FIGURE 6.4 Kaplan-Meier survival curves for freedom from major adverse events in 553 patients following percutaneous transluminal coronary angioplasty. (From Schnyder, G. et al., JAMA, 288, 973, 2000. With permission.)

damage and dysfunction,199206 (3) encouraging oxidation of LDL,207,208 (4) smooth muscle proliferation,209210 and (5) endothelium-leukocyte interactions.211 Although endothelial cells initially respond to homocysteine by increasing nitric oxide synthesis,212 prolonged exposure213 and high homocysteine concentrations214 lead eventually to a fall in nitric oxide production.

Homocysteine may also promote thrombogenesis both by increasing factor V activity,215 reducing antithrombin III216 and protein C217 activity, and impairing fibrinolysis.218

Homocysteine levels rise with age, which may be a reflection of particularly poor intake of vitamins B12 and B6 and folate in the elderly population.219 High folate levels seem to be protective for cardiovascular disease.192,220 Homocysteine can be lowered with folic acid and vitamin b6.221,222 This therapy is associated with a decreased occurrence of abnormal exercise tests223 and an improvement in endothelial function.224 Homocysteine-lowering therapy reduced the incidence of events225 and restenosis226 in 533 patients randomised to vitamin supplementation (B12, folate, and vitamin B6) or placebo following percutaneous coronary intervention (Figure 6.4).

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