High stress regions in saphenous vein bypass graft atherosclerotic lesions

Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.

OBJECTIVES. Our aim was to test the hypothesis that maximal stresses in saphenous vein atherosclerotic stenoses are greater than those in native coronary artery stenoses. BACKGROUND. The patency of coronary artery saphenous vein bypass grafts decreases with time, usually because of thrombosis. Plaque rupture has been described as one mechanism of vein graft thrombosis. METHODS. Twenty-six nonruptured human lesions were studied. Fourteen lesions were from native coronary arteries, and 12 were from saphenous vein bypass grafts placed a mean +/- SD of 9.8 +/- 3.3 years before pathologic study. The finite element method was used to determine the distribution of stress in the lesion, using estimates of material properties from previous measurements of human tissues. RESULTS. Maximal circumferential stresses were significantly higher in the saphenous vein lesions (median 352 kPa [interquartile range 161 to 475]) than in the coronary artery lesions (median 104 kPa [interquartile range 75 to 185]) (p = 0.05). Thin-walled cylinder formulations predict that stresses are proportional to the radius of the vessel and inversely proportional to the minimal wall thickness. In this study, there was a good correlation between the maximal stress in the 26 lesions and the ratio of the square root of lumen area to minimal fibrous cap thickness (r = 0.83, p < 0.001). CONCLUSIONS. Maximal circumferential tensile stresses in saphenous vein bypass graft stenoses are higher than in native coronary artery atherosclerotic stenoses. These data suggest that strategies that decrease stresses in bypass graft atherosclerotic lesions, such as prevention of lipid accumulation, could reduce the probability of plaque rupture in bypass grafts.

This article has been cited by other articles:

				S.-A. Hassantash, B. Bikdeli, S. Kalantarian, M. Sadeghian, and H. Afshar Pathophysiology of Aortocoronary Saphenous Vein Bypass Graft Disease Asian Cardiovasc Thorac Ann, August 1, 2008; 16(4): 331 - 336. [Abstract] [Full Text] [PDF]

				M J A Williams, C J S Low, G T Wilkins, and R A H Stewart Randomised comparison of the effects of nicardipine and esmolol on coronary artery wall stress: implications for the risk of plaque rupture Heart, October 1, 2000; 84(4): 377 - 382. [Abstract] [Full Text]

				O Gurne, P Chenu, M Buche, Y Louagie, P Eucher, B Marchandise, E Rombaut, D Blommaert, and E Schroeder Adaptive mechanisms of arterial and venous coronary bypass grafts to an increase in flow demand Heart, September 1, 1999; 82(3): 336 - 342. [Abstract] [Full Text] [PDF]

				Y. Sakakibara Minimally Invasive Axillary-Coronary Artery Bypass Ann. Thorac. Surg., April 1, 1998; 65(4): 1197 - 1197. [Full Text] [PDF]

				R. T. Lee, F. J. Schoen, H. M. Loree, M. W. Lark, and P. Libby Circumferential Stress and Matrix Metalloproteinase 1 in Human Coronary Atherosclerosis: Implications for Plaque Rupture Arterioscler. Thromb. Vasc. Biol., August 1, 1996; 16(8): 1070 - 1073. [Abstract] [Full Text]