Effect of Coronary Artery Occlusion on Dog's Heart with Total Coronary Sinus Ligation. ∗

Abstract

One of us (L.G.) 1 described 3 vascular mechanisms in the blood supply to the human heart which probably serve as compensatory means to ward off the results of coronary artery narrowing or occlusion. The first and most important of these is a gradual and consistent widening of anastomotic channels which occurs with increasing age. It was shown that many of these anastomotic channels are situated in the interventricular septum. The second compensatory mechanism is the age period development of rami telae adiposae, vessels which lie in the epicardial mantle and anastomose with the myocardial vascular ramifications on the one hand, and with periaortic and peripulmonic vessels on the other. The third mechanism is the existence of anastomoses between the myocardial and pericardial vascular ramifications and the extracardiac vessels (bronchial arteries, arteriae mammariae internae and diaphragmmatic vessels). These studies were subsequently confirmed and extended by Campbell, 2 Davis, 3 Robertson, 4 Hudson, Moritz and Wearn, 5 and by Gross and Kugel. 6

Recently, augmentation of these extracardiac anastomoses was attempted by Moritz, Hudson and Orgain 7 by means of epicardiectomy (stripping of epicardium) with resulting pericardial adhesions. Using this procedure, Beck, Tichy and Moritz 8 observed that some dogs may recover after gradual coronary artery occlusion covering a period of 2 years and that no infarctions were produced in the hearts. Robertson 9 produced pericardial adhesions by tying off coronary veins in stages. In many cases such dogs tolerated coronary occlusion, also produced in stages. If the adhesions were separated, however, the dogs died with fresh infarcts. Robertson believed that the progressive adhesions supplied nutrition to the heart.

Apart from the fact that these techniques involve extensive operative procedures, the question arises as to whether the results obtained were due to the added vascular supply by way of the pericardium or to the compensatory vascular dilatation within the myocardium made possible by the slow occlusion of the coronary arteries.