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Original communication| Volume 9, ISSUE 1, P1-24, January 1941

The physiology, pathology, and clinical significance of experimental coronary sinus obstruction

Its relation to cardiac surgery, coronary thrombosis, and nutrition of the heart by thebesian vessel or coronary sinus backflow
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      Abstract

      • 1.
        1. Variations in cardiac function and morphology, produced by coronary sinus occlusion, or by occlusion of the veins of the heart, depend on the varying number and efficiency of the venous and thebesian anastomoses which drain the heart wall. Thus, with insufficient or inefficient venous and thebesian anastomoses large enough degrees of venous occlusion may produce congestion of the heart wall, slowing of the heart, dilatation of the veins and the arteries of the heart, and myocardial necrosis.
        The coronary sinus of dogs, cats, and monkeys in many instances can be completely and suddenly occluded, where it enters the right auricle, without producing any significant change in cardiac function or morphology. Sometimes, however, in dogs especially, left heart congestion occurs, with slowing of the heart, dilatation of both the arteries and the veins, and a moderate to severe degree of myocardial necrosis. Such a reaction does not usually endanger cardiac function gravely. In a large series of dogs no death occurred from the effects of coronary sinus ligation, but the myocardial changes produced would not prove beneficial to a heart already suffering from other pathology.
        Individual cardiac veins in the dog, cat, and monkey can usually be tied without change or with very slight change in cardiac morphology. Ligation of the larger veins or of groups of veins sometimes leads to a small amount of myocardial necrosis, but produces no marked change in cardiac function or morphology.
      • 2.
        2. Thebesian vessels can be dilated by tying the coronary sinus. In most hearts they dilate so readily that, when the coronary sinus is closed, the venous blood of the left ventricle is rapidly forced into the left ventricular cavity and no congestion ensues.
      • 3.
        3. When venous congestion of the left heart wall occurs, following coronary sinus closure, it gives rise to a vasodilatation of the coronary vessels and to slowing of the heart. This reaction resembles that seen after intravenous or intracardiac administration of adenosine or similar substances and suggests the local application of such substances to the heart in cases of coronary thrombosis.
      • 4.
        4. This study supports the contention that tying the main vein, from a part already deprived of its main arterial supply, is likely to cause muscular necrosis, sometimes of serious enough degree to offset any possible advantages of the procedure. Such a procedure, if it causes significant vascular congestion with increased oxygen utilization and vascular dilatation, apparently may induce muscular necrosis in the affected part.
      • 5.
        5. A consideration of the coronary sinus outflow and pressure curves, in relation to the cardiac cycle and cardiac pressure curves, prejudices one against either a thebesian vessel backflow of a coronary sinus backflow as a source of nutrition to hearts deprived of their ordinary blood supply.
      • 6.
        6. The occlusion of coronary veins makes no change in electrocardiographic curves. Occlusion of the coronary sinus, if no congestion and cyanosis of the left heart wall ensues, makes no change in the electrocardiographic curves. If congestion and cyanosis ensue, then splintering, M or W in form, of the QRS complex is seen. It may be that lack of oxygen in ventricular muscle accounts for this phenomenon, as it disappears in acute experiments the moment congestion is relieved by unclamping the sinus; and in survival experiments it disappears in twenty-four to forty-eight hours when left heart congestion has disappeared.
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