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Animal experiments were done to learn the degree of coronary narrowing required to produce the larger intercoronary collateral channels, their speed of development, and the degree of protection afforded the myocardium. Twelve or more days of 75 per cent narrowing were required to produce sufficiently rich anastomotic communications to protect the myocardium from damage, and to permit survival after superimposed acute complete occlusion. The physiologic and pathologic significance of the intercoronary collateral communications and the clinical implications in coronary artery disease are discussed.T HE CLINICAL manifestations of acute myocardial infarction are no longer regarded to be solely the result of an acute occlusion of a coronary artery. In some instances, acute myocardial infarction occurs in the absence of fresh narrowing or occlusion'-while in other hearts the effects of acute occlusion may be partly neutralized by the presence of collateral circulation consequent to previous narrowing. Thus, acute myocardial infarction is to be regarded rather the resultant of two opposing processes; namely, the obstruction to blood flow by occlusive processes, and the compensatory development of collateral circulation which serves to offset the dire effects of coronary narrowing and occlusion.Despite excellent studies of the collateral coronary circulation, the speed with which interarterial connections develop and the degree to which they protect the myocardium are imperfectly understood. Clinical and pathologic data on hearts with old coronary occlusion and with collateral circulation do not yield decisive answers. On examining such a human heart post mortem, only the net end result of the obstructive process and the compensatory bypasses is witnessed; one cannot determine accurately, even by microscopic study, how long previously the narrowing or complete occlusion

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