No abstract

Since a report by Prinzmetal and Kennamer (1954) illustrating the return of sinus rhythm in a case of heart block after an injection of corticotrophin, a number of reports on the use of corticosteroids in this context has been published. Some of these have continued to show recovery of sinus rhythm as the principal effect (Phelps and Lindsay, 1957;Aber and Jones, 1960;Dall andBuchanan, 1961, 1962), while others have found this to be not a constant feature but regard the abolition of Stokes-Adams seizures as the chief benefit (Friedberg et al., 1960;Pay and Waverley, 1961;Caramelli and Tellini, 1960). This discrepancy has resulted in three theories as to the effect of steroids in these cases. The original authors suggested an "anti-inflammatory" effect; Friedberg et al. (1960), influenced by the abolition of Stokes-Adams attacks even when heart block persisted, suggested an "arousal of the ventricular pacemaker"; and Lown et al. (1955) studying the electrocardiogram in cases of Cushing's syndrome and Addison's disease noted significant shortening of the P-R interval in the presence of excessive adrenocortical activity, and conversely significant lengthening when there was a reduction in corticosteroid secretion. They suggested that corticosteroids had a "facilitating" effect on atrio-ventricular conduction. To evaluate these theories, the effect of corticosteroids on the P-R interval in patients in whom it was "normal" at the outset has been compared with control subjects. A further group of patients with heart block has been given a course of steroid therapy, and the effect on rhythm, A-V conduction, and Stokes-Adams attacks has been observed during and after the treatment. SUBJECTS AND METHODS Group 1: Normal Conduction. Twenty-five patients with acute myocardial infarction were given a 14-day course of oral prednisolone decreasing from 30 mg. daily to nil over that period. The P-R interval was recorded on an initial electrocardiogram, on the eighth day (in the middle of the steroid course), and a final record at four weeks (i.e. two weeks after stopping steroids), and these readings were analysed (Table I).A further 25 patients with infarct were studied in the same way but had no steroids, and these formed a control series. The two groups were obtained by random sampling of 50 consecutive cases of established myocardial infarct. All records were taken on a direct-writing electrocardiogram: all measurements of P-R were made from lead II of the tracing. In both treated and control groups patients were lost by death. Complete sets of readings were obtained in 17 patients treated with steroids, and in 18 controls.

No abstract

No abstract

No abstract