<![CDATA[ABSTRACT Hyperhomocysteinemia appears to be an independent risk factor for coronary heart disease. Elevated levels of plasma total homocysteine (tHcy) was caused by genetic or nutrient-related disturbances in the transsulfuration or remethylation pathways for homocysteine metabolism. This study observed premature myocard infarct acute patients with hyperhomocysteinemia.The aim of the research was to determine Cystarhionine-β Synthase and Methylenetetrahydrofolate Reductase genes mutations in premature acute myocard infarct patients with hyperhomocysteinemia.This study was a cross sectional study in premature acute myocard infarct patients. Twenty three patients were examined for plasma total homocysteine, vitamin B6, vitamin B12 folic acid and lipid profile. Total DNA isolated from patients with hyperhomocystememia and normal folic acid, vitamin B6, vitamin B12 levels and lipid profile. Five patients were assayed for Cystathionine-β Synthase and gen Methylenetetrahydrofolate Reductase genese mutations by Polymerase Chain Reactions (PCR). Five from 23 patients ( 21,7% ) plasma total]]>
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