Homocysteine

Although homocysteine is widely assumed to be an established risk factor for atherosclerotic disease, little prospective clinical trial or epidemiologic evidence supports this (Christen and Ridker, 2000). It has been known for decades that patients with homocystinuria have increased risk for CAD, stroke, PAD, and thromboembolic events (Handy and Loscalzo, 2003). Many documented enzyme mutations are etiologic for hyperhomocysteinemia, which is associated with increased endothelial dysfunction and hypercoagulability. Mutations in methylenetetrahydrofolate reductase, cystathionine-p-synthase, methionine synthase, and y-cystathionase can lead to elevations in serum homo-cysteine levels. The supplementation of patients with folate and vitamins B6 (pyridoxine) and B12 (cyanocobalamin) frequently helps to normalize the levels of patients with hyper-homocysteinemia. These three vitamins are available in a single combination formulation (Folbee, Foltx).

Two clinical trials evaluating folate/B6/B12 supplementation in patients with CAD and undergoing percutaneous transluminal coronary angioplasty (PTCA) demonstrate the contradictory nature of some data in this field. In one study, triple-vitamin therapy resulted in reduced rates of atheromatous plaque progression, in-stent restenosis, and need for subsequent revascularization of the target lesion (Schnyder et al., 2001). In a subsequent study, triple-vitamin therapy showed increased rates of plaque progression as well as increased in-stent restenosis and need for target lesion revascularization (Lange et al., 2004). The AHA and American College of Cardiology (ACC) currently discourage widespread screening for hyperhomocysteinemia. Seven different randomized, placebo-controlled trials (RCTs) are pro-spectively evaluating whether treatment of homocystinemia reduces risk for cardiovascular morbidity and mortality.

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