Cardiovascular Disease and Risk Factors

Based on prospective and experimental data, mild to moderate elevation of homocysteine is a stabilized and independent risk factor for cardiovascular disease. The hyperhomocystenemia is consequence of inhibition of transsulphuration pathway or inhibition of remethylation pathway of homocysteine metabolism, transsulphuration is mediated by CBS and remethylation is mediated directly by MS and indirectly by MTHFR. The SNPs in the genes, express these enzymes may or may not responsible for mild to moderate hyperhomocystenemia. The elevated homocysteine choke the vessels by endotelial cell injury by increased oxidative stress and reduced bioavalibility of nitric oxide, increased platelet adhesiveness, enhanced LDL deposition on arterial wall and activation of coagulation cascade. The some environmental factors are known to contribute in progression of disease may also associated with elevated homocysteine concentration.