Records and objectives: This study is planned with the objective of identifying new efficacious risk vascular markers. For this work the hyperhomocysteinemia as independent thrombotic vascular risk factor, atherosclerosis as inflammatory illness and Heat Shock Proteins (HSP70i) as molecules likely involved in the vascular damage are considered.

Subjects and methods: Workers of the HGGM have volunteered and given their consent. 53 male (M) and 54 female (F) were studied randomly. Anamnesis and epidemiological questionnaire were performed. Arterial pressure was measured and blood samples were taken for neutrophils leukocytes isolation by gradient, biochemical study and DNA extraction. We performed quantification of homocysteine (tHcy)

by HPLC; Reactive-C-Protein (RCP), serum and intraleukocitary HSP70i, and HSP70i antibodies by ELISA; molecular study of the polymorphism of C677T of the enzyme metilentetrahidropholatereductase (MTHFR) by PCR-RFLP. Task force of coronary risk was applied for the population classification.

Results: The studied population present [tHcy] ≥ 11 umol/L in the 12% of the cases. The mutation C677T appears in heterozygote subjects (CT) in the 45% of the cases and in homozygote subjects in the 17%.

Subjects were classified into 3 groups: G-0, without vascular risk factors, n=77 (32M and 45F); G-1, with a moderated risk factor (>10%) but without illness n=26 (18M and 8F) and G-2, with an evident atherosclerotic illness n=4 (3M and 1F)

Conclusions: The following correlations have been proved:

  1. Inverse (p<0.05) between [tHcy] and [HSP70i] in neutrophils in females G-0 and males G1 wild type (CC)

  2. Inverse (p<0.05) between [tHcy] and serum [HSP70i] in males G-1 homozygotes (TT)

  3. Direct (p<0.05) between [tHcy] and [RCP] in females G-0 heterozygotes (CT)

  4. Direct (p<0.05) between [tHcy] and cholesterol in females G-0 homozygotes (TT)

  5. Direct (p<0.01) between [tHcy] and HTA in males G-0 heterozygotes (CT)

This study has been partially financed by FIS 03/1308

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