Only marginal influence of metabolic control on blood rheology in insulin-dependent diabetic patients without manifest angiopathy

Abstract

To evaluate the influence of metabolic quality on blood rheology plasmatic and cellular determinants were studied in otherwise healthy, young insulin-dependent diabetic patients with excellent (A; n=12; age: 32.1 ± 13 a (x ± SD); HbA1c: 5.2 HbA1c 0.4%), moderate (B; n=12; 26.4 ± 7.8 a; HbA1c: 7.7 ± 0.5%) and insufficient (C; n=14; 26.3 ± 7.9 a; HbA1c: 11.5 ± 1.8%) metabolic control, as well as in patients with manifest microangiopathy (= retinopathy) (D; n=10; 33.1 ± 8.6; HbA1c: 7.2 ± 1.9%) and in heal thy age-matched non-diabetic controls (N; n=12; 28.3 ± 4.7 a; HbA1c: 5.3 ± 0.2%). While plasma fibrinogen, (N: 242 ± 46 mg/dl; A: 259 ± 51 mg/dl; B: 277 ± 45 mg/dl; C: 287 ± 68 mg/dl; D: 307 ± 69 mg/dl) and alpha-2-macroglobulin (A: 185 ± 41 mg/dl; B: 207 ± 70 mg/dl; C: 211 ± 89 mg/dl; D: 228 ± 73 mg/dl) tended to increase with worsening of metabolic control and presence of microangiopathy, we found no significant differences between the groups in plasma viscosity (N: 1.61 ± 0.03 mPa.s; A: 1.64 ± 0.05 mPa.s; B: 1.70 ± 0.11 mPa.s; C: 1.68 ± 0.16 mPa.s; D: 1.66 ± 0.12 mPa.s) and in red cell aggregation (in stasis, arb. units) (N: 4.98 ± 1.04 aU*; A: 5.31 ± 0.78 aU*; B: 6.45 ± 1.55 aU; C: 5.57 ± 1.57 aU*; D: 7.33 ± 2.32 aU;* p<0.05 vs D; analysis of variance) in dependance of metabolic control. In contrast, red cell aggregation (stasis) was higher in patients with microangiopathy (n=10; 7.33 ± 2.32 aU) than in those without (n=52; 5.55 ± 1.36 aU; p<0.015) under comparable metabolic control (HbA1c; 7.2 ± 1.9% vs 7.5 ± 2.9%; n.s.), resembling the results for red cell aggregation at low shear rate (3/s) (with retinopathy: 9.2 ± 2.4 aU; without: 7.8 ± 1.5 aU; p<0.05).

Our data suggest that rheological parameters depend only marginally on metabolic control in young insulin-dependent diabetic patients without manifest macro- and microangiopathy. Thus, changes in blood rheology in patients with manifest macro- and microangiopathy should be interpreted rather as aggrevating consequence of the underlying vessel disease than as primary causal factor.