Rheumatic fever in Hawaii: Alfred S. Hartwell, M.D., Honolulu, T. H., Hawaii

Abstract

1.1. By means of a specially designed plunge electrode, intraventricular leads were recorded from multiple sites throughout the walls, papillary muscle, septum and cavities of thirty-two dogs during normal sinus rhythm. A series of experiments was performed which established (a) that the presence of the plunge electrode in the myocardium did not alter the normal course of depolarization, and (b) that the depolarization complexes registered by the plunge electrode represented essentially local potentials.2.2. Pure QS or rS waves were recorded throughout at least the innermost two-thirds of the intramural myocardium in both ventricles as well as from all levels of the left papillary muscle. Intraseptal leads also exhibited essentially negative deflections, although considerable positivity was noted in the center and right side of the septum. Only the epicardial surface and a thin subjacent layer of the walls yielded predominantly positive depolarization complexes. In general, negative potentials were found to predominate in roughly 80 per cent of the musculature during ventricular depolarization while about 20 per cent of the myocardium was predominantly positive. This observation indicates that the ventricular wall does not depolarize in the same manner as the auricles.3.3. Pure QS waves consistently were obtained throughout the left ventricular cavity as well as from all portions of the right ventricular cavity except in the immediate vicinity of the septum. Cavity leads recorded near the right septal surface occasionally displayed a small R wave derived from the initial positivity of the right septal surface.4.4. The velocity of the depolarization wave was measured in twenty animals by timing the onset of the downstrokes in intramural leads from multiple depths of the left ventricular wall. As determined by this method, the rate of depolarization appears to be considerably more rapid in the innermost two-thirds of the wall than in the superficial layers.5.5. Currents of injury, manifested by RS-T segment elevation, always occurred for a brief period following the introduction of the plunge electrode into the myocardium. The RS-T segment deviation was markedly less in subendocardial leads than in subepicardial leads, indicating that subepicardial muscle characteristically is capable of producing more intense injury currents than are the deeper layers of the myocardium.6.6. The observed weakness of subendocardial injury currents in experimental animals suggests that the downward RS-T segment deviation, which is seen clinically in angina pectoris, is not attributable to subendocardial anoxia as is generally believed. On the basis of the same experimental observation, a new theory concerning the cause of RS-T segment elevation following coronary occlusion is proposed which appears to reconcile apparent discrepancies among the electrocardiographic, anatomic, and pathologic findings.