Culprit Lesion Coronary Arterial Remodelling and Clinical Outcome

Posted On 2013-07-17 14:56:24
Based on the seminal work by Seymour Glagov and others, arterial remodeling of the coronary arteries was first described as an adaptive process maintaining luminal dimensions despite atherosclerotic plaque accumulation (1). Subsequent imaging studies hypothesized that positive (expansive) arterial remodelling was one of the morphological characteristics of the vulnerable plaques (lesions responsible for acute coronary syndromes) (2,3). However, limited data were available on a long-term outcome of acute coronary syndrome (ACS) patients with culprit lesion positive arterial remodelling (PR). Such data would provide proof that PR is a marker of instability.

In a study recently published in the European Heart Journal, intravascular ultrasound (IVUS) was performed to assess target lesion remodelling before percutaneous coronary intervention in 134 patients with ACS. PR was defined as the ratio of the external elastic membrane cross-sectional area at the target lesion to that of at the proximal reference of >1.05, and intermediate or negative remodelling (IR/NR) was defined as that of ≤1.05. Major adverse cardiac event (MACE) was defined as a composite of death, ACS, and target lesion revascularization. During the follow-up (median 5.8 years), MACE-free survival was significantly lower in the PR group than that in the IR/NR group (log-rank, P = 0.005). Survival and ACS-free survival were also significantly lower in the PR group than that in the IR/NR group (log-rank, both P = 0.04). By multivariable Cox regression analysis, PR (hazard ratio = 2.4, P = 0.02) and diabetes (hazard ratio = 1.9, P = 0.03) were independent predictors of MACE

The authors conclude that culprit lesion PR was associated with a poor long-term prognosis in patients with ACS. These data provide further evidence that coronary PR is a marker of plaque vulnerability.


REFERENCES:
  1. 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):1371-5.
  2. Pasterkamp G, Schoneveld AH, van der Wal AC, Haudenschild CC, Clarijs RJ, Becker AE, Hillen B, Borst C. Relation of arterial geometry to luminal narrowing and histologic markers for plaque vulnerability: the remodelingparadox. J Am Coll Cardiol. 1998 Sep;32(3):655-62.
  3. Schoenhagen P, Ziada KM, Kapadia SR, Crowe TD, Nissen SE, Tuzcu EM. Extent and direction of arterial remodeling in stable versus unstable coronary syndromes : an intravascular ultrasound study. Circulation. 2000 Feb 15;101(6):598-603.
  4. Okura H, Kataoka T, Matsushita N, Shimeno K, Yoshiyama M, Yoshikawa J, Yoshida K. Culprit lesion remodelling and long-term prognosis in patients with acute coronary syndrome: an intravascular ultrasound study. Eur Heart J Cardiovasc Imaging. 2013 Aug;14(8):758-764. Epub 2012 Nov 9.