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. 1994 Mar 1;73(7):431-7.
doi: 10.1016/0002-9149(94)90671-8.

Effects of cyclic flexion of coronary arteries on progression of atherosclerosis

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Effects of cyclic flexion of coronary arteries on progression of atherosclerosis

P D Stein et al. Am J Cardiol. .

Abstract

The purpose of this investigation was to test the hypothesis that cyclic flexion of the coronary arteries contributes to the progression of atherosclerotic plaques. Coronary arteriograms were evaluated in 33 unselected patients who underwent 2 studies over a period of 25 +/- 16 months (mean +/- SD). Among the 33 patients, 103 plaques were identified. Plaques that showed progression were compared with plaques that showed no progression. The angle of flexion that occurred during systole at the site of the plaque was measured on the first arteriogram. In comparing progression versus no progression, the interval between arteriograms was 29 +/- 18 versus 23 +/- 14 months (p = NS) and percent stenosis at the first arteriogram was 42 +/- 28 versus 45 +/- 19% (p = NS). Percent stenosis at the time of the second arteriogram among plaques that progressed was 78 +/- 21%, and by definition, it remained 45 +/- 19% among those that did not progress. Among arteries with plaques that showed a progression of stenosis, the angle of flexion during systole was 19 +/- 13 degrees versus 9 +/- 15 degrees among arteries with plaques that did not progress (p < 0.01). Linear regression showed that the correlation of the angle of flexion with percent change of stenosis was relatively low (r = 0.32) but statistically significant (p < 0.005). Mathematic modeling of flexible and stiff plaques showed stresses approximately 1.5 to 1.9 times greater with 20 degrees than with 10 degrees flexion. Stresses due to flexion were usually greatest proximal and distal to the plaque along the subendothelial layer of the inner wall of the curved vessel. Data show that the angle of cyclic flexion, and consequently the stresses due to cyclic flexion of the artery were greatest in the region of plaques that progressed over the period of observation. Such stresses may have contributed to tissue damage of fatigue resulting in a more rapid progression of the atheromatous plaques.

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