Coronary artery bypass grafting surgery is associated with a marked reduction in serum homocysteine and folate levels in the early postoperative period.

OBJECTIVE It has been suggested that cardiac surgery-related ischemia-reperfusion injury to the myocardium is caused by the oxidative stress, derived from the formation of reactive oxygen species in the early phases of the reperfusion. The availability of cysteine, mostly deriving from homocysteine (Hcy) via the trans-sulfuration pathway, is determinant for the synthesis of glutathione (GSH), which in turn acts as a first line of defence against oxidative stress. Indeed, an increased consumption of Hcy in response to oxidative stress has been described. Previous research has shown that Hcy levels increase during the first weeks or months after coronary artery bypass grafting (CABG). This study was designed to evaluate the Hcy metabolism in CABG patients during the early postoperative period. METHODS Serum Hcy and folate were measured by an automatic immunometric system on blood samples obtained from 48 (mean age 67+/-10 years) consecutive patients undergoing CABG, preoperatively and at 0, 12, 48, and 120 h after surgery. A subgroup of 22 of these patients was also studied 6 months postoperatively. RESULTS A significant decrement of Hcy and folate was observed throughout the study (P<0.0001) from 17.3+/-9.3 to 8.5+/-5.6 micromol/l at 12 h postoperatively for Hcy, and from 5.1+/-2.8 to 2.5+/-1.5 ng/ml at 48 h for folate. The reduction of Hcy and folate levels remained significant after correction for haemodilution (as assessed by measurement of plasma proteins). Furthermore, the use of cardiopulmonary bypass significantly interacted with the time of sampling in affecting the Hcy levels. Hcy levels returned to near-baseline values 48 h postoperatively, and were similar to base-line at follow-up. CONCLUSION Our study indicates that serum Hcy and folate levels are markedly reduced during the early postoperative period after CABG. This reduction is at least in part independent of haemodilution, and may be caused by an altered Hcy turnover, due to an increased consumption of GSH during and soon after CABG.