Editorial 363/78 British Heart Journal, 1979, 41, 257-262

The concept of thyrocardiac disease was introduced by Samuel Levine (Levine and Sturgis, 1924) who described atrial arrhythmias, congestive cardiac failure, and cardiac enlargement in hyperthyroidism occurring even in the absence of overt evidence of thyroid disorder. His clinical descriptions are as pertinent today as when they were written but it has always been a matter for conjecture whether thyroid disease in any of its forms can produce either specific pathological changes in the heart or an identifiable cardiac syndrome. The consensus from published work indicates that thyrocardiac disease as such is a clinical entity (Sandler and Wilson, 1959a; Staffurth and Morrison, 1968). Probably too much emphasis has been given to alterations in cardiac rhythm, a phenomenon symptomatic of associated muscle excitability. This survey discusses some of the experimental and clinical aspects of thyrocardiac disease and shows that a spectrum of response exists which may have a-bearing on the nature of cardiomyopathy itself. Action of thyroid hormones The precise mode of action of thyroid hormones, thyroxine and tri-iodothyronine, is uncertain but contemporary view accepts that they have a direct inotropic and chronotropic effect on the heart. Much data have come from experimentally produced thyrotoxicosis and caution should be exercised in relating the results of aniimal experiments to the clinical situation in man, especially as the level of thyroxine dosage employed may exert effects at pharmacological and not physiological levels (Bernal and Refetoff, 1977). DeGroot (1972) has sum-marised the various ways the heart may be affected by thyroid hormones; the effects may be secondary to an increased cardiac output from a raised total body oxygen consumption, in turn the result of