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47 - Pathophysiology of arterial thrombosis

from PART III - PATHOLOGY

Published online by Cambridge University Press:  10 May 2010

Lina Badimon
Affiliation:
Cardiovascular Research Center, CSIC-HSCSP-UAB, Barcelona, Spain
Juan-Jose Badimon
Affiliation:
Cardiovascular Institute, Mount Sinai School of Medicine, New York, USA
Valentin Fuster
Affiliation:
Cardiovascular Institute, Mount Sinai School of Medicine, New York, USA
Paolo Gresele
Affiliation:
Università degli Studi di Perugia, Italy
Clive P. Page
Affiliation:
Sackler Institute of Pulmonary Pharmacology and Therapeutics, Guy's, King's and St Thomas' School of Biomedical Sciences, London
Valentin Fuster
Affiliation:
Mount Sinai Medical Center and School of Medicine, New York
Jos Vermylen
Affiliation:
Universiteitsbibliotheek-K.U., Leuven
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Summary

During the past few years we have witnessed a remarkable advance in our understanding of the pathophysiology of coronary atherosclerosis–thrombosis. Here we focus on thrombosis with specific emphasis on the coronary arteries.

Lesion classification and progression of atherosclerosis–thrombosis

According to the criteria of the American Heart Association Committee on Vascular lesions, plaque progression can be divided into the five phases and various lesion types shown in Fig 47.1. The so-called ‘vulnerable’ type IV and type Va lesions (phase 2) and the so-called ‘complicated’ type VI lesion (phase 4) are the most relevant to acute coronary syndromes (ACS). The acute type VI lesion that results in an ACS, rather than being characterized by a small mural thrombus, consists of an occlusive thrombus.

Type IV and type Va lesions, although not necessarily stenotic at angiography, may be prone to disruption because of their softness due to a high lipid content and macrophage-dependent chemical properties. Type IV lesions consist of confluent cellular lesions with a great deal of extracellular lipid intermixed with fibrous tissue covered by a fibrous cap, whereas type Va lesions possess a predominant extracellular lipid core also covered by a thin fibrous cap. Phase 2 can evolve into acute phase 3 or 4, and either of them can evolve into a fibrotic phase 5.

Type
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Information
Platelets in Thrombotic and Non-Thrombotic Disorders
Pathophysiology, Pharmacology and Therapeutics
, pp. 725 - 737
Publisher: Cambridge University Press
Print publication year: 2002

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