pmc logo image
Logo of heartHeartCurrent TOCInstructions to authors

Formats:

Heart. 2001 August; 86(2): 207–211.
doi: 10.1136/heart.86.2.207.
PMCID: PMC1729857
Relation between coronary artery remodelling (compensatory dilatation) and stenosis in human native coronary arteries
A Varnava and M Davies
British Heart Foundation Department of Cardiovascular Pathology, St George's Hospital Medical School, Cranmer Terrace, London SW17 ORE, UK. Email: avarnava/at/sghms.ac.uk
Abstract
OBJECTIVES—To investigate the contribution of plaque size and vessel remodelling to coronary artery stenosis and to assess the role of vessel shrinkage (negative remodelling) across a wide range of lesions.
DESIGN—Postmortem study of coronary remodelling in perfusion fixed hearts.
SUBJECTS—24 men and 24 women who died suddenly with coronary artery disease.
MAIN OUTCOME MEASURES—Percentage stenosis, percentage plaque burden, percentage remodelling, and arc of normal vessel were measured and related to age, sex, smoking status, and history of hypertension.
RESULTS—There was a positive relation between percentage stenosis and percentage plaque burden (r = 0.6, p < 0.0001) and an inverse relation between percentage stenosis and percentage remodelling (r = -0.4, p < 0.0001). Multilinear regression modelling showed that luminal stenosis = 1.0 (plaque burden) − 0.4 (vessel remodelling). Remodelling was greater in lesions that would not have been significant at angiography ([less-than-or-eq, slant] 25% stenosis) than in the remaining lesions (25.9 (26)% v 10.0 (21.1)%, p < 0.0001, respectively) and was reduced in segments with circumferential plaques (12.7 (24.5)% v 20.7 (24.3)% in eccentric plaques, p = 0.001). Remodelling did not correlate with age, sex, or smoking. Negative remodelling was present in 62 lesions with a stenosis > 25% versus 10 lesions with [less-than-or-eq, slant] 25% stenosis (p < 0.0001). Lesions with negative remodelling had greater plaque burden and luminal stenosis and a reduced arc of normal segment.
CONCLUSION—Outward arterial remodelling negates the stenosing effect of increasing plaque size. Significant coronary stenoses arise from a failure of this outward remodelling in the face of a large plaque burden. Coronary arterial remodelling is unrelated to sex or smoking and is plaque specific.


Keywords: coronary artery disease; vessel remodelling; pathology
Full Text
The Full Text of this article is available as a PDF (163K).
Selected References
These references are in PubMed. This may not be the complete list of references from this article.
  • Glagov S, Weisenberg E, Zarins CK, Stankunavicius R, Kolettis GJ. Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med. 1987 May 28;316(22):1371–1375. [PubMed]
  • McPherson DD, Sirna SJ, Hiratzka LF, Thorpe L, Armstrong ML, Marcus ML, Kerber RE. Coronary arterial remodeling studied by high-frequency epicardial echocardiography: an early compensatory mechanism in patients with obstructive coronary atherosclerosis. J Am Coll Cardiol. 1991 Jan;17(1):79–86. [PubMed]
  • Hermiller JB, Tenaglia AN, Kisslo KB, Phillips HR, Bashore TM, Stack RS, Davidson CJ. In vivo validation of compensatory enlargement of atherosclerotic coronary arteries. Am J Cardiol. 1993 Mar 15;71(8):665–668. [PubMed]
  • Losordo DW, Rosenfield K, Kaufman J, Pieczek A, Isner JM. Focal compensatory enlargement of human arteries in response to progressive atherosclerosis. In vivo documentation using intravascular ultrasound. Circulation. 1994 Jun;89(6):2570–2577. [PubMed]
  • Pasterkamp G, Borst C, Post MJ, Mali WP, Wensing PJ, Gussenhoven EJ, Hillen B. Atherosclerotic arterial remodeling in the superficial femoral artery. Individual variation in local compensatory enlargement response. Circulation. 1996 May 15;93(10):1818–1825. [PubMed]
  • Varnava A. Coronary artery remodelling. Heart. 1998 Feb;79(2):109–110. [PubMed]
  • Pasterkamp G, Wensing PJ, Post MJ, Hillen B, Mali WP, Borst C. Paradoxical arterial wall shrinkage may contribute to luminal narrowing of human atherosclerotic femoral arteries. Circulation. 1995 Mar 1;91(5):1444–1449. [PubMed]
  • Mintz GS, Kent KM, Pichard AD, Satler LF, Popma JJ, Leon MB. Contribution of inadequate arterial remodeling to the development of focal coronary artery stenoses. An intravascular ultrasound study. Circulation. 1997 Apr 1;95(7):1791–1798. [PubMed]
  • Nishioka T, Luo H, Eigler NL, Berglund H, Kim CJ, Siegel RJ. Contribution of inadequate compensatory enlargement to development of human coronary artery stenosis: an in vivo intravascular ultrasound study. J Am Coll Cardiol. 1996 Jun;27(7):1571–1576. [PubMed]
  • Smits PC, Bos L, Quarles van Ufford MA, Eefting FD, Pasterkamp G, Borst C. Shrinkage of human coronary arteries is an important determinant of de novo atherosclerotic luminal stenosis: an in vivo intravascular ultrasound study. Heart. 1998 Feb;79(2):143–147. [PubMed]
  • Wong CB, Porter TR, Xie F, Deligonul U. Segmental analysis of coronary arteries with equivalent plaque burden by intravascular ultrasound in patients with and without angiographically significant coronary artery disease. Am J Cardiol. 1995 Sep 15;76(8):598–601. [PubMed]
  • Tronc F, Wassef M, Esposito B, Henrion D, Glagov S, Tedgui A. Role of NO in flow-induced remodeling of the rabbit common carotid artery. Arterioscler Thromb Vasc Biol. 1996 Oct;16(10):1256–1262. [PubMed]
  • Lerman A, Cannan CR, Higano SH, Nishimura RA, Holmes DR., Jr Coronary vascular remodeling in association with endothelial dysfunction. Am J Cardiol. 1998 May 1;81(9):1105–1109. [PubMed]
  • Abbruzzese TA, Guzman RJ, Martin RL, Yee C, Zarins CK, Dalman RL. Matrix metalloproteinase inhibition limits arterial enlargements in a rodent arteriovenous fistula model. Surgery. 1998 Aug;124(2):328–335. [PubMed]
  • Bassiouny HS, Song RH, Hong XF, Singh A, Kocharyan H, Glagov S. Flow regulation of 72-kD collagenase IV (MMP-2) after experimental arterial injury. Circulation. 1998 Jul 14;98(2):157–163. [PubMed]
  • Mann J, Davies MJ. Mechanisms of progression in native coronary artery disease: role of healed plaque disruption. Heart. 1999 Sep;82(3):265–268. [PubMed]
  • Flugelman MY, Virmani R, Correa R, Yu ZX, Farb A, Leon MB, Elami A, Fu YM, Casscells W, Epstein SE. Smooth muscle cell abundance and fibroblast growth factors in coronary lesions of patients with nonfatal unstable angina. A clue to the mechanism of transformation from the stable to the unstable clinical state. Circulation. 1993 Dec;88(6):2493–2500. [PubMed]
  • von Birgelen C, Mintz GS, de Vrey EA, Kimura T, Popma JJ, Airiian SG, Leon MB, Nobuyoshi M, Serruys PW, de Feyter PJ. Atherosclerotic coronary lesions with inadequate compensatory enlargement have smaller plaque and vessel volumes: observations with three dimensional intravascular ultrasound in vivo. Heart. 1998 Feb;79(2):137–142. [PubMed]
  • DeBakey ME, Lawrie GM, Glaeser DH. Patterns of atherosclerosis and their surgical significance. Ann Surg. 1985 Feb;201(2):115–131. [PubMed]
Figures and Tables
Figure 1
Figure 1
Figure 1  
Luminal stenosis against plaque burden.
Figure 2
Figure 2
Figure 2  
Luminal stenosis against vessel remodelling.
Figure 3
Figure 3
Figure 3  
Number of lesions with positive versus negative remodelling according to percentage luminal stenosis.
An external file that holds a picture, illustration, etc.
Object name is hrt-tflm.f1.jpg
An external file that holds a picture, illustration, etc.
Object name is hrt-tflm.f1.jpg