Nowadays, vascular disease is the leading cause of death and disability in the western world, and then we could be anxious by the numbers. According to the World Health Organization report, 16.6 million people around the globe die of cardiovascular diseases each year. For example in 2001 there were 7.2 million deaths from heart disease and 5.5 million from stroke (American Heart Association, AHA).
Another 15 million each year survive minor strokes and may use drugs for better life.
We could also remember that 60 million people with high blood pressure are at risk of heart attack, stroke and cardiac failure. To summarize the situation, cardiovascular diseases contributed in 2001 to nearly one third of global death. Cardio-vascular disease risks factors in developing countries are the following: prevalence of high blood pressure, economic transition, urbanization, industrialization and globalization bring about lifestyle changes that promote stress and heart disease, tobacco (it generate approximately 30% of cardio-vascular deaths worldwide), high cholesterol (estimated to cause about 4.4 million death and a level of less 5.0 mmol/l is suggested for both primary and secondary prevention of cardiovascular diseases), global burden of diabetes in adults, overweight and obesity, and finally, excessive alcohol intake (near than 38% of men and 21% of women consume more than the recommended daily benchmarks) (AHA).
A response to this disease was found with the development of various therapeutic drugs corresponding to the diversity of the diseases, but this clinical care is costly, prolonged and we have to note that diseases affect individuals in their peak mid life years, disrupting the future of the families dependent on them and undermining the development of nations by depriving them of workers in their most productive years (AHA). In the other hand, another risk factor sort out, hyperhomocysteinemia.
In this domain pioneers who first described this factor were Buty and du Vigneau in 1932; the association between elevated homocysteine levels and human disease was suggested in 1962 by Carson and Neil and in 1969 Mc CulIy described the vascular pathology in this patients (smooth muscle proliferation, progressive arterial stenosis, haemostatic changes). Homocysteine, an amino acid, precursor of cysteine and glutathione, is generated in almost all tissues in the human body and approximatively eighty percent is bound to proteins in human body and the remaining 20% is found in three forms: oxidized, mixed disulfide cysteine and a small amount of free homocysteine. Normal range of homocysteinemia is about 8.0 to 14.0 mmol/l for male and 6.0 to 12.0 for female. High levels of homocysteine in the body due to metabolic abnormalities (5,10-methylenetetrahydrofolate reductase deficiency, cystathionine beta synthase) can lead to the auto-oxidation of homocysteine and converting to toxic free radicals.
So, we can find different forms of hyperhomocysteinemia: moderate (16-30 mmol/l), intermediate (31-100 mmol/l) and severe (> 100 mmol/l).
The prevalence of hyperhomocystememia, is 5% in general population and 13-41% among patients with symptomatic atherosclerotic vascular disease and the Mechanisms of homocysteine toxicity could be classify in Endothelial dysfunction generation (impairment of nitric oxide production, over production of reactive oxygen species, increased of Von willebrand factor and thrombomodulin, increased tissue factor production), effect on coagulation factors, participation to oxidation stress, oxidation of low density lipoproteins. Now we could insist on the worst effect of high extracellular levels homocysteine and its correlation with endothelin-1 defect (homocysteine decrease endothelin-1 expression by interfering with the AP-1 signalling pathway), and the possibility of L-homocysteine sulfinic acid and other acidic homocysteine derivatives are potent and selective metabotropic glutamate receptor agonists. Growth effect of homocysteine on vascular smooth muscle cells may be mediated by a novel NMDA-like glutamate gated calcium ion channel receptor, a receptor with anatomic and physiological properties distinct from other NMDA receptors.

Homocysteine blood levels is affecting by age, sex (explain by effects of sex hormones on the homocysteine metabolism), smoking and genetic factors.

Recently it appeared that hyperhomocysteinemia may contribute to heart failure and results showed that high homo-cysteine levels were associated with a risk of heart failure in both men and women but appeared to be more consistent in women than men (Vasan and colleagues report). And while there is not strong evidence to suggest that lowering homocysteine levels is beneficial, we could say that people at high risk should be sure to get enough folic acid, from foods as leafy greens and fortified breakfast cereals, as well as two other B vitamins, 6 and 12, these vitamins are knows to aid the breakdown of homocysteine in the body and other treatment (symptomatic or curative) are required for the diseases which could be associated with hyperhomocysteinemia such neural tube defects, pernicious anaemia, renal impairment, hypothyroidism, malignancy, severe psoriasis, myocardial infarction or thrombogenesis.