Abstract
Conclusion: Aggressive lipid-controlling therapy may be effective in preventing saphenous vein graft disease after coronary artery bypass grafting (CABG). Summary: About 25% of saphenous vein grafts occlude ≤1 year of CABG, and 50% occlude ≤ 10 years (Am Heart J 1990;119:1164-84). Despite their relative unfavorable natural history, saphenous vein grafts are still used in >70% of CABG procedures. It appears that plaque rupture with thrombus formation are a major cause of long-term saphenous vein graft disease after CABG (Circulation 2007;71:286-7). It also appears that lowering low-density lipoprotein cholesterol (LDL-C) <100 mg/dL may be effective in reducing atherosclerosis in saphenous vein grafts. In this study, the authors sought to investigate the efficacy of aggressive statin therapy on angioscopic-determined progression of saphenous vein graft disease after CABG. There were 21 patients after CABG divided into two groups. Group I comprised 10 patients whose serum LDL-C levels and LDL/high-density lipoprotein (HDL) ratios could be controlled to <80 mg/dL and <1.5, respectively. Group II consisted of 11 patients whose LDL-C levels and LDL/HDL ratios were >100 mg/dL and >2.5, respectively. Twenty-seven saphenous vein grafts were assessed by intravascular ultrasound (IVUS) and angioscopy at 12 to 16 months postoperatively. Serum LDL-C levels in group I were 64.1 vs 130.2 mg/dL in group II. LDL/HDL ratios in group I were 1.36 vs 2.64 in group II. High-sensitivity C-reactive protein in group I was 0.045 ± 0.1 vs 0.116 ± 0.02 mg/dL in group II. All values were significantly lower in group I. In group II, IVUS detected eccentric plaques in 11 of 14 saphenous vein grafts (78.6%). Yellow plaque was present in all 14 saphenous vein grafts by angioscopy, and 11 of these grafts had thrombi. The 13 saphenous vein grafts in group I had no eccentric or yellow plaques, and no thrombi were visible. The intima was entirely clear white. Comment: The mechanism of failure of saphenous vein grafts in the coronary circulation may be different than that in the peripheral circulation. However, the idea that driving down LDL-C and C-reactive protein levels may improve vein graft patency is intriguing for the peripheral vascular surgeon as well. Indeed, there is evidence suggesting higher primary assisted and secondary patency in lower extremity vein grafts in patients treated with statins (J Vasc Surg 2004;39:1178-85). Well-designed prospective data are needed to assess the effects of statins on suppression of peripheral vein graft lesions.
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