Bundle branch and intraventricular block in acute coronary artery occlusion

Abstract

1. 1. Intraventricular block, including bundle branch block, was present in 15 per cent of 375 cases of acute coronary artery occlusion. 2. 2. Patients in this group were older than controls and presented clinical and pathologic evidence of severe heart disease. Congestive heart failure, antecedent hypertension, cardiac enlargement and evidence of previous attacks were the rule. 3. 3. The conduction defect was usually observed on the first day and was usually permanent. In six patients it was transient. 4. 4. Intraventricular or bundle branch block could not be diagnosed clinically since there were no specific symptoms or physical signs. Gallop rhythm was present in 60 per cent of the cases, but was probably due to the associated wevere heart failure. 5. 5. Left bundle branch block occurred in 51 per cent of the group, typical or atypical right bundle branch block in 28 per cent and intraventricular block in 21 per cent. The configuration of the ventricular complexes as well as the axis deviation often varied in serial records. 6. 6. In the presence of intraventricular block characteristic electrocardiographic signs of myocardial infarction failed to appear in one-third of the cases. 7. 7. The precordial lead may be of diagnostic importance, for progressive S-T and T-wave changes may occur only in this lead. Absence or marked diminution in the initial positive deflection in this lead is usually due to anterior wall infarction even when bundle branch block is present, although occasionally the latter alone is the cause. 8. 8. Intraventricular block was often associated with impaired auriculoventricular conduction. Other arrhythmias were not more common than in coronary occlusion in general. 9. 9. The sudden appearance of defective intraventricular conduction should suggest recent coronary occlusion. Since bundle branch or intraventricular block following coronary occlusion is usually permanent, it may be the only evidence that the patient has suffered a coronary occlusion in the past. Repeated attacks of coronary occlusion may result in a progressive increase in the QRS duration. 10. 10. The presence of defective intraventricular conduction in coronary occlusion adds to the seriousness of the prognosis, the mortality rate being 42 per cent. The more severe the conduction defect was, the higher the mortality rate, but there was no correlation with the type of block. 11. 11. The anatomical basis for the conduction defect was septal infarction, which was present in four-fifths of the hearts. 12. 12. Correlation between the vessels occluded or the location of the septal infarct and the type of conduction defect could not be made; occlusion of the right coronary artery was as frequent as that of the left and anterior infarction was as common as posterior infarction, regardless of the type of block. 13. 13. The persistence of normal conduction in many cases with septal infarction was attributed mainly to the presence of adequate collateral circulation in the septum. 14. 14. Transient bundle branch block was probably due to anoxemia resulting from shock, tachycardia, and heart failure. 15. 15. The vagus nerve probably played no role in bundle branch block since the latter was not affected by the injection of atropine. 16. 16. The relation between cardiac enlargement and bundle branch block was discussed, and the influence on the electrocardiogram of cardiac enlargement and bundle branch involvement contrasted. 17. 17. The treatment is that of coronary occlusion in general, with special attention to heart failure. The value of aminophyllin and oxygen was emphasized. Quinidine and digitalis should be used only when there is persistent rapid ventricular rate with failure.