It is well known that blood viscosity is increased in patients with occlusive cerebrovascular disease (OCVD) and also that red blood cell aggregation (RBC-A) is one of the most important determinants of blood viscosity, especially at low shear rate. In this paper, RBC-A in OCVD is discussed with particular attention to the distinction between perforating branch infarction (POI) and cortical branch infarction (CBI).
The subjects comprised 64 cases with occlusive CVD, (34 PBI, 30 CBI) and 67 age-matched controls. Heparinized whole blood was sampled and RBC-A was quantitated by measuring light transmission through the blood after stasis. Values of RBC-A · T1/2 were 5.0 ± 1.4 sec, 4.8 ± 1.0 sec, 5.3 ± 1.7 sec and 6.4 ± 2.0 sec in whole OCVD, PBI, CBI and controls, respectively. RBC-A · T1/2 was shortened (accelerated) in occlusive CVD as compared with the control group (p<0.01). RBC-A · T1/2 was more shortened in PBI than in CBI, although the difference was not statistically significant. Duration after onset and volume of infarction were not related to RBC aggregation time.
Whole OCVD patients were divided into two groups, cerebral thrombosis and embolism. Values of RBC-A · T1/2 were 5.2 ± 1.5 sec (thrombosis) and 4.7 ± 1.1 sec (embolism) and there was no significant difference between them.
Red blood cell volume (RBV), hematocrit (Hct) and plasma proteins, [total protein (TP), albumin (Alb), gamma globulin (γ-G1) and fibrinogen (Fib)] were studied in these patients. RBV and Hct were slightly but significantly higher (although the value was within normal limits) in occlusive CVD than in the controls (p<0.05). In the control group, there were significant negative correlations of RBC-A · T1/2 with Hct, TP, γ-Gl and Fib, but no correlation with Alb. In occlusive CVD, there was no correlation between RBC-A · T1/2 and these parameters, suggesting that the higher RBC and higher Hct did not influence the acceleration of RBC-A. Serum Alb level was higher in PBI (p<0.05), but other parameters showed no significant difference between PBI and CBI. There was no correlation between RBC-A · T1/2 and plasma factors in PBI. In CBI, there was only a negative correlation between RBC-A · T1/2 and γ-Gl [R=-0.449 (n=25), p<0.05]. These results indicate that the plasma factors which affect RBC-A in controls may not contribute to the acceleration of RBC-A in OCVD. In occlusive CVD, some factors in RBC themselves may contribute to the acceleration of RBC-A.
Clinical risk factors such as hypertension (HT), atrial fibrillation (Af), diabetes mellitus (DM) or glucose tolerance impairment (GTI), hyperlipidemia (HL), cigarette smoking and alcohol drinking were also studied. HT and smoking were more frequent in PBI, and Af was more frequent in CBI. However there was no relation between RBC-A and such risk factors.
Acceleration of RBC-A may be determined by intrinsic properties of the RBCs themselves as mentioned above. Under the influence of atherosclerosis or stenotic change of cerebral vessels and so on, such properties of RBC would lead to a reduction of cerebral blood flow, especially in low flow areas such as distal parts of the perforating branch which would be easily affected by hemorheological change.
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