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Cardiovascular Research 2002 56(3):347-349; doi:10.1016/S0008-6363(02)00693-4
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

A new altruist on the block: effects of adrenomedullin after myocardial infarction

Ian M.C. Dixon*,1

Department of Physiology, Institute of Cardiovascular Sciences, University of Manitoba. 351 Tache Avenue, Winnipeg, Canada R2H 2A6

idixon@sbrc.ca

* Tel.: +1-204-235-3419; fax: +1-204-233-6723

Received 24 September 2002; accepted 24 September 2002

The first 150 words of the full text of this article appear below.

See article by Nakamura et al. [15] (pages 373–380) in this issue.

The first few weeks after myocardial infarction (MI) are critical to the evolution of compensated to decompensated heart failure; it is generally agreed that the rapidity of cardiac dysfunction in these hearts depends on the magnitude of the initial insult [1]. From a clinical standpoint, it stands to reason that any process that may interrupt or abrogate secondary ventricular remodeling with attendant loss of normal chamber geometry may also attenuate the rate of functional decline of the remnant heart. The hallmark of maladaptive change in the post-MI heart is increased myocyte size; this change is associated with decreased intrinsic cardiac performance [2]. Alternatively, the premise that post-MI heart failure stems from not only abnormalities in cardiac myocytes but may also be linked to unusual behaviour of non-myocytes, i.e., myofibroblasts, seems to be borne out by data . . . [Full Text of this Article]


   1 Early events in wound healing after myocardial infarction
 

   2 Adrenomedullin: an endogenous anti-remodeling factor?
 

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