Cerebral Blood Flow and Neurological Change in Chronic Heart Failure

Abstract

In their article in this issue of Stroke , Gruhn et al report that cerebral blood flow (CBF) is reduced about 30% in patients with NYHA III/IV heart failure but has normalized when retested in 5 subjects 30 days after successful heart transplantation. The authors suggest that (1) the reduced CBF found before transplantation is responsible for neurological signs and symptoms reported in patients with chronic heart failure (CHF), and (2) that the resolution of such symptoms after transplantation, as reported in other studies, and the normalization of CBF, as found in their investigation, are parallel phenomena, both resulting from an improvement in central hemodynamics. This editorial explores whether the increase in CBF 30 days after transplantation found by Gruhn et al could be on another basis—a perisurgical fall in hematocrit—and whether the reduced CBF values found before surgery are sufficient to cause neurological disturbances. It also considers the types and etiologies of neurological changes in CHF. Hematocrit is the main determinant both of whole-blood viscosity1 and arterial O2 content,2 each of which has powerful effects on CBF. Viscosity accounts for 56% of the decrease in CBF that occurs as hematocrit rises from 20% to 40%.3 In dilated cardiomyopathy, viscosity is further increased due to elevated fibrinogen and decreased red cell deformability,4 which can compound the inverse effect of hematocrit on CBF. A reduction in arterial oxygen content can account for 40% to 60% of the increase in CBF that accompanies a fall in hematocrit.2 A drop in hematocrit can occur perisurgically from blood loss or relative hemodilution. Some years ago we noted (data reported at meetings but unpublished) that paired CBF measurements, done shortly before and after unilateral carotid endarterectomy (CEA) in patients with single-vessel disease, showed a statistically significant postoperative increase in …