A new altruist on the block: effects of adrenomedullin after myocardial infarction
Authors: I Dixon
Journal: Cardiovascular Research (2002)

maladaptive hypertrophy remains dismal, and (ii) the list in this issue.of new agents for treatment of this disease has not grown appreciably in the last 10 years, an understanding of The first few weeks after myocardial infarction (MI) are naturally occurring factors that tend to oppose cardiac critical to the evolution of compensated to decompensated remodeling per se is well worth further investigation.An heart failure; it is generally agreed that the rapidity of improved understanding of endogenous adaptive changes cardiac dysfunction in these hearts depends on the mag-of the myocardium may provide a basis for exploitation in nitude of the initial insult [1].From a clinical standpoint, it delaying the onset of maladaptive hypertrophy.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 1 .Early events in wound healing after myocardial hallmark of maladaptive change in the post-MI heart is infarction increased myocyte size; this change is associated with decreased intrinsic cardiac performance [2].Alternatively, Wound healing and scar formation following myocardial the premise that post-MI heart failure stems from not only infarction is marked by inflammation and clearance of abnormalities in cardiac myocytes but may also be linked necrotic myocytes followed by proliferation of interstitial to unusual behaviour of non-myocytes, i.e., myofibroblasts, fibroblasts where they synthesize new extracellular matrix seems to be borne out by data from recent studies [3,4].proteins and mediate contraction of the infarct scar [5,6].Recent attention has focused on the acute pattern of Multiple cell types in the surviving tissues and in the changes that transpire in the healing infarct scar and infarct zone undergo phenotypic changes and participate in remnant myocardium, loosely connected by the general subsequent cardiac remodeling.Myocytes grow larger and hypothesis that events in early post-MI healing may serve express a characteristic subset of protein isoforms specific to set the pace for the onset of cardiac decompensation.In to the fetal gene programming, while fibroblasts tend to this context, basic cardiovascular research specializing in a proliferate and undergo a phenotypic change to become subset of novel factors that may have anti-growth and actin-expressing contractile myofibroblasts.These changes anti-proliferative properties for cardiac cells is burgeoning.are initiated by, and tend to offset, increased net me-In this scenario, multiple factors with opposing functions chanical stress of the ventricular wall.Various cell medi-(operating via autocrine or paracrine modes) may partici-ators and cytokines are well known to play integral roles in pate in the acute phase of wound healing and continue to this phenomenon, including angiotensin II, endothelin-1, exert their effects in the chronic post-MI heart.As (i) the and transforming growth factor b. Nonetheless, the number prognosis for patients who manage to survive the acute of putative players that may participate in the acute and net phase of a large MI and who yet go on to develop heart function in vivo is increasing.For example, recent discoveries of the ACE homologue, ACE2, and cardiotrophin-1 (CT-1; a member of the IL-6 family of cytokines) and that of their effects on cardiac-specific cell