The dilated cardiomyopathies: experimental aspects

Abstract

Dilated cardiomyopathy is characterized by the primacy of systolic dysfunction. Experimental animal models have contributed greatly to our current knowledge and promise to continue to expand our understanding, especially as methods of cellular and molecular biology are increasingly applied. Although specific etiologies dominate in some forms of dilated cardiomyopathy, the cause is generally multifactorial--that is, the full expression results from the interplay of a number of etiologic and enhancing factors. Recognition of these factors paves the way for therapy as well as primary and secondary prevention. This article has focused chiefly on experimental models of dilated cardiomyopathy associated with congestive heart failure and on interventions producing or aggravating heart failure. Many factors associated with the production or aggravation of experimental myocardial necroses have not been considered here. Even so, this overview reaffirms the concept that dilated cardiomyopathies are pluricausal. In Table 3, the major processes identifies as pathogenetic in experimental dilated cardiomyopathy are listed. Table 4 presents a list of major categories of enhancing factors. The evidence offered in this article indicates that in most models many pathogenetic mechanisms and enhancing factors may be operative, and this is also believed to be the case in human dilated cardiomyopathy Recognition of the multifactorial etiologies of the dilated cardiomyopathies is an important first step in therapeutic and preventive interventions. Experimental work in human dilated cardiomyopathy has not been included in this article, but some recent studies provide challenging insights.