The Reduction of Infarct Size — An Idea Whose Time (For Testing) Has Come

EARLY IN THIS CENTURY, cardiovascular physiologists began to direct their attention to the study of the control of myocardial oxygen consumption (MVO2). Evans and Matsuoka, in Starling's laboratory in London,' and Rohde, in Heidelberg,2 called attention to the importance of intraventricular pressure as a principal determinant of M'/O2. Technical developments during subsequent decades allowed a systematic reexamination of this problem in the mid-1950s,3 resulting in more precise elucidation of the role of intraventricular tension, myocardial fiber shortening, contraction frequency, and external cardiac work in regulating the heart's oxygen needs. Later, the roles of myocardial contractility,4 the basal oxygen needs of the noncontracting heart,5 the costs of electrical depolarization of the myocardium,6 and the effect of shortening against a load7 on MVO2 were defined.8 While of considerable interest to physiologists, an understanding of the determinants of MVO2 has considerable clinical implications as well. After all, myocardial ischemia, the principal consequence of coronary arteriosclerosis, is characterized by an imbalance between myocardial oxygen needs and availability, which results in chest discomfort, as well