Pd. Stein et al., EFFECTS OF CYCLIC FLEXION OF CORONARY-ARTERIES ON PROGRESSION OF ATHEROSCLEROSIS, The American journal of cardiology, 73(7), 1994, pp. 431-437
The purpose of this investigation was to test the hypothesis that cycl
ic flexion of the coronary arteries contributes to the progression of
atherosclerotic plaques. Coronary arteriograms were evaluated in 33 un
selected patients who underwent 2 studies over a period of 25 +/- 16 m
onths (mean +/- SD). Among the 33 patients, 103 plaques were identifie
d. Plaques that showed progression were compared with plaques that sho
wed no progression. The angle of flexion that occurred during systole
at the site of the plaque was measured on the first arteriogram. In co
mparing progression versus no progression, the interval between arteri
ograms was 29 +/- 18 versus 23 +/- 14 months (p = NS) and percent sten
osis 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 a 1
9% 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 pla
ques that did not progress (p <0.01). Linear regression showed that th
e 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 ap
proximately 1.5 to 1.9 times greater with 20 degrees than with 10 degr
ees flexion. Stresses due to flexion were usually greatest proximal an
d distal to the plaque along the subendothelial layer of the inner wal
l of the curved vessel. Data show that the angle of cyclic flexion, an
d consequently the stresses due to cyclic flexion of the artery were g
reatest in the region of plaques that progressed over the period of ob
servation. Such stresses may have contributed to tissue damage or fati
gue resulting in a more rapid progression of the atheromatous plaques.