Author + information
- Received March 3, 1994
- Revision received June 3, 1994
- Accepted June 30, 1994
- Published online December 1, 1994.
- ↵∗Address for correspondence: Dr. Richard T. Lee, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis Street, Boston, Massachusetts 02115.
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.
↵1 Dr. Loree is the recipient of National Research Service Award 2 T32 GM07753-12 from the National Heart, Lung, and Blood Institute National Institutes of Health, Bethesda, Maryland.
☆ This study was supported in part by a Grant-in-Aid from the American Heart Association, Massachusetts Affiliate, Framingham, Massachusetts.
- Received March 3, 1994.
- Revision received June 3, 1994.
- Accepted June 30, 1994.