High serum pentosidine in branch atheromatous disease among small vessels occlusion.

BACKGROUND

Cerebral branch atheromatous disease (BAD) are more likely to experience progressing stroke and neurological deterioration compared with lacunar infarction, although these small vessels occlusions are difficult to discriminate in acute phase of ischemic stroke. Advanced glycation end products including pentosidine have been implicated in atherosclerosis, and were associated with atheroma plaque progression. However, little is known about a relationship between serum pentosidine and small vessels occlusion.

METHODS

Serum pentosidine levels were measured in 56 patients (BAD: N.=21; lacunar: N.=35) with small vessels occlusion among consecutive 208 patients with acute ischemic stroke at initial hospitalization as well as other risk factors of stroke. Univariate and multivariate logistic regression analyses were performed to analyze relationship between risk factors including pentosidine and small vessels occlusion. Sensitivity and selectivity of pentosidine to discriminate BAD from lacunar were calculated.

RESULTS

Serum pentosidine was significantly higher in BAD group than lacunar group (0.081±0.081 µg/mL and 0.046±0.043 µg/mL, P<0.05). In the univariate logistic regression analyses, BAD was significantly related to high serum pentosidine (P=0.01), absence of dyslipidemia (P=0.04), and worse outcome measured by modified Rankin Scale (P=0.03). Multivariate logistic regression analysis showed that only high level of serum pentosidine was the independent risk factor for BAD (P=0.03). Sensitivity and specificity were 90% and 44%, respectively.

CONCLUSIONS

High level of serum pentosidine in acute phase of stroke was associated with BAD, which led to worse outcome among patients with small vessels occlusion.