To clarify the relationship between arteriosclerosis obliterans (ASO) and cerebral infarction (CI), brain CT was performed and the risk factors for atherosclerosis were assessed. Thirty-five male and 5 female patients with intermittent claudication and/or leg ulceration were angiographically diagnosed as having ASO. According to CT findings, these patients were divided into three groups [no low-density areas (NLDA), hemorrhage, and infarction (CI)]. CI was subdivided as lacunar, cortical, and watershed infarction. Thirteen patients were in the NLDA group and 26 in the CI group (17 lacunar, 3 cortical and 6 mixed infarcts), indicating a CI incidence of 65%. Comparing the risk factors of the CI group with those of the NLDA group, hypertension (53.8%), diabetes (34.6%), and cigarette smoking (69.2%) was often seen in the CI group, although hypercholesterolemia (53.8%) and ischemic heart disease (42.3%) was the same in both groups. Multivariate analysis revealed that smoking had the strongest effect on the occurrence of CI in ASO patients. Furthermore, the number of combined risk factors (hypertension, diabetes, smoking, hypercholesterolemia) had a significant positive correlation with cortical infarction. As to the chronological relationship between the onset of ASO and CI, CI was present in 14 of 27 ASO patients on CT when the ischemic leg symptoms appeared, while symptomatic cortical infarction preceded ASO in 5 patients. CI patients increased gradually over a decade to 26 out of 40, among whom 16 patients with lacunae had silent infarcts. These findings suggested that ASO is frequently associated with CI, due not only to atherosclerosis of the main trunks of the cerebral vessels, but also to arteriolosclerosis of the perforating arteries.

View full abstract

As previously reported, cerebral infarction (CI) is found in 65% of the patients with arteriosclerosis obliterans (ASO), and occurs in the presence of risk factors such as smoking. On the other hand, the incidence of ASO in CI patients is still unknown due to the difficulty of detecting ASO. To determine this incidence and to elucidate the risk factors for ASO, we measured the ankle pressure index (API) by Doppler velocimetry in 46 patients with cerebral thrombosis. Based on API, these patients with neurological deficits were divided into two groups, the normal API (API≥0.9) group and the low API (API≤0.9) group. The low API elderly patients were taken to have ASO, even if ischemic symptoms were not present. Since 29 patients were in the normal API group and 17 in the low API group, the incidence of ASO was 37%. For these two groups, we compared the risk factors for atherosclerosis, the brain CT findings, and biochemical data. Mean age (78.4 years), duration since CI (3.5 years), and gender (M: 7/F: 10) were similar in both groups, but hypertension (82.4%), diabetes (23.5%), cigarette smoking (41.2%), and ischemic heart disease (35.3%) were seen more often in the low API group. Furthermore, the combination of four risk factors (hypertension, diabetes, smoking, hypercholesterolemia) had a significant positive correlation with ASO. Brain CT findings were classified as lacunar (23 patients), cortical (10), watershed (9), and mixed-type infarction (4). API in cortical infarction (0.86±0.17) tended to be lower than in the other types. Multivariate analysis revealed that diabetes, cortical/watershed infarction, and hypertension had a strong relationship to the occurrence of ASO in CI patients. Serum lipids (total cholesterol, triglycerides, HDL cholesterol, apo-AI, and apo-B) showed no differences in the two groups, while significantly higher levels of β-thromboglobulin and lower levels of 6keto-PGF_1α were found in the low API group. These findings suggest that platelets were activated and that endothelial cell damage was present in patients with CI and ASO. In conclusion, ASO complicated by cerebral thrombosis (especially cortical infarction) and the risk factors mentioned above was shown to be a state of advanced atherosclerosis associated with a functional imbalance between platelets and endothelial cells.

View full abstract