Cardiocyte Adaptation to Chronically Altered Load

The long-standing multidisciplinary interest in myocardial hypertrophy re­ cently has evolved from a description of specific forms of this entity to a more general consideration of the basic mechanisms by which the entire potential spectrum of cardiac loading conditions regulates the biology both of the myocardium and of the constituent striated muscle cell of this tissue, the cardiocyte. This is not to suggest that the understanding of hypertrophied myocardium is now complete. Although there have been significant recent refinements in the pathophysiologically relevant models of cardiac hypertro­ phy, the most important work in this area, which may lead to a clearer understanding of the bases for the transition from compensated cardiac hypertrophy to decompensated cardiac failure, remains to be done. Nonethe­ less, other recent work having a broader scope is clarifying the relative importance of loading conditions and other potential regulatory factors to the control of myocardial biology. A natural outgrowth of this investigative interest would be the elucidation of the mechanisms controlling growth and differentiation in both neonatal and adult mammalian myocardium. The expectation that such an approach may allow the basis for cardiocyte adapta­ tion to chronically altered loads to be understood at the molecular level is one of the most exciting prospects in cardiovascular physiology.