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(1966). Assistances circulatoires pulsees, applications cliniques. La Houille Blanche: Vol. 52, No. 2, pp. 181-188.

Summary Electrical systole duration has been studied in two groups of 23 patients (39 M and 7 F) admitted in the coronary care units of two different hospitals for documented acute myocardial infarction (AMI). The mean QT interval duration corrected for heart rate (QTc) was obtained from three measurements of non consecutive complexes in five different leads and compared to the ideal electrical systole duration of a normal population with the same cardiac cycle length. During the evolution of AMI, QT interval increased in both groups of patients (11.5% and 14.8% respectively) and was prolonged (17.6% and 21.5% respectively) at the 48th hour. Prolongation of electrical systole can be best measured using the ratio: QTc (according to Bazett)/normal QT (according to Ashman).

Experimental and clinical studies demonstrate the antifibrillatory effectiveness of bretylium tosylate: Experimental ventricular fibrillation induced either by electrical stimulation or by ischemia is prevented by bretylium. In 2,000 acute myocardial infarction patients who received bretylium prophylactically primary ventricular fibrillation occurred in less than 1% of cases. In a randomized hemodynamic study in acute myocardial infarction patients bretylium induced a significant decrease in heart rate, systolic and mean left ventricular pressures, and in systolic and mean aortic pressures. In addition, a parallel and significant decrease in total pulmonary and systemic resistances was seen, accompanied by decreases in tension time and left ventricular (delta P/delta V) indexes. Bretylium tosylate induces stabilization of electrical systole duration (QTc) in acute myocardial infarction patients. The conclusions of the present review strongly support those of the United States Food and Drug Administration, approving bretylium for prophylaxis and treatment of ventricular fibrillation.

Extension of the duration of electric systol in the acute phase of coronary thrombosis can be analysed in satisfying conditions whatever the physiological frequencies by the measurement (formula; see text) represents the average QT measurement of three non-consecutive complexes in five derivations (DI, DIII, aVF, VI and V6). This extension is of prognostic value when the QTc is greater than 44 c/s. Out of 1 255 acute phase thrombosis patients, 18 Out of 20 cases of ventricular fibrillation revealed a QTc greater than 44 c/s in the 24 hours preceding sudden death. Therapeutic intervention with anti-andrenergic drugs such as bretylium tosylate or beta-blocking agents appears to reduce the QTc of these patients and thus prevent sudden death.

The electrical systole duration (QTc), heart rate, and the QTc/QTt ratio were studied during the hospital course of an uncomplicated AMI in 13 patients treated with bretylium tosylate (10 mg/mg/24 hr over 5 days since confirmation of AMI) and in 19 controls. The QTc/QTt ratio showed prolongation of electrical systole duration in control subjects with a maximal value at the second day after AMI. QTc increased in these patients from day 1 to day 2 after AMI (402 +/- 4 msec vs. 430 +/- 3 msec, p less than 0.05) and decreased in the following days (p less than 0.05). During hospitalization cardiac rate was constant in both groups. In contrast, patients treated with bretylium tosylate showed a stable duration of QTc and the QTc/QTt ratio did not indicate prolongation of electrical systole duration. After drug discontinuation a slight increase in QTc duration was noticed (391 +/- 6 msec vs. 413 +/- 5 msec, p less than 0.05). These observations may contribute to the understanding of the antiarrhythmic action of bretylium and would indicate its usefullness in AMI patients with prolonged QTc and high risk of life-threatening arrhythmias.

Recent reports have drawn attention to the association between long QT intervals and sudden death in myocardial infarction and certain congenital syndromes. This study was undertaken to determine the relationship between lengthening of the QT interval and primary ventricular fibrillation in acute myocardial infarction. Thirteen cases were chosen out of a total of 21 cases of primary ventricular fibrillation (5.09% of 412 cases of myocardial infarction hospitalised during this period). Ten other cases of myocardial infarction with the same features apart from the arrhythmia were used as controls. Three series of electrocardiogrammes recorded under the same technical and chronological conditions (2 before and 1 after ventricular fibrillation) were analysed. The average QT interval was corrected for heart rate (RR) with Bazett's formula. The average QTc in acute myocardial infarction was longer than the theoretical QTc (p less than 0.05). The graph showing this increase reached a peak at the 48th hour. The average QTc in patients with primary ventricular fibrillation was longer than in the control patients (p less than 0.05) and significantly longer than the theoretical value (p less than 0.001). The average QTc in survivors of ventricular fibrillation was not significantly longer than that of the control group but was longer than the theoretical value (p less than 0.01). These results justify the strict surveillance of the length of electrical systole in the first hours of the acute phase of myocardial infarction. In this series, values greater than 440 ms were associated with a high risk of ventricular fibrillation in the first week after myocardial infarction.

Acute occlusions of the proximal left circumflex coronary arteriovenous pedicle were performed in open chest anaesthetised dogs. Twenty eight dogs were randomly allocated to receive acebutolol (3 mg X kg-1 twice daily) or placebo given blindly by mouth for five days; a control group of 14 dogs without any pretreatment underwent the same procedure. Coronary ligations in the randomised study were performed during seven consecutive days, and four dogs were operated on each day. This schedule was chosen in order to measure acebutolol plasma concentrations just before ligation from 60 to 540 min after the last dose of the drug. Long term oral treatment with acebutolol protected against postischaemic ventricular fibrillation and significantly reduced the incidence of both early phase (0-10 min postocclusion) ventricular arrhythmias and ventricular fibrillation. As a result the outcome was significantly improved after 60 min of ischaemia in acebutolol compared with placebo treated animals. The results in the control animals were similar to those in the placebo treated dogs. The protective effect of long term oral treatment with acebutolol lasted for nine hours and was apparently independent of the plasma concentrations of the drug. These data show that improved outcome in this canine model is due to the prevention of ischaemia induced ventricular fibrillation by long term beta adrenoceptor blockade, which is able to overcome the effect, if any, of partial agonist activity of acebutolol. A direct myocardial anti-ischaemic effect might explain the effectiveness of long term oral treatment, which is independent of plasma concentrations of the drug.

The aim of this prospective study is comparing long-term prognosis in patients implanted with a VVI pacemaker (group A) with those implanted with a sequential pacing device, AAI or DDD, (group B). Both groups of 45 patients each, were comparable as regards to age, sex, pacing indications, underlying heart disease, and technical conditions of implantation and were followed-up over 55 months. Atrial arrhythmias (A.A.) incidence was higher in group A: 24.4% than group B: 8.8% (P less than 0.05). Arterial embolisms (A.E.) occurred in group A patients only. Worsening or occurrence of exercise limitation was more frequent in group A: 35.6% as compared to group B: 13.3% (P less than 0.05) and deaths related to these complications, occurred in seven cases in group A versus four cases in group B. In group A, all patients who experienced a worsening or occurrence of an A.A. or an A.E., had a ventriculoatrial conduction (VAC). No statistical difference was observed in worsening or occurrence of exercise limitation between patients with VAC and those without VAC: nine (42.8%) and seven (29.2%) but they respectively experienced at least one complication in 16 cases (76.2%) and seven cases (29.2%) (P less than 0.01). In conclusion, long-term prognosis in patients implanted with VVI pacing as compared to patients implanted with sequential pacing is poorer. The presence of VAC in patients treated with permanent VVI pacing is a major factor for complications and deaths related to A.E. and cardiac failure. Thus VVI pacing should be avoided in patients with VAC.

A critical review of the available data on QT interval is presented to delineate techniques useful to the development of a QT-sensitive cybernetic pacemaker. The reason for the development of this unit stems from the ability of QT prolongation to predict the onset of life-threatening ventricular arrhythmias in some clinical situations; the QT interval is physiologically related to the cardiac cycle length, therefore providing adequate information to drive both ventricuiar and atrioventricuiar sequential rate-responsive pacemakers. This unit might also monitor cardiac rhythm and detect the pathophysioiogic precursors of advanced grades of ventricular arrhythmias. A therapeutic role, both pharmacologic and electrical, may also be possible in the future. Integration of these concepts and cooperation between interested physicians, technicians and manufactors will be necessary to produce such a unit at a low cost-benefit ratio. The potential clinical application of this pacemaker deserves attention for the prophylaxis and treatment of sudden arrhythmic death.