THE DYNAMIC FACTOR IN ENLARGEMENT OF CORONARY ARTERIAL ANASTOMOSES, AND PARADOXICAL CHANGES IN THE SUBENDOCARDIAL PLEXUS

Most investigators are agreed that frequent arterial anastomoses of relatively large size may be demonstrated in the coronary circulation in the presence of obliterative coronary artery disease. Evidence has been presented which shows that the enlarged anastomotic channels found in disease may in fact be derived from pre-existing, pre-capillary communications (Fulton, 1960, 1963a,b). Although there is a considerable body of information concerning the effects of coronary artery ligation on collateral blood flow in the experimental animal (Gregg, 1950) and on the increased incidence of readily injectable intercoronary communication in the presence of coronary occlusion (Zoll, Wessler, and Blumgart, 1951a), knowledge about the exact anastomotic pathways concerned and detail of their structural change is still somewhat sketchy. Enlargement of anastomoses on the surface of the heart has tended to attract greater notice than have changes taking place in the deeper vessels. This is probably attributable to the relative ease with which the superficial vessels may be demonstrated. However, an arterial network in the -inner zone of the left ventricle was described independently in the normal heart by Spalteholz (1907, 1924) and by Gross (1921), and the subendocardial network has been shown to undergo great enlargement and to exert profound influence on the distribution of blood to the heart in coronary artery disease (Fulton, 1956, 1960, 1964b). Apart from the observations made in the present investigation, enlargement of the vessels composing the subendocardial plexus of the left ventricle appears to have received little attention in pathology. It is perhaps for this reason that the apparent paradox of enlargement of these vessels under conditions of severe restriction of total blood flow to the heart has excited so little comment hitherto. The manner in which the subendocardial arterial plexus of the left ventricle enlarges in the presence of coronary artery disease, and some factors that promote anastomotic enlargement at this -site, and elsewhere in the heart, are considered in this communication.

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