Homocyst(e)ine, nitrous oxide and atherosclerosis

Post-operative myocardial infarction (PMI) remains a significant health care problem. Recent evidence notes that its peak incidence is the first post-operative night, temporally implicating an intra-operative event. Beta-blockers have been shown to decrease post-operative myocardial ischaemia, PMI and to increase long-term survival although the mechanism of their benefit is unknown. However, many patients with known coronary artery disease (CAD) or associated risk factors for CAD are either already receiving beta-blockers or have contraindications to their use, necessitating other treatment approaches. Homocyst(e)ine when chronically elevated is a risk factor for coronary artery, cerebrovascular, vascular and venous thromboembolic disease. Acute elevations of homocyst(e)ine have been shown to produce endothelial dysfunction. Nitrous oxide, which inhibits methionine synthase, has been shown to cause elevations in post-operative homocyst(e)ine levels. This has recently been associated with increased post-operative myocardial ischaemia. Pre-operative treatment with folate and vitamins B6and B12appears to blunt the effect of nitrous oxide on plasma homocyst(e)ine levels.