Spread of activation in the left ventricular wall of the dog. III.: Transmural and intramural analysis

Abstract

Important information as to the course of activation in the heart wall can be obtained from the transmural wall curve. This is but little influenced by the other parts of the heart, a fact that can be demonstrated by studying the influence of septum activation on it. The wall curve is highly asymmetric, and its fall has a very steep part. This fast portion is synchronous with the fast part of the corresponding unipolar epicardial lead. The P-R interval of the epicardial lead differs from that of the transmural lead: the former is 10 to 15 milliseconds longer than the latter. This is explained by the course of the cavity potential and the wall curve. The descending part of the cavity curve and the ascending part of the wall curve are nearly identical. The causes of this remarkable phenomenon are analyzed. The cavity potential comprises potential contributions from the wall activation and septum activation. The transmural potential originates nearly totally from activation of the free wall. Since the electrodes lie on either side of the activation front, the transmural potential is higher than that part of the cavity potential that originates from the wall activation. The contribution of the septum activation to the cavity potential makes the latter more or less equal to the transmural potential. In view of the fact that even the wall curve can give only a rough picture of the activation of the wall, the latter has been examined by means of needle electrodes. It was shown that despite the movements of the heart it is possible to fix the electrodes satisfactorily. The lesion effects following insertion of the needle disappear within 15 minutes at the most. The surrounding tissue remains sufficiently intact. Unipolar intramural leads and partial wall curves were registered synchronously. The latter were registered between an intramural leadpoint and a cavity electrode, placed close to the endocardium of the wall area in question. The unipolar intramural curves were strongly negative in a large part of the wall; R-waves occurred only in the outermost layers. The complex at the epicardial surface is the smallest of the series. The partial wall curves of the innermost layers show, in correspondence to this, a low voltage. Only in the outer layers does the shape of the partial wall curve approach that of the wall curve for the region in question. Both the unipolar intramural and the partial wall curves show larger or smaller fast portions; these are due to the activation of the layer in which the leadpoint in question is situated. A more accurate analysis can be achieved by taking bipolar leads from the closely-spaced leadpoints of an electrode needle and by the use of a differential needle electrode. In this way it has been shown that the innermost layers are more or less synchronously activated. In consequence of this the activation front in these layers is irregular in shape and the voltage does not reach the same values as in the outermost layers. In the bipolar leads this is shown by the small, irregular complexes. The activation of the outer layers, on the other hand, gives rise to regularly formed complexes, the width of which is proportional to the distance between the leadpoints. This indicates that the front is regular in form and sharply bounded. The velocity of propagation in these layers is approximately 50 cm./sec. Between the synchronously activated inner layers, which account for approximately two-fifths of the thickness of the wall and the outer layers there is in some areas a transitional region in which complexes, often regular in shape, are found which are indicative of activation in epi-endocardial direction. A hypothesis accounting for these facts is presented.