No abstract

No abstract

In IO patients with severe myocardial infarction and left ventricular failure, bretylium tosylate was used in the treatment of ventricular arrhythmias which had proved refractory to lignocaine and procainamide; 6 cases had also failed to respond to phenytoin. In 7 patients stable sinus rhythm was achieved and 5 of these survived to leave hospital. For the period during which bretylium was used, the only observed side-effect was sinus bradycardia.The anti-arrhythmic effect of bretylium tosylate was first described in I965 when Leveque reported its protective effect in experimentally-induced atrial fibrillation in dogs. In the following year, Bacaner (1966) showed that bretylium protected the dog heart against ventricular fibrillation by raising the fibrillation threshold, and later demonstrated (Bacaner, I968a) that it was more effective in this respect than lignocaine, procainamide, quinidine, phenytoin, and propranolol. Since then,

Ischaemia reduces membrane excitability and conduction of myocardial depolarisation. This would alter the synergy of electromotive forces that contribute to a resultant force at any instant. Changes in magnitude and direction of resultant forces are reflected in electrocardiographic signals. Here we show a method for obtaining the coordinates of resultant electrical forces during exercise derived from a bipolar orthogonal lead system for calculation of electrical vectors in three planes. In a trial, analysis of changes in vectors indicated that the extent of reduction in magnitude with exercise was significantly greater in groups of patients categorized by impaired effort tolerance and signs of ischaemia. Measurement of changes in the spectrum of depolarisation vectors during exercise has the potential for non-invasive assessment of myocardial ischaemia. This could be the basis of a portable, low-cost tool for investigation of patients with symptoms suggestive of coronary artery disease.

The electrocardiograms in this study of parasystolic rhythm were tape recorded and then analysed with a special purpose hybrid computer. The rate of appearance of specific inter-ectopic intervals was shown to change significantly with small changes in either the sinus or parasystolic pacemaker period. Natural changes in the period of the ectopic pacemakers were observed over several hours. Changes amounting to 14% within 10 min and 18% overall were observed in one patient, and a gradual lengthening of 10% over 3 h in another. A previously undescribed form of exit block has been discovered in one patient where the block remained active for a given time only after propagation from the parasystolic focus. Different interectopic intervals were shown to contribute to specific and restricted coupling interval locations in diastole. Hence this form of exit block, by preventing some inter-ectopic intervals from propagating, limited the locations in diastole in which parasystolic ectopic complexes could appear. In this case later diastolic complexes were inhibited and hence fusion complexes were completely absent. Parasystolic rhythm, with and without the exit block described, was simulated successfully by a digital computer. The simulations aided our understanding of the clinical data.