Complete heart block complicating acute myocardial infarction, and the role of artificial pacing in its management

Abstract

To determine the effect of artificial pacing on the natural history of complete heart block (CHB) complicating acute myocardial infarction, 100 patients with this disorder of conduction were studied under conditions of continuous electrocardiographic monitoring and intensive care with pacing immediately available. The clinical and electrocardiographic features in these patients and the necropsy findings in those patients who died were examined and related to the need for and effects of pacing. To determine the circulatory alterations associated with heart block in acute infarction and their response to pacing, haemodynamic measurements were carried out in 13 consecutive patients soon after the onset of CHB and were repeated on the second and subsequent days of heart block and after the return of normal atrioventricular conduction in five. In order to assess the long -team outlook of patients who had required pacing during the course of an acute infarct complicated by CHB, the first 27 of the 100 patients who survived to be discharged from hospital were reviewed at the end of one year.

CHB occurred early in the course of acute myocardial infarction and had developed prior to admission to hospital in many patients. However, when CHB was observed to develop, it was usually preceded by a premonitory disorder of conduction: second degree atrioventricular block in the case of inferior or inferolateral infarction, and complete bundle branch block in the case of anterior infarction. The most unfavourable immediate prognosis occurred in patients with anterior infarction or a QRS complex of greater than 0.12 second duration caring CHB. These patients usually had severe myocardial damn ge and pacing made little impact on their outlook. Inferior infarction with a QRS complex of less than 0.12 second duration was associated with a mortality little higher than that of patients with acute infarction uncomplicated by heart block. In the majority of these patients pacing was not required, but in a proportion of those with attacks of asystole or evidence of a low cardiac output, it produced striking improvements in clinical and haemodynamic features.

The prognosis during the remainder of the first year after discharge from hospital was no worse for patients who had been benefited by pacing during the acute attack than the outlook for patients with complete block in whom pacing had not been required. Moreover, the long-term prognosis for patients who survived an acute myocardial infarction complicated by CHB was no worse than that of patients with infarcts of similar severity but without heart block.

Because patients in whom bradycardia or asystole had been corrected by pacing and who survived the acute attack had a relatively good long -term prognosis, it was concluded that pacing does have a role to play in the management of CHB complicating acute myocardial infarction. Since 50% of patients with second degree heart block progressed to CHB and because it was not possible to predict which patients with block would eventually require pacing or when they would require it, it was also concluded that electrodes should be introduced in all patients with either second degree of complete heart block. On the other hand, although 30% of patients with complete bundle branch block progressed to CHB and most subsequently required pacing, electrodes should not be inserted prophylactically in this group of patients because pacing did not reduce mortality and because electrode insertion was associated with a high incidence of serious arrhythmias.

Because of the dangers associated with electrode insertion and pacing, special facilities inoluding continuous electrocardiographic monitoring and intensive care are required when this form of treatment is used. When such facilities are available, it was concluded that pacing is superior to drug therapy in treating patients with ventricular asystole and patients in whom bradycardia is responsible for clinical deterioration.