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Editorials

MRI of the Microarchitecture of Myocardial Infarction

Are We Seeing New Kinds of Structures?

Leon Axel, PhD, MD

From the Department of Radiology, NYU Langone Medical Center, New York, NY.

Correspondence to Leon Axel, PhD, MD, Department of Radiology, NYU Langone Medical Center, 660 First Ave, Room 411, New York, NY 10016. E-mail leon.axel@nyumc.org

Key Words: Editorials

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

Myocardial infarction (MI) is a leading cause of death and disability. In addition to the immediate incidence of death in acute infarction caused by pump failure or arrhythmias related to the immediate loss of functioning cardiac tissue and the possibility of later progression to intractable pump failure in the subacute or chronic phases of infarction, a significant number of patients with prior MI have sudden death,¹ presumably largely caused by arrhythmias related to the infarction. There are various theories about the mechanisms of infarction-related arrhythmias, many centering around the idea that the altered transmission through the region of the infarction can alter the propagation of waves of electric activation in such a way that they can set up self-perpetuating foci of electric activity. However, there is still much uncertainty about the area.

Article see p 206

In MI, there is ischemia of a portion of the heart wall that is sufficiently severe and prolonged that cells in the heart wall start to die. Whereas the myocytes, with their relatively high metabolic demands, are likely to be irreversibly damaged by such a significant period of ischemia and thus lost from the wall, the fibroblasts in the heart wall are more resistant to the effects of ischemia and thus are more likely to survive. In the healing phases of MI, these fibroblasts can become activated and effectively "patch" the wall with a meshwork of collagen. The resistance of the heart wall to the effects of ischemia is species-dependent, in part reflecting the . . . [Full Text of this Article]

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