THE EFFECT OF CORONARY OCCLUSION ON MYOCARDIAL CONTRACTION

Abstract

An optical myograph suitable for recording localized contractions from a ventricular surface and a technique for its correct application are descr. Normal myograms recorded simultaneously with aortic or ventricular pressure curves, though slightly deformed by oscillations during the isometric contraction and relaxation phases, clearly show the natural shortening which occurs during ventricular ejection and the lengthening which follows isometric relaxation. Occlusion of a main coronary branch is followed by an evolving series of myographic changes which indicate progressive enfeeblement of contraction to the extent that approx. within a minute the area stretches during isometric contraction, remains stretched during systolic ejection and shortens quickly during isometric relaxation; in short, the myogram is completely inverted. Similar changes in contraction of the right ventricle occur following ligation of the right coronary artery. These observations demonstrate convincingly the functional inadequacy of described collateral circulation in normal hearts. Reestablishment of the normal blood supply is followed by a reversed series of myographic changes with restoration of normal vigorous contractions provided the period of ischemia is not too long in duration. Failure of shortening is due to enfeeblement or abrogation of contraction and not to failure of impulses to reach the areas involved, or to excite them. The O requirements for maintaining efficient contractions in the normally working heart are high as evidenced by the authors'' failure to maintain efficient contractions when an area is perfusing with highly oxygenated Locke''s soln. The observations supply tangible proof for the correctness of Orias'' hypothesis that coronary occlusion produces an early abbreviation of total ventricular systole with little or no decline of systolic pressure through a progressive decrease in amplitude and duration of contraction in the ischemic area. The results suggest further that the tendency for development of hypodynamic ventricular beats following coronary occlusion may not necessarily be due to fatigue of the remaining contracting fibers, but can be explained by loss of pressure in expanding the regions in which contractions are enfeebled or absent.