Compensatory enlargement of human atherosclerotic coronary arteries


Glagov S, Weisenberg E, Zarins CK, et al. Reference

N Engl J Med 1987; 316: 1371-1375 Abstract

Whether human coronary arteries undergo compensatory enlargement in the presence of coronary disease has not been clarified. We studied histological sections of the left main coronary artery in 136 hearts obtained at autopsy to determine whether atherosclerotic human coronary arteries enlarge in relation to plaque (lesion) area and to assess whether such enlargement preserves the cross-sectional area of the lumen. The area circumscribed by the internal elastic lamina (internal elastic lamina area) was taken as a measure of the area of the arterial lumen if no plaque had been present. The internal elastic lamina area correlated directly with the area of the lesion (r = 0.44, p less than 0.001), suggesting that coronary arteries enlarge as lesion area increases. Regression analysis yielded the following equation: Internal elastic lamina area = 9.26 + 0.88 (lesion area) + 0.026 (age) + 0.005 (heart weight). The correlation coefficient for the lesion area was significant (p less than 0.001), whereas the correlation coefficients for age and heart weight were not. The lumen area did not decrease in relation to the percentage of stenosis (lesion area/internal elastic lamina area x 100) for values between zero and 40% but did diminish markedly and in close relation to the percentage of stenosis for values above 40% (r = -0.73, p less than 0.001). We conclude that human coronary arteries enlarge in relation to plaque area and that functionally important lumen stenosis may be delayed until the lesion occupies 40% of the internal elastic lamina area. The preservation of a nearly normal lumen cross-sectional area despite the presence of a large plaque should be taken into account in evaluating atherosclerotic disease with use of coronary angiography.


In this seminal post-mortem study of human coronary arteries, Dr Glagov et al. systematically described the relation between plaque size and luminal dimension, and suggested that early plaque accumulation was frequently not reflected in luminal change because of an outward bulging or "remodelling" of the overall vessel size. The results are reminiscent of Crawford and Levene's observation (Paper no. 1).

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Related References

1. McPherson DD, Sirna SJ, Hiratzka LF, et al. Coronary arterial remodeling studies by high-frequency epicardial echocardiography. J Am Coll Cardiol 1991; 17: 79-86.

2. Hermiller JB, Tenaglia AN, Kisslo KB, et al. In vivo validation of compensatory enlargement of atherosclerotic coronary arteries. Am J Cardiol 1993; 71: 665-668.

3. Armstrong ML, Heistad DD, Marcus ML, Megan MB, Piegors DJ. Structural and hemodynamic responses of peripheral arteries of macaque monkeys to atherogenic diet. Arteriosclerosis 1985; 5: 336-346.

4. Varnava AM, Mills PG, Davies MJ. Relationship between coronary artery remodeling and plaque vulnerability. Circulation 2002; 105: 939-943.

5. Burke AP, Kolodgie FD, Farb A, Weber D, Virmani R. Morphological predictors of arterial remodeling in coronary atherosclerosis. Circulation 2002; 105: 297-303.

Key message

Our findings do indicate that many persons have an adequate, if not normal, lumen cross-sectional area in the presence of advanced atherosclerosis and that such a possibility should be taken into account in evaluating the extent and severity of disease with angiography. The arrest of progression and the stabilization of a plaque before cross-sectional stenosis exceeds 40% could be consistent with preservation of an adequate, if not normal lumen area in such patients. Identification of the clinical, functional and anatomical factors that influence plaque stabilization could have important clinical consequences, even if the disease is not reversible and regression is not achieved.

Why it's important

This and subsequent papers explained why plaque accumulation was not always associated with luminal stenosis.


1. Systematic observation of early atherosclerotic lesions in human post-mortem arteries.

2. The authors suggest an explanation for the dissociation between plaque and lumen size, which subsequently will have significant influence on our current understanding of coronary artery disease (CAD).


Owing to the cross-sectional design of post-mortem studies, the findings regarding plaque development needed confirmation in serial studies.


The simultaneous description of the compensatory changes of vessel size during plaque development in post-mortem and imaging studies provided the rational for tomographical imaging of coronary atherosclerosis.

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