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Previous Volume 338:1838-1839 June 18, 1998 Number 25 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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Over the past two decades, clinical and pathological studies have examined the pathophysiology of the acute coronary syndromes, unstable angina, and non–Q-wave and Q-wave myocardial infarction. In these conditions, rupture of atherosclerotic plaques leads to varying amounts of platelet adhesion and aggregation, vasoconstriction, and the formation of partially or totally occlusive thrombus. Although the inhibition of platelet aggregation and thrombus formation and the restoration of antegrade flow in occluded coronary arteries improve survival and reduce the incidence of recurrent ischemia and infarction, residual coronary-artery stenosis may cause ischemia, infarction, or even death. As a result, there has been considerable interest . . . [Full Text of this Article]

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Management of Non–Q-Wave Myocardial Infarction
Bedell S. E., Graboys T. B., Ravid S., Thompson R. C., Roe M. T., Bowen T. E., Topol E. J., Huitink J. M., Bax J. J., Boden W. E., O'Rourke R. A., Crawford M. H.
Extract | Full Text  
N Engl J Med 1998; 339:1395-1398, Nov 5, 1998. Correspondence

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