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Positive remodeling for ralph


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Positive remodeling for ralph

  1. 1. Editorial Slides VP Watch, March 4, 2002, Volume 2, Issue 9 Positive Remodeling, A Surrogate Marker of Plaque Inflammation and Vulnerability? By: Gerard Pasterkamp, M.D., Ph.D. Inter University Cardiology Institute of the Netherlands
  2. 2. Determinants of Atherosclerotic Luminal Narrowing  In the long term: i. Plaque formation ii. The mode of geometrical remodelling a) Expansive remodeling prevents whereas b) Constrictive remodeling accelerates luminal narrowing  Acutely: >> plaque rupture/erosion with subsequent thrombus formation. * In some cases, plaque rupture goes silent and the healing process results in fibrous cap formation and further luminal narrowing.
  3. 3. Seymour Glagov: Compensatory Enlargement of Human Atherosclerotic Coronary Arteries ”Positive Remodeling” <50% stenosis <80% stenosis Luminal area is not endangered until more than 40% of internal elastic lamina is destructed and occupied by plaque. Coronary artery disease is a disease of arterial wall not lumen.
  4. 4. Arterial Remodeling Gradual Luminal Narrowing Expansive Remodeling Constrictive Remodeling
  5. 5. Histological Characteristics of the Plaque that is Prone to Rupture
  6. 6. Plaque Rupture
  7. 7.  Previous studies demonstrated that: a. Histologically: an association between expansive remodeling and markers for plaque vulnerability in unruptured plaques. 1,2 b. Clinically: an association between expansive remodeling and unstable clinical syndromes. 3,4
  8. 8.  As highlighted in VP Watch, Varnava et al. studied the associaton between de novo atherosclerotic remodeling and histological markers for plaque vulnerability in plaques (n=108) obtained from patients (n=88) that died of coronary artery disease.
  9. 9. Results: 64/108 plaques revealed expansive remodelling. 44/108 revealed constrictive remodelling. Lipid core was larger in expansively remodelled plaques (39+/-21 % versus 22+/- 23%). Macrophage count was higher in expansively remodelled segments.
  10. 10. Conclusion: I. In patients that died acutely of coronary artery disease, expansive remodeling is associated with a vulnerable plaque phenotype. II. This observation may explain why acute coronary syndromes often originate from locations with minor luminal stenosis (but with outward remodelled plaques).
  11. 11. Questions: 1. Studies are cross-sectional, thus no causal of prognostic inferences are allowed. The question is what is the predictive value of the remodelling mode for the occurrence of plaque rupture and an acute cardiovascular event?  To answer this, serial (IVUS) studies are necessary.
  12. 12. Questions: 2. Remodelling is a double edged sword: in the long term expansive remodeling prevents luminal narrowing by plaque formation. In the short term these plaques are more prone to rupture giving rise to an acute cardiovascular event. How can we induce expansive remodeling without destabilizing the plaques?  To answer this, good animal models are needed that develop both types of geometrical remodeling
  13. 13. Questions: 3. In this study, positive (expansive) remodeling was present in 72%, however negative (constrictive) remodeling was also present in 50%, the question is how these two correlate with each other? 4. If expansive remodeling correlate with macrophage count and thin cap and can be a surrogate marker of vulnerability, what is the predictive value of constrictive remodeling (stenosis in angiography) in predicting presence of expansive remodeling and vulnerability to rupture in other plaques in the same patient?
  14. 14. Suggestion: Editorial Suggestion: - Please email your thoughts to: or
  15. 15. 1- Atherosclerotic arterial remodeling and the localization of macrophages and matrix metalloproteases 1, 2 and 9 in the human coronary artery; Atherosclerosis 2000; 150(2):245-253 ; Gerard Pasterkamp, Arjan H. Schoneveld, Dirk Jan Hijnen, Dominique P. V. de Kleijn, Hans Teepen, A. C. van der Wal and Cornelius Borst 2- Relation of arterial geometry to luminal narrowing and histologic markers for plaque vulnerability: the remodeling paradox, J American Coll Cardio 1998; 32(3):655-662 Gerard Pasterkamp, Arjan H. Schoneveld, Allard C. van der Wal, Christian C. Haudenschild, Ruud J. G. Clarijs, Anton E. Becker, Berend Hillen and Cornelius Borst 3- Coronary artery disease: arterial remodelling and clinical presentation Heart 1999; 82: 461-464. P C Smits, G Pasterkamp, M A Quarles van Ufford, F D Eefting, P R Stella, P P T de Jaegere, and C Borst 4- Extent and Direction of Arterial Remodeling in Stable Versus Unstable Coronary Syndromes : An Intravascular Ultrasound Study; Paul Schoenhagen, Khaled M. Ziada, Samir R. Kapadia, Timothy D. Crowe, Steven E. Nissen, and E. Murat Tuzcu; Circulation 2000 101: 598 - 603. 5 Compensatory Enlargement of Human Atherosclerotic Coronary Arteries. Seymour Glagov: New England Journal of Medcine 1987 May 28;316(22):1371-5 References