In series of patients with stroke, selected by random (n = 68), mean age 62.44 +/- 9.12 years (range 39-82 yrs), there were 23 females (33.8%), mean age 65.43 +/- 10.11 yrs and 45 males (66.2%) mean age 60.8 +/- 8.3 yrs. Lp(a) reference values have been obtained from a group of 283 healthy individuals (age ranging from 15 to 65 years). The cholesterol, triacyglycerol, Apo B reference values come from the database of the Department of Clinical Biochemistry. There were 52 hypoxemic stroke patients in the whole observed group. Triacylglycerol serum level TAG < or = 2.89 mmol/l was observed in 47 cases (90.3%), the serum level TAG > 2.89 mmol/l was present in 5 cases (9.7%). The occurrence of TAG normal serum level was significantly more frequent than its pathologic increase (p < 0.001). Apolipoprotein Apo B < or = 1.67 g/l serum level was present in 41 (78.8%) and Apo B > 1.67 g/l in 11 (21.2%) cases (p < 0.001). Apo B < or = 1.67 g/l serum levels in 23 cases (82.1%) and Apo B > 1.67 g/l in 5 cases (18%) were observed among the stroke diabetes mellitus patients (n = 28)--statistic difference in 1/1000 level. In the total hypoxemic stroke group (n = 52), Lp(a) < or = 0.278 g/l was observed in 44 cases (84.6%), Lp(a) > 0.278 g/l serum level was present in 8 cases (15.4%)/ - p < 0.001. According to EASD consensus the serum level of Lp(a) = 0.278 g/l has been considered as "cut-off limit". Similar distribution of Lp(a) serum levels was observed in the diabetes mellitus stroke group (n = 28), the ischemic heart group (n = 54), the group with aortosclerosis (n = 16) and in the group with arterial hypertension (n = 50). Elevated TAG serum levels were not in correlation with the number of sites where atherosclerotic changes were proved by arteriography, ultrasound investigation e.g. in the extracranial brain supplying arteries. Elevated Lp(a) serum levels did not correlate with the stage of ischemic heart disease and they correlated with the stage of functional CNS defect in arterial hypertension and atherosclerosis. Metabolic disorders of lipoprotein and apolipoprotein, namely genomic transcription of lipoprotein seem to be more significant risk stroke factors, but, if they are present, they contribute to the occurrence of arteriosclerosis of some larger arteries. Elevated Lp(a) serum levels did not correlate with the stage of the heart ischemic disease and aortosclerosis, but they correlate with the stage of functional CNS defect due to arteriosclerosis and arterial hypertension, hence the increase in Lp(a) serum level as an indicator of arteriosclerotic evolution of cerebral arteries is significant. Our results, hence, do confirm a common supposition for Lp(a) serum level as an independent arteriosclerotic risk factor of the brain arteries. (Fig. 7, Tab. 1, Ref. 22.)