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Heart 2004;90:1392-1394; doi:10.1136/hrt.2004.034975
Copyright © 2004 BMJ Publishing Group Ltd & British Cardiovascular Society
Heart 2004;90:1392-1394
© 2004 by BMJ Publishing Group & British Cardiac Society

MINI-SYMPOSIUM

Plaque stabilisation by systemic and local drug administration

J C Spratt1, E Camenzind2

1 Royal Infirmary of Edinburgh, Edinburgh, UK
2 University Hospital of Geneva, Geneva, Switzerland

Correspondence to:
Correspondence to:
Dr Edoardo Camenzind
University Hospital Geneva, Rue Micheli-du-Crest 24, 1211 Geneva 4, Switzerland; edoardo.camenzind@hcuge.ch

Abbreviations: ACE, angiotensin converting enzyme; ACS, acute coronary syndrome; CRP, C reactive protein; Gp, glycoprotein; HDL, high density lipoprotein; IVUS, intravascular ultrasound; LDD, local drug delivery; LDL, low density lipoprotein; LMWH, low molecular weight heparin; MACE, major adverse cardiac events; M-CSF, macrophage colony stimulating factor; MMP, matrix degrading metalloproteinases; PCI, percutaneous coronary intervention; TMMP, tissue inhibitor of MMP; UFH, unfractionated heparin

Keywords: acute coronary syndrome; drug administration; local drug delivery; plaque stabilisation

The first 150 words of the full text of this article appear below.

Clinical manifestations of coronary atherosclerosis are mainly a consequence of one of the following pathogenesis:

  • Stable coronary artery plaque without thrombus formation causing variable degrees of luminal narrowing and stable angina
  • Superficial plaque erosion, defined as endothelial erosions that may result in thrombus formation and acute coronary syndromes (ACS) (cause ~30–40% of ACS, more common in younger patients and women)1
  • Deep plaque rupture defined as fibrous cap rupture with exposed lipid core resulting in in-situ thrombus formation and varying degrees of coronary ischaemia (cause ~60–70% of ACS).2

The lack of a linear relation between stenosis severity and the probability of developing an ACS is well recognised.3 Indeed the majority of plaques (~70%) leading to acute myocardial infarction are not of angiographic significance, implying that factors other than stenosis severity determine the probability of vessel closure. The term "vulnerable" plaque defines the vascular substrate most subject to superficial erosion or . . . [Full text of this article]


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This article has been cited by other articles:

  • Bonvini, R. F., Hendiri, T., Camenzind, E. (2005). Inflammatory response post-myocardial infarction and reperfusion: a new therapeutic target?. Eur Heart J Suppl 7: I27-I36 [Abstract] [Full Text]  

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