caa a22 4500 47582380X CHVBK 20180406123825.0 cr unu---uuuuu 170329e20000101xx s 000 0 eng 10.1023/A:1018675624181 doi (NATIONALLICENCE)springer-10.1023/A:1018675624181 Homocysteine and Risk of Cardiovascular Disease [Elektronische Daten] [Felicita Andreotti, Francesco Burzotta, Alessandro Manzoli, Killian Robinson] This pictorial introduction to homocysteine illustrates at a glance the nature of homocysteine and its role in cardiovascular disease by means of eight simple figures and an essential bibliography. Homocysteine is a sulfur-containing metabolite of methionine. Conversion back to methionine or transsulfuration to cysteine are the two major metabolic pathways that reduce total homocysteine (tHcy) concentrations in cells and blood. B vitamins are essential cofactors in homocysteine metabolism. Median fasting total homocysteine levels in adult males are ∼10 µmol/L. Increased plasma tHcy concentrations are found with methionine-rich diets, low vitamin B intake, male gender, age, impaired renal function, and genetically determined defects of the enzymes involved in homocysteine metabolism. An inverse relation exists between plasma tHcy and circulating folate or vitamin B6 concentrations, and folic acid supplements of 0.5 mg/d can reduce tHcy levels by ∼25%. Homocystinuric patients, who have severe hyperhomocysteinemia, die prematurely of atherothrombotic disease. Many (but not all) cross-sectional and prospective studies indicate, on average, that plasma tHcy levels <.10 µmol/L are associated with, or predict the development of, coronary, cerebral, and peripheral vascular disease. The risk conferred by hyperhomocysteinemia is graded and is independent of traditional risk factors, with an estimated odds ratio for ischemic heart disease of 1.4 for every 5 µmol/L increase in plasma tHcy. In vitro and in vivo, tHcy has been found to impair endothelial function. It is now well established that tHcy represents a marker of current or subsequent ischemic vascular disease. However, irrefutable proof that hyperhomocysteinemia actually causes atherothrombosis will come only if interventions to lower plasma tHcy will produce concomitant reductions in cardiovascular events. Kluwer Academic Publishers, 2000 homocysteine nationallicence cardiovascular disease nationallicence risk nationallicence Andreotti Felicita Institute of Cardiology, Catholic University, Rome, Italy aut Burzotta Francesco Institute of Cardiology, Catholic University, Rome, Italy aut Manzoli Alessandro Institute of Cardiology, Catholic University, Rome, Italy aut Robinson Killian Department of Cardiology, The Cleveland Clinic Foundation, Cleveland, Ohio, USA aut Journal of Thrombosis and Thrombolysis Kluwer Academic Publishers 9/1(2000-01-01), 13-21 0929-5305 9:1<13 2000 9 11239 https://doi.org/10.1023/A:1018675624181 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1023/A:1018675624181 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Andreotti Felicita Institute of Cardiology, Catholic University, Rome, Italy aut NATIONALLICENCE 700 1- Burzotta Francesco Institute of Cardiology, Catholic University, Rome, Italy aut NATIONALLICENCE 700 1- Manzoli Alessandro Institute of Cardiology, Catholic University, Rome, Italy aut NATIONALLICENCE 700 1- Robinson Killian Department of Cardiology, The Cleveland Clinic Foundation, Cleveland, Ohio, USA aut NATIONALLICENCE 773 0- Journal of Thrombosis and Thrombolysis Kluwer Academic Publishers 9/1(2000-01-01), 13-21 0929-5305 9:1<13 2000 9 11239 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer