Abstract
The exact mechanism by which the myocardium is nourished in the presence of chronic obstruction of the coronary arteries is still controversial. 1 , 2 The reason for this appears to be that the studies have been largely anatomical and give only qualitative data regarding collateral blood flow. 3 In the normal heart the controversy has been cleared to a large extent by physiological studies. The majority view is best expressed by Wiggers: 4 “The collateral flow is extremely small and insufficient to support contraction in an area rendered [acutely] ischemic by ligation of a main [coronary artery] branch.” However, since anatomical connections normally exist between a given coronary artery and (a) other coronary arteries, 5 (b) extra-cardiac arteries 6 and (c) ventricular cavities, 7 the work of Wiggers does not rule out the possibility of enlargement of existing collateral channels or the development and enlargement of new connections. Indeed, it is known that following acute experimental occlusion of a coronary artery, the infarcted area is generally much smaller than the area originally supplied by the occluded artery. 8 We have, therefore, attempted to devise ways and means of stimulating the development of such an accessory circulation and to study its physiological extent.
It seemed to us that the ultimate solution of the problem of the development, source, and determinants of collateral coronary flow might be reached by studying the peripheral coronary pressure (P.C.P.) and blood flow from coronary arteries that have been occluded for varying lengths of time and in hearts with increasing extent of coronary arterial occlusion.
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