AIM: Homocysteine (Hcy), a sulfur-containing amino acid product of methionine metabolism, may play an important role in the development of cardiovascular disease. In this paper we review available knowledge on the pathways leading to synthesis and degradation of Hcy, as well as on the genetic and environmental factors affecting its plasma levels, focussing on its potential role in the development of coronary heart disease. DATA SYNTHESIS: Hyperhomocysteinemia (HHcy) is determined by genetic and environmental factors and represents a modifiable cardiovascular risk factor since vitamin supplementation has been shown to effectively lower plasma homocysteine levels. While case-control and cross-sectional studies consistently showed an association of HHcy with cardiovascular disease, prospective studies have given conflicting results. Thus, the role of HHcy in the development of coronary heart disease is still under debate. Furthermore, it remains unclear which patients should be screened for HHcy and treated to correct HHcy. CONCLUSIONS: Available information collectively suggests that although HHcy can be regarded as a minor risk factor for coronary heart disease, it interacts with other risk factors in triggering new events in patients with known CAD. Thus, the treatment of mild HHcy with folate supplementation is appropriate in particular in high risk patients or patients with established CAD who do not present with the "traditional" risk factors.
AIM: Homocysteine (Hcy), a sulfur-containing amino acid product of methionine metabolism, may play an important role in the development of cardiovascular disease. In this paper we review available knowledge on the pathways leading to synthesis and degradation of Hcy, as well as on the genetic and environmental factors affecting its plasma levels, focussing on its potential role in the development of coronary heart disease. DATA SYNTHESIS: Hyperhomocysteinemia (HHcy) is determined by genetic and environmental factors and represents a modifiable cardiovascular risk factor since vitamin supplementation has been shown to effectively lower plasma homocysteine levels. While case-control and cross-sectional studies consistently showed an association of HHcy with cardiovascular disease, prospective studies have given conflicting results. Thus, the role of HHcy in the development of coronary heart disease is still under debate. Furthermore, it remains unclear which patients should be screened for HHcy and treated to correct HHcy. CONCLUSIONS: Available information collectively suggests that although HHcy can be regarded as a minor risk factor for coronary heart disease, it interacts with other risk factors in triggering new events in patients with known CAD. Thus, the treatment of mild HHcy with folate supplementation is appropriate in particular in high risk patients or patients with established CAD who do not present with the "traditional" risk factors.