Corticotrophin and corticosteroids in the management of acute and chronic heart block.

Abstract

Clinical studies and individual case reports indicate that corticotrophin and corticosteroids frequently help to restore sinus rhythm in acute complete A-V heart block associated with recent myocardial infarction (Prinzmetal and Kennamer, 1954;Phelps and Lindsay, 1957;Aber and Wyn Jones, 1960;Caramelli and Tellini, 1960;Friedberg et al., 1960;Dall and Buchanan, 1962; Dalil, 1964). However, the true value of this form of treatment in chronic A-V block is less certain. Tung, Lu, and Fu (1957) and Litchfield, Manley, and Polak (1958) each reported two patients with long-standing block who reverted to sinus rhythm under corticotrophin therapy, and Pay and Waverley (1961) restored sinus rhythm in 5 out of 6 patients with chronic heart block, using oral corticosteroids. On the other hand, Caramelli and Tellini (1960) failed to improve A-V conduction in 10 patients, and in Dall's series (Dall, 1964) only 2 of the 14 patients with long-standing block regained sinus rhythm while receiving "steroid" therapy.Our experience of corticotrophin and corticosteroids in the treatment of heart block has been less pessimistic. Restoration of sinus rhythm or improved A-V conduction has not only been achieved in most patients with acute heart block, but also in an appreciable number with heart block of considerable duration. SUBJECTS AND METHODSBetween 1958 and 1964 we studied the effects of corticotrophin (ACTH) and corticosteroids on 36 patients with complete A-V block. These patients form 2 groups.Group I: 10 patients (6 men and 4 women) with acute heart block (less than 48 hours' duration) following recent myocardial infarction. The mean age was 60 years (range 43-80 years) and the mean duration of heart block before the start of "steroid" therapy was 16fi5 hours (range 4-48 hours) (Tables I and III). Group II: 26 patients (8 men and 18 women) with chronic heart block (longer than 1 month's duration). Of these, 11 had undoubted coronary artery disease. In the remaining 15 reliable evidence of coronary artery disease was lacking. The mean age was 61 years (range 34-77 years) and the mean duration of heart block in this group was assessed at 8 months (range 5 weeks to 30 months) (Tables II and III). In several patients accurate assessment of the duration of block was not possible; therefore some of the values recorded in Table II may have been underestimated. Selection and Management ofPatients. Corticotrophin or corticosteroids were given to all patients with acute heart block in association with recent myocardial infarction (Group I). Patients with chronic heart block (Group II) were selected for "steroid" therapy if they were experiencing either incapacitating StokesAdams syncope or were in either right or left heart failure and had failed to respond to more conventional treatment.The following criteria determined the initial management of these two groups of patients (Tables I and II). 916

Outcomes for children with acute myocarditis

“…The use of immunosuppression for treatment of myocarditis probably began nearly 40 years ago. 7,8 Early clues regarding the role of activation of the immune system, and viral infection, in the pathogenesis of myocarditis came to light shortly thereafter. [9][10][11][12] Das went so far as to suggest the possibility of viral infection in, and subsequent alteration of, myocardial tissue, thereby making it immunogenic.…”

Corticosteroids in the Management of Sinoatrial Block

“…Encouraging results have been reported by some [9][10][11], suggesting that corticosteroids frequently re store sinus rhythm, particularly in acute complete A-V block [10][11][12]. Others, how ever, reported complete or almost complete failure [13,14], To the best of our knowledge, no such therapy has been reported in S-A block.…”

“…As no inflammatory pro cess could be diagnosed in our patients, the anti-inflammatory action of steroids does not seem to provide an explanation for the improvement in S-A conduction in these cases. It is conceivable that the metabolic effect of steroids on the myocardium and changes in the intracellular-extracellular el ectrolyte flux [11] consistently reduce stimu latory threshold by altering cellular mem brane permeability, and led to a 'facilitating effect' [19] on the S-A conduction. It is known that steroids shorten the P-R interval [19] and are therapeutically used to treat 'pacemaker exit block', and a similar phe nomenon may occur in the S-A conduction.…”