ABSTRACT
Homocyst(e)ine refers to a family of sulfated amino acids associated with premature, systemic atherosclerosis and prothrombotic disorders. In 1962, the first observation of elevated homocyst(e)ine associated with cerebrovascular disease was reported in children and young adults with homozygous homocystinuria secondary to deficiency of cystathionine synthase (1,2). In 1969, McCully suggested that moderate levels of homocyst(e)ine could be associated with atherosclerosis (3). Boers and co-workers reported in 1985 that homocyst(e)ine levels of 14 mmol/L or higher were present in approximately 30% of patients with symptomatic peripheral and cerebrovascular disease, but not coronary artery disease (4). This observation was corroborated by Clarke et al. who noted that about 30% of patients with premature atherosclerosis have plasma homocyst(e)ine levels >14 mmol/L (5). Several observational studies have shown that elevated homocyst(e)ine is associated with a high risk of ischemic stroke (6-11). Plasma homocyst(e)ine >10.2 mmol/L doubles the vascular risk of patients with lower levels (12). If plasma homocyst(e)ine rises above 20 mmol/L, then vascular risk increases 8-fold compared to levels below 9 mmol/L (13).
