An increased concentration of total homocysteine is a still disputable as a independent risk factor for cardiovascular diseases and also a predictor of cerebrovascular diseases, especially of stroke (1). There is no doubt that hyperhomocysteinemia plays an important role in the atherosclerotic and thromboembolic process and promotes them. The mechanisms of these processes are very complicated and depend on many factors like the concentration of foliate, vitamin B12 and B6. It is also important that the concentration of increased serum homocysteine correlates with the state of vascular damage. Experimental data suggest that homocysteine has an influence on the oxidative arterial injury, damaging the vascular matrix and augmenting the proliferation of vascular smooth muscle. Homocysteine also alters the coagulation properties of the blood and impairs endothelium-dependent vasomotor regulation.
The reference value of the normal homocysteine concentration is between 5-15 μmol/l and this value is widely and commonly used. In this paper we present and discuss the association between hyperhomocysteinemia and types of stroke according to the Oxfordshire Community Stroke Project (OCSP) (2).
We examined 193 patients (tab. 1a, 1b, 2) with acute ischemic stroke (83 men and 110 women, aged 53 to 96 years, mean 71.60 years), successively admitted to the Department of Neurology and Epileptology of the Center for Postgraduate Medical Education in Warsaw. The diagnosis of ischemic stroke was based on a history of sudden onset of a fixed neurological focal deficit of presumed ischemic origin lasting more than 24 hours. CT of the brain was performed on all patients to exclude other causes of neurological symptoms. Patients were classified into one of four stroke types according to the OCSP classification: TACI (Total anterior circulation infarction), PACI (Partial anterior circulation infarction), LACI (Lacunar infarction) and POCI (Posterior circulation infarction) (2). Group characteristics (stroke patients and controls with other neurological disease) are summarised in table 3. The local Ethics Committee of the Center for Medical Postgraduate Education in Warsaw approved this study.
Table 1a. Demographic data of group: gender and age.
Table 1b. Demographic data of group: gender and age.
Table 2. The concentration of homocysteine in group patients with stroke and controls.
Table 3. Demographic data of group HC1 (patients with homocysteine concentrations over 15 μmol/l) and HC2 (patients with homocysteine concentrations below 15 μmol/l).
Peripheral blood was obtained in the first 48 hours after onset of symptoms of stroke. The blood has been immediately centrifuged. Serum was stored at -20oC. Total plasma homocysteine concentrations were measured by fluorescence polarisation immunoassay (FPIA-ABBOTT) (3). We considered a homocysteine concentration > 15 μmol/l as pathological basing our findings on Ueland’s study (4). Therefore patients for analysis were divided into two groups: patients with the homocysteine concentration in sera < 15 μmol/l and the homocysteine concentration in sera > 15 μmol/l.
The statistical analyses were performed by Statistica (StatSoft, USA) version 6.0. For descriptive purposes, univariate analysis with either the chi-square test or Fisher’s exact test (depending on the sample size) was used to perform evaluation of frequency distribution proportionality for categorical variables, while one-way analysis of variance (ANOVA) was used for continuous variables. The statistical significance of differences between groups was evaluated by the non-parametric Mann-Whitney U test. Multivariate logistic regression with odds ratio (OR) was performed.
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