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Previous Volume 351:1716-1718 October 21, 2004 Number 17 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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Enormous progress made during the past few decades has dramatically enhanced our understanding of the pathobiology and pathophysiology responsible for acute myocardial infarction. Investigations in vascular biology have elucidated the critical role of growth factors, the proliferation of smooth-muscle cells, and the central role of inflammation in the initiation and progression of atherosclerosis.¹ Research has also focused on the initiating events or "triggers" that qualitatively alter the stable or quiescent phase of coronary atherosclerosis and initiate a cascade of events that culminates in acute myocardial infarction. Some triggering phenomena may exert a single, transient effect on the pathophysiologic process, such . . . [Full Text of this Article]

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From the Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston.

Related Letters:

Traffic and Myocardial Infarction
Tosteson D. C., Greenbaum D. S., Lebwohl B., Stone P. H.
Extract | Full Text | PDF  
N Engl J Med 2005; 352:623-624, Feb 10, 2005. Correspondence

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