An endocrine experimental model for myofibrillar disarray as found in hypertrophic cardiomyopathy.

The various etiologic suggestions for hypertrophic cardiomyopathy in man have been reviewed and experimental studies for endogenous pathways have been investigated experimentally. Intramuscular administration of triac to adult rats resulted in severe myocardial hypertrophy but no disarray. When studying the effect of triac on the myocardium of developing rats profound changes of disarray as well as hypertrophy were produced, mimicking the ultrastructural changes of hypertrophic cardiomyopathy in man. By using a variety of compounds with beta-adrenergic blocking action or predominantly membrane stabilizing properties or agonist action together with triac, the site where triac exerts its effect has been shown to be the cell membranes. A mechanism for production of cellular disarray has been delineated. Extrapolating to man, these experiments lend support to the suggestion that an endogenous hormonal mechanism may be operative in some patients with hypertrophic cardiomyopathy.