Differential enlargement of artery segments in response to enlarging atherosclerotic plaques

Abstract

We studied the relationships among intimal plaque area, lumen area, and artery size in 481 sections of the left anterior descending (LAD) coronary artery taken at four standard sampling sites in 125 pressure-perfusion-fixed postmortem adult human hearts. The internal elastic lamina area was considered to be a measure of artery size or potential lumen area. Artery size correlated strongly with intimal plaque area at each LAD level (p less than 0.0001). Stepwise regression analysis revealed that plaque area was the principal determinant of artery size at each LAD level (r2 = 0.20 to 0.33). Sections of arteries with the most intimal plaque (highest quartile) were compared with those with the least plaque (lowest quartile) at each sample site. In the proximal LAD artery, the most severely diseased arteries increased in size 62% but lumen area decreased 25%. In the midportion of the LAD artery, plaque area was 10 times greater in the most diseased arteries, but lumen area remained normal because of an 80% increase in artery size. In the most severely diseased distal LAD artery sections, despite a fourteenfold increase in plaque area, lumen area almost doubled because of a marked increase in artery size. If no enlargement had occurred, the most severely diseased arteries in the proximal LAD segment would have developed a 92% lumen stenosis rather than the observed 25% lumen stenosis. In the distal LAD artery, without enlargement there would have been a 65% lumen stenosis rather than the 85% increase in lumen area that was found.(ABSTRACT TRUNCATED AT 250 WORDS)

Longitudinal study of vascular remodeling in coronary arteries after heart transplantation

“…This initial enlargement of the vessel may even overcompensate for the amount of plaque area and dilation of the vessel that occurs. Other authors including Zarins et al 3 have found that the distal left anterior descending coronary artery segments demonstrated a greater propensity to enlarge in response to expanding plaque than the proximal segments. This author postulated that smaller coronary arteries may have more smooth muscle and fewer elastic and collagen fibers than larger ones.…”

Flow affects development of intimal hyperplasia after arterial injury in rats.

“…There is evidence that shear may modulate structure in diseased vessels as well. Glagov et al 25 and Zarins et al 26 found that human coronary arteries dilate as atherosclerotic plaque accumulates, perhaps in response to increased blood velocity and shear. Fatty streaks in cholesterol-fed animals, atherosclerotic plaques in humans, and wall thickening in vein grafts all tend to occur in areas of low fluid shear.…”

Coronary arterial remodeling in differing clinical presentations of unstable angina pectoris—an intravascular ultrasound study

“…38 In- vestigators have previously demonstrated by IVUS that the plaques at the site of the culprit lesion in patients with acute coronary syndromes are larger and have more remodeling. [10][11][12][13][14][15][16][17][18] Our study shows that such large plaques are even more prevalent in the subset of patients with new-onset angina. These lesions have been characterized as more vulnerable, and the natural history of recent onset unstable angina has been shown to be more adverse than that in patients who have progressive or accelerating angina.…”

“…[5][6][7][8][9] Vascular remodeling was first described pathologically as compensatory enlargement of the diseased artery. [10][11][12][13][14][15][16][17][18] More recently, pathology and IVUS studies have also shown that compensatory enlargement is often inadequate to preserve lumen size completely, and that some vessels may not remodel or, paradoxically, may even shrink at the lesion site. [19][20][21][22][23][24][25][26] Positive remodeling and larger plaques have been associated with acute coronary syndromes.…”