ACTIVE rheumatic carditis is a self-limited process in which the severity of any attack cannot be predicted. The cardiac damage usually sustained in any one attack depends on the duration and the severity of the inflammatory process. This has been demonstrated in both pathological and long-term clinical studies reported by Wilson and other investigators.1
It has been shown that certain inflammatory conditions are arrested by the administration of corticotropin (ACTH). Complete termination of self-limited ophthalmological disorders has been reported by Gordon and McLean2 and by Olson and co-workers.3 In severe burns, early corticotropin therapy has resulted in decreased inflammation and minimal permanent tissue damage, as reported by Whitelaw.4
From these and other observations it was considered that if the acute inflammatory phase of active rheumatic carditis could be terminated by the use of corticotropin before irreversible tissue damage occurred, permanent cardiac damage might be prevented or