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(Circulation. 2008;118:1780-1782.)
© 2008 American Heart Association, Inc.

Editorial

The Emerging Role of Thrombus Aspiration in the Management of Acute Myocardial Infarction

Y.L. Gu, MD; M.L. Fokkema, BSc; F. Zijlstra, MD, PhD

From the Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.

Correspondence to F. Zijlstra, Department of Cardiology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, PO Box 30001, 9700 RB Groningen, the Netherlands. E-mail f.zijlstra@thorax.umcg.nl

Key Words: Editorials • angiography • myocardial infarction • prognosis • thrombus

An extract of the first 250 words of the full text is provided, because this article has no abstract.

An acute thrombotic event resulting in total occlusion of a coronary artery is considered the principal mechanism of ST-segment elevation myocardial infarction (STEMI). De Wood et al¹ were the first to show that total coronary occlusion was visible on the coronary angiogram in a large majority of patients presenting during the early hours of STEMI. Thrombus could be retrieved in 52 of 59 patients with angiographic, and in 5 of 20 patients without, features of thrombus, suggesting that thrombus formation plays a major role in the pathophysiology of total occlusion and subsequent infarction. Total coronary artery occlusion has also been described, though less frequently, in a range of nonthrombotic events such as intraplaque hemorrhage, vasospasm, spontaneous coronary artery dissection, coronary emboli, coronary arteritis, and compression by myocardial bridging.^2,3

Article p 1810

Acute coronary thrombosis is caused primarily by the rupture of a coronary atherosclerotic plaque, responsible for approximately 75% of all coronary thrombi leading to myocardial infarction or death,⁴ or by plaque erosion or calcified nodules. After rupture of the fibrous cap covering the atherosclerotic plaque, fragments of the lipid-rich core are exposed to the arterial lumen. This highly thrombogenic material causes platelet aggregation within the lipid core and on the ruptured fibrous cap, forming a mural thrombus consisting mainly of platelets, resulting in early coronary obstruction.³ In this early stage of thrombus formation, intermittent flow is often present, because the platelet aggregates are unstable and embolize into the microcirculation.^4,5 As a consequence of a balance between thrombotic and thrombolytic . . . [Full Text of this Article]

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