[A study on the etiology and epidemiology of familial aggregation in arteriosclerotic cerebral infarction].

A case-control study including 214 pedigrees (109 cases and 105 controls) was carried out to explore the etiology of family aggregation of arteriosclerotic cerebral infarction in Yi-Xing city, March 1997. The results showed that the family member in both cases and control groups were comparable. The total prevalence rate of the first-degree relatives in cases was 5.12%, significantly higher than (1.63%) that noticed in controls, with chi 2 = 16.40 (P < 0.01). The same results was also found in their parents and siblings. Results from binominal distribution analysis showed that the number of cases in the families of arteriosclerotic cerebral infarction was significantly higher than the theortical range which indicated that there was significant familial aggregation in the occurance of arteriosclerotic cerebral infarction. Logistic regression model also showed that genetic factor was one of the most important risk factors in Xi-xing, Jiangsu. Dose-response was observed in this model. The heritability and the segregation ratio of arteriosclerotic cerebral infarction were the same as seen in other chronic diseases, such as coronary heart disease and esophageal cancer.

[Analysis on the interaction among agents in arteriosclerotic cerebral infarction].

An 1:1 matched case-control study including 105 arteriosclerotic cerebral infarction cases and 105 controls was carried out to estimate the etiologic interaction, in Yi-xing city, March 1997. Results showed that the major risk factors were high levels of serum TG, Lp(a) and BMI while serum level of HDL-C was the only protective factor. When several levels were divided on Lp(a) and BMI, a significantly dose response relation was found. Considering the correlation among serum concentration of lipids, we analysed the interaction of different factors, using Log-Linear models. Results showed that there were significant interactions between arteriosclerotic cerebral infarction and TC, TG, HDL-C and Lp(a). There were also interactions between TC, TG, HDL-C and LDL-C. However, the strongest interaction is expected to happen at what level remains further investigations.