Lipoprotein(a) and other risk factors for cerebral infarction

The serum concentration of lipoprotein(a) [Lp(a)], lipids, lipoproteins, apolipoprotein A-I, and apolipoprotein B were determined in 228 patients with cerebral infarction, composed of 87 cases of asymptomatic lacunar infarction, 99 cases of lacunar infarction, and 42 cases of atherothrombotic infarction, and in a control group of 138 healthy subjects with normal MRI. Observations were made on the distribution of Lp(a), Lp(a) and other risk factors for cerebral infarction and these were statistically analyzed, primarily by multiple logistic regression analysis. The diagnosis of these cases was based on the Classification of Cerebrovascular Diseases III of the National Institute of Neurological Disorders and Stroke. The following results were obtained. 1) Lipoprotein (a) (1) Lp(a) did not show a normal distribution with the curve showing a gradual declining slope to the right. It was therefore considered not appropriate in our analysis to use as a means or standard deviation. (2) The 25th percentile, 50th percentile, and 75th percentile of the control group were 5.0 mg/dl, 11.0 mg/dl, and 22.4 mg/dl, respectively. In studying the distribution in these percentile ranges by subtypes of infarction, an increase in cases showing values greater than the median of the control group was observed in asymptomatic lacunar infarction, lacunar infarction, and atherothrombotic infarction, when compared to the control group. In asymptomatic lacunar infarction and lacunar infarction in particular, Lp(a) showed a significantly higher value compared to the control group. (3) However, by multiple logistic regression analysis to adjust for age and sex, Lp(a) did not show a significant odds ratio for asymptomatic lacunar infarction, lacunar infarction and atherothrombotic infarction. 2) Various serum lipids and other parameters (1) The various serum lipids did not show any involvement in asymptomatic lacunar infarction. However, involvement of HDLC and Apo A-I in lacunar infarction and atherothrombotic infarction was observed with the odds ratios in lacunar infarction being 4.2 with a confidence interval of 2.9-9.4 and 4.7 with a confidence interval of 2.2-10.1, and the odds ratios in atherothrombotic infarction being 3.1 with a confidence interval of 1.1-9.0 and 9.6 with a confidence interval of 3.0-30.5, respectively. (2) Involvement of diabetes mellitus in asymptomatic lacunar infarction and lacunar infarction was small, but a strong involvement in atherothrombotic infarction was observed with the odds ratio being 4.3 with a confidence interval of 1.2-16.2. (3) Involvement of hypertension in asymptomatic lacunar infarction and lacunar infarction was observed with the odds ratios being 2.6 with a confidence interval of 1.4-5.2 and 5.6 with a confidence interval of 2.4-13.0, respectively, but the involvement in atherothrombotic infarction was low. The foregoing results indicated that there was no involvement of Lp(a) as a risk factor for any type of cerebral infarction, unlike its involvement in coronary heart diseases. Only blood pressure was involved as a risk factor for asymptomatic lacunar infarction, but for lacunar infarction not only blood pressure but also HDLC and Apo A-I were involved as risk factors. HDLC, Apo A-I, and diabetes mellitus were involved as risk factors for atherothrombotic infarction, but the involvement of hypertension was minimal.