The normal sequence of ventricular recovery proceeds from epicardium to endocardium, but on the epicardium the pattern of ventricular recovery is similar to the pattern of activation. Data concerning ventricular repolarization have been obtained from analyses of electrocardiographic recordings, suction potential recordings, a limited number of recordings of transmembrane action potentials, and from measurements of refractory periods. Normal ventricular repolarization has now been characterized in sufficient detail that it can be used with theoretic models to derive T waves with forms that correspond closely to recorded T waves. These models provide insights concerning the body surface manifestations of the electrophysiologic events of ventricular repolarization and should contribute to a more physiologic approach to interpreting T wave abnormalities in clinical electrocardiograms. A relationship between inhomogeneity of ventricular refractory period duration and arrhythmia vulnerability has also been documented. Because inhomogeneity of ventricular repolarization is a factor in both T wave-form and arrhythmia vulnerability, methods of analysis of the T wave for determining patients at risk of developing arrhythmias should be possible. One such analysis is presented. The method has been tested on experimental animals before and after interventions designed to increase arrhythmia vulnerability and in a limited number of patient studies. The results to date are encouraging and suggest that in the future electrocardiographic examination will be used as a prognostic tool in addition to its already established diagnostic function.
Functional distributions of individual cardiac nerves distal to the stellate ganglia were determined in 30 open-chest, anesthetized dogs by mapping sites of refractory-period shortening during stimulation of the nerves. On the right, recurrent cardiac nerve stimulation produced marked shortening of refractory periods in the interventricular septum, and lesser changes on the anterior heart surface. On the left, ventromedial cardiac nerve stimulation shortened refractory periods in a similar distribution, but changes were not marked as with the recurrent cardiac nerve. The other left-side nerve that produced repolarization changes, the ventrolateral cardiac nerve, produced marked refractory-period changes on the posterior heart surface. Its distribution showed little overlap with that of the ventromedial or recurrent cardiac nerves. T waves inverted in an electrocardiographic Y lead during recurrent cardiac and ventromedial cardiac nerve stimulation, while ventrolateral cardiac nerve stimulation increased the positivity of T waves in that lead. The cardiac distributions of individual nerves documented in this study provide an anatomical basis for localized alterations in ventricular electrophysiologic properties.
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