 +/- 0.01 mPa s) (P < .05, respectively). After including 6 lipoprotein parameters in a g eneral linear model, plasma viscosity, blood viscosity, and RCA were higher in familial hypertriglyceridemia compared with healthy controls and famili al hypercholesterolemia (P < .05, respectively). As most of the hemorrheolo gic abnormalities were still significant after adjusting for lipoprotein co ncentrations, they seem to be at least partly independent from direct lipop rotein effects. Hemorrheologic abnormalities in familial hypertriglyceridem ia (low atherosclerotic risk) were at least as marked as in dyslipoproteine mias with high atherosclerotic risk, suggesting that it might be most impor tant to determine lipoprotein concentrations and to define exactly the type of dyslipoproteinemia for estimating the individual cardiovascular risk in these patients. Copyright (C) 2001 by W.B. Saunders Company.