Poster presentation | Open | Published:
Role of homocysteine in the development of the cerebral and cardiovascular pathology in young persons
Critical Carevolume 10, Article number: P366 (2006)
Cerebral and cardiovascular pathology is the leading cause of the death and invalidity in industrially developed countries. During recent years new data allowed to increase significantly the presentations of the pathogenesis of these diseases. They revealed that hyperhomocysteinemia increases the risk of early development of atherosclerosis and thrombosis of the coronary, cerebral and peripheral arteries independently of the traditional risk factors and it is the prognostic marker of the lethal outcome.
The objective of this study was to appreciate the role of homocysteine in the development of the cerebral and cardiovascular pathology (ischemic stroke, myocardial infarction) in young persons. We examined 28 patients during an acute period of the ischemic stroke (IS) and 10 patients with acute myocardial infarction (AMI) (mean age 45.1 ± 1.15 and 40.9 ± 2.34 years). Clinical evaluation of the neurological status of the patients with IS was conducted traditionally and according to the international clinical scales determining neurological deficiency (Bartela, NIH-NINDS, Orgogoso, Scandinavian, Index of the Disorders of Adoptive Activity) at patient's admission. The control group consisted of 15 healthy subjects (mean age 44.7 ± 1.02 years). The homocysteine concentration in the blood was analyzed in all fasting patients on the immunochemoluminescent analyzer 'IMMULITE One' (USA) using the assay kit of 'DPC' production (USA).
We revealed the presence of the moderate hyperhomocysteinemia in the patients with IS and AMI. The mean concentration of the serum homocysteine exceeded the mean concentration of this metabolite in healthy subjects by 57% and 48%, respectively.
The patients with IS had dependence of the clinical course of the disease on the homocysteinemia level. In mild (n = 7) and moderate (n = 9) neurological deficiency, the mean concentration of homocysteine was 8.1 ± 0.65 and 10.8 ± 1.44 μmol/l respectively. In expressed and gross (n = 11) neurological deficiency, the mean concentration of homocysteine was 16.0 ± 2.44 μmol/l, which exceeded the control value by 85%. In two patients with gross neurological deficiency and the highest values of homocysteine, the disease finished by fatal outcome. All patients with increased homocysteine concentration had atherosclerotic changes of the vessels that were uncharacteristic for their age. All patients had the atherothrombotic subtype of IS.
The development of AMI and the severe degree of the atherothrombotic subtype of IS in young persons may thus be conditioned by increased homocysteine concentration provoking early formation of the atherosclerotic changes of the vessels and thrombosis. The obtained data may be useful in the composition of programs of the prophylactic measures.