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Previous Volume 330:1006-1007 April 7, 1994 Number 14 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Heart attacks and strokes are usually caused by thrombo-occlusive events at sites of atherosclerotic stenosis and plaque rupture¹. These thrombotic processes are generally mediated by thrombin, dependent on the action of platelets, and not completely responsive to conventional therapy with aspirin and heparin^2,3. Resistant thrombi may also form after vascular procedures commonly performed for the treatment of symptomatic atherosclerotic disease, including coronary angioplasty, various types of atherectomy, placement of endovascular stents, endarterectomy, and implantation of small-caliber vascular grafts^4,5. In fact, abrupt vessel closure and coronary restenosis are the two most difficult problems limiting the success of coronary . . . [Full Text of this Article]

References

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• Harker, L. A., Marzec, U. M., Kelly, A. B., Chronos, N. R. F., Sundell, I. B., Hanson, S. R., Herbert, J.-M. (1998). Clopidogrel Inhibition of Stent, Graft, and Vascular Thrombogenesis With Antithrombotic Enhancement by Aspirin in Nonhuman Primates. Circulation 98: 2461-2469 [Abstract] [Full Text]  
• Sobel, M., Bird, K. E., Tyler-Cross, R., Marques, D., Toma, N., Edward Conrad, H., Harris, R. B. (1996). Heparins Designed to Specifically Inhibit Platelet Interactions With von Willebrand Factor. Circulation 93: 992-999 [Abstract] [Full Text]  
• (1994). MONOCLONAL ANTIBODY REDUCES VESSEL CLOSURE AFTER ANGIOPLASTY. JWatch General 1994: 2-2 [Full Text]