Experimental studies on the pathogenesis of damage in the heart.

Abstract

Radiation-induced heart disease has been observed in a significant number of patients following mediastinal radiotherapy of Hodgkin’s disease or postoperative radiotherapy of breast cancer. Following higher radiation doses and especially following treatments delivering a particularly high dose to the anterior pericardium, a reversible exudative pericarditis can occur within the first 2–3 years (Pierce et al. 1969; Byhardt et al. 1975; Gottdiener et al. 1983; Greenwood et al. 1974; Applefeld and Wiernik 1983). A compilation of clinical data has shown that the incidence of pericarditis rises sharply with radiation dose to the anterior pericardium (Schultz-Hector 1991a). Since modern radiation techniques achieve a more homogeneous dose distribution, pericarditis has become a rare event and is no longer a major clinical concern (Carmel and Kaplan 1976; Watchie et al. 1987; Morgan et al. 1985). With increasing survival times, particularly in Hodgkin patients, late radiation effects on myocardial function have been observed. In a significant number of patients, left ventricular ejection fractions were reduced at 5–25 years postirradiation (Morgan et al. 1985; Burns et al. 1983; Savage et al. 1990; Gomez et al. 1983). Although these patients were asymptomatic, one has to assume that the cardiac reserve capacity, i.e., the ability to compensate for cardiac stress of other origin, is reduced in these patients. We therefore developed an animal model to study the pathogenesis of radiation-induced myocardial dysfunction.