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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:2207.)
© 2004 American Heart Association, Inc.

Editorials

Propagation of Arterial Thrombi

Local and Remote Contributory Factors

Shinya Goto

From the Department of Medicine, Tokai University School of Medicine, Kanagawa, Japan.

Correspondence to Shinya Goto, MD, FACC, Department of Medicine, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa 2591193, Japan. E-mail sgoto3@mac.com

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

It is a common understanding that the rupture of an atheroma in the coronary arteries is the initial event in the onset of arterial thrombosis resulting in myocardial infarction.¹ Ex vivo perfusion experiments using human blood have clearly demonstrated that platelet accumulation occurs immediately when the subendothelial matrix, such as collagen, is exposed to the blood stream.² However, initiation of platelet thrombus formation after endothelial disruption resulting in exposure of the subendothelial matrix does not directly represent the onset of symptomatic atherothrombotic diseases, such as myocardial infarction, which were caused by thrombotic arterial occlusion. For example, coronary intervention, while causing damage to the endothelium, does not, in most cases, result in any symptomatic myocardial ischemia. Moreover, recent advances in clinical imaging techniques, such as intracoronary ultrasonography, have revealed a much higher incidence of atheroma rupture than of symptomatic atherothrombotic coronary artery diseases, including myocardial infarction and unstable angina pectoris.^3,4 These observations suggest the contribution of propagating factors for thrombus growth, besides exposure of the subendothelial matrix due to endothelial disruption, in the onset of symptomatic arterial thrombotic diseases.

See page 2420

In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Yamashita et al have elegantly demonstrated in experimental studies the importance of 2 factors in the formation of arterial occlusive thrombi, namely increased vascular wall thrombogenicity induced by the accumulation of tissue factor and reduction of the total arterial blood flow by increased vascular resistance.⁵ The former explains the difference between the onset of myocardial infarction induced by the . . . [Full Text of this Article]

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