In 12 dogs on right-heart bypass with heart rate, stroke volume, and aortic pressure constant, the velocity of contraction was augmented comparably by three fundamentally distinct interventions in the same heart: 1) sustained postextrasystolic potentiation produced by paired, electrical stimulation; 2) norepinephrine infusion; and 3) calcium infusion. In each instance the correlation between velocity of contraction and MVo2 was striking. During paired stimulation, maximum rate of left ventricular ejection increased by an average of 50.3% ± 3.8% (se of mean) above control, MVo2 increased by 1.96 ± 0.10 ml/100 g per min (39.8% ± 1.6% above control), while the tension-time index (TTI) fell 12.4% ± 1.1%. With norepinephrine, and with calcium, left ventricular ejection rates were increased 52.9 ± 3.2% and 55.1 ± 3.2%, respectively, and MVo2 was augmented 2.03 ± 0.08 ml/100 g per min and 1.87 ± 0.04 ml/100 g per min, while the TTI decreased 15.9 ± 0.6% and 12.4 ± 2.4%. Since MVo2 always increased substantially while TTI fell, tension cannot be considered to be the sole determinant of MVo2. Since comparable increases in velocity of contraction produced by different interventions were associated with similar large augmentations of MVo2, it appears that the velocity of contraction is an important determinant of MVo2. Furthermore, it is likely that the so-called O2 wasting effect exerted by norepinephrine on myocardial metabolism may be explained largely by an increased velocity of contraction.

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A study was designed to correlate changes in bipolar epicardial electrograms recorded from normal and acutely infarcted myocardium with the onset of ventricular arrhythmias. Electrodes were sewn to selected sites on the left ventricle, and after control electrograms and ECG's were recorded, the left anterior descending coronary artery was doubly ligated close to its origin. Electrograms recorded from within the infarct initially manifested diminished amplitude and increased duration of the deflection which reflected depolarization. The appearance of ventricular arrhythmias during phase 1 of Harris was associated with the appearance in electrograms recorded from within the infarct of continuous electrical activity which extended beyond the T wave of the preceding beat and preceded the onset of the arrhythmia. During the continuous electrical activity, it was not possible to delineate which deflections of the electrogram reflected depolarization or repolarization and it was suggested that the continuous electrical activity was localized fibrillation. For three experiments in which no arrhythmias occurred during phase 1 of Harris and for all animals which survived into phase 2 of Harris, the absence of ventricular arrhythmias was correlated with the absence of continuous electrical activity or locallized fibrillation recorded from within the area of the infarct.Additional Indexing Words: Acute myocardial infarction Ventricular electrograms Localized fibrillation Ventricular arrhythmias IT IS well known that ventricular arrhythmias are associated with myocardial infarction.' Wilson's group2 3 was the first to study experimentally produced myocardial infarction by recording epicardial electrograms and to correlate changes in the local electrogram with changes in the ECG which occurred during the experimentally produced infarction. Since then, there have been numerous studies which have contributed to the understanding of the nature of arrhythmias associated with myocardial infarction. In 1943, Harris and Rojas4 used a string galvonometer to record epicardial electrograms from ischemic areas of the canine heart following acute occlusion of the left anterior descending coronary artery. They reported that as the ischemia developed, electrograms recorded from within the area of the infarct demonstrated a progressive loss of amplitude and increase in duration, until in many cases, no electrogram could be recorded. Recent studies using more sophisticated electronic recording technics 7 have demonstrated that bipolar electrograms could be recorded from areas of ischemic myocardium. The present study was designed to reexamine the observations of Harris and Rojas by recording bipolar electrograms from acutely infarcted regions of the canine myocardium and correlating the electrical activity thereby recorded with the occurrence arrhythmias involving the remainder of the ventricles. From the Methods Twenty-five mongrel dogs weighing 15-25 kg were anesthetized with intravenously administered pentobarbital, 30 mg/kg. For each anim...

When a depolarizing stimulus is delivered to the ventricle immediately following the refractory period, little extrasystolic contraction occurs and repetitive paired stimulation then results in a marked and sustained improvement of ventricular performance which has been termed electroaugmentation. The present study characterizes this augmentation and its effects on myocardial oxygen consumption (MV O O 2 ). In 45 experiments on 14 dogs in which mean aortic pressure and stroke volume were held constant by right heart bypass, a change from single to paired stimulation at identical contraction rates markedly increased the performance of the left ventricle as evidenced by shortening of ejection time increase in left ventricular dp/dt, stroke power, and peak ejection rate, and sometimes a fall in end diastolic pressure. Similar resul were obtained after administration of resepine or nethalide. In 15 experiments on 11 dogs the stroke volume of the left ventricle was varied during single and paired stimulation. Improvement in left ventricular performance during paired stimulation was always evidenced by increased speed of contractic and an upward displacement of the curvesrelating end diastolic pressure to stroke powe mean and peak ejection rates, and some times by an upward displacement of the curves relating end diastolic pressure to stroke volume and stroke work. In eight experiments MV · O O 2 was determined during single and paired stimulation, stroke volume, mean aortic pressure, and contraction rate being held constant. Paired stimulation always increased MV · O O 2 the average increase being 35%. Despite the rise in MV · O O 2 , a reduction in the tension-time index always occurred. These studies indicate that repetitive paired stimulation exerts a powerful and sustained positive inotropic in fluence on the mammalian ventricle and that at a relatively constant level of external world the increased velocity of ventricular contraction which accompanies this effect results in an increase in MV · O O 2 .