© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
Atherosclerotic plaque rupture – pathologic basis of plaque stability and instability
affl1Department of Cardiovascular Pathology, Academic Medical Center, University of Amsterdam, P.O. Box 22700, 1100 DE Amsterdam, Netherlands
* Corresponding author. Tel.: +31-20-5665-633; fax: +31-20-914-738; e-mail a.c.vanderwal@amc.uva.nl
Received 5 June 1998; accepted 31 July 1998
KEYWORDS Atherosclerosis; Plaque rupture; Pathology; Macrophages; Smooth muscle cells; Acute coronary syndromes; Human
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1 Introduction |
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Atherosclerosis continues to be one of the main subjects in pathology research. The intriguing complexity of its pathogenesis as well as the importance of its clinical sequelae provide a rationale for this [1]. A large number of diseases with totally different clinical presentations are basically atherosclerosis related, and among these, myocardial infarction, stroke, abdominal aneurysms and lower limb ischemia determine to a large extent the morbidity and mortality in Western style populations. But, despite this broad spectrum of clinical disease, most of the acute manifestations of atherosclerosis share a common pathogenetic feature: rupture of an atherosclerotic plaque [2–4]. Plaque disruptions may vary greatly in extent from tiny fissures or erosions of the plaque surface to deep intimal tears which extend into the soft lipid core of lesions; in all these instances, at least some degree of thrombus formation occurs [5, 6]. The abdominal aorta is the arterial
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2 Stable and unstable plaques |
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2.1 Ratios of fibrous tissue and lipids in plaques
2.2 Inflammatory activity in the plaque
2.2.1 Acute myocardial infarction
2.2.2 Unstable angina
2.2.3 Stable angina
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3 Instability and stability: a balance between inflammation and repair |
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3.1 Smooth muscle cells: repair cells of the plaque
3.2 Lipids and inflammatory cells
3.3 Pathologic evidence derived from coronary atherectomy studies
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4 The acute ischemic event: a multifactorial process |
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4.1 The spectrum of plaque disruption and thrombus formation
4.2 Plaque volume and stenosis rate
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5 Classical risk factors and acute plaque complications |
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6 Conclusions |
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