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European Heart Journal 2003 24(20):1804-1806; doi:10.1016/j.ehj.2003.08.008
Copyright © 2003 by the European Society of Cardiology.
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Editorial

Type II secretory phospholipase A2: The emerging role of biochemical markers of plaque inflammation

Jan J. Pieka,* and Robbert J. de Wintera

a Amsterdam Medical Center, Cardiologie, Meibergdreef 9, postbus 22660, 1100 DD Amsterdam, Netherlands

* Corresponding author: Prof. J. J. Piek. Tel.: +31-20-5662609; fax: +31-20-6962609

Received 22 August 2003; accepted 28 August 2003

The first 10% of the full text of this article appears below.

See doi:10.1016/j.ehj.2003.07.003for the article to which this editorial refers

In his classical clinical-pathomorphological studies, Fulton described for the first time the thrombotic sequelae underlying acute coronary events.1However, it took several decades before these thrombo-embolic complications were related to local plaque composition and the extent and/or location of plaque inflammation. Subsequent studies were conducted using atherosclerotic plaque specimen derived by directional coronary atherectomy during cardiac catheterization. These studies demonstrated that the clinical manifestation of coronary syndromes is positively associated with the extent of plaque inflammation of the culprit lesions, i.e. patients with unstable angina exhibit more activated macrophages and/or T-lymphocytes and less smooth muscle cells as compared to patients with stable angina.2The intimal infiltration of activated macrophages and/or T-lymphocytes promotes plaque rupture and subsequent local thrombus formation resulting in micro-embolization and/or acute thrombotic occlusion resulting in acute coronary syndromes.

. . . [Full Text of this Article]

1. Revascularization procedures

2. Death, unstable angina and myocardial infarction


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