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PubMed · 9330735

Ventricular remodeling: from bedside to molecule.

R Jaffe·M Y Flugelman·D A Halon·B S Lewis
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Abstract

The multiple mechanisms that bring about the decompensation of the hypertrophic remodeled myocardium are synergistic and not fully understood. Our current hypothesis is that the increased stress on the ventricle is initially offset by compensatory myocardial hypertrophy. In many instances, however, progressive ventricular dilatation and heart failure occur as a result of maladaptive hypertrophy (abnormal myosin-actin production), programmed cell death (apoptosis) and/or changes in the interstitial vasculature and collagen composition. The molecular and genetic background to these processes includes changes in myocardial gene expression, activation of the local tissue renin-angiotensin and other neurohormonal systems, increased matrix metalloproteinase activity (including collagenase), and expression of certain components of the immune system, such as TNF-alpha. Future research will hopefully provide better methods for limiting the remodeling-ventricular dilatation process by novel pharmacotherapies, gene therapy and, possibly, surgical therapy, and determine the impact of such interventions on survival.

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AnimalsCardiomegalyCoronary VesselsGene ExpressionHeart FailureHeart VentriclesHumansNeurosecretory SystemsRenin-Angiotensin SystemJournal ArticleReview

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R Jaffe, M Y Flugelman, D A Halon, B S Lewis. 1997. Ventricular remodeling: from bedside to molecule.. https://doi.org/10.1007/978-1-4615-5959-7_22

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