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ALTHOUGH the clinical presentation of angina pectoris is familiar to most physicians, the pathophysiologic basis of this syndrome has only become evident within the last decade. Before this time there had been almost no hemodynamic and metabolic information regarding the anginal state. Today, by contrast, the number and variety of studies in this field have been great enough to create confusion regarding primary mechanisms. The purpose of the present review is to clarify some of the better documented aspects of this syndrome, as well as to indicate those areas requiring further elucidation. Discussion will be primarily concerned with abnormalities of ventricular pressure, volume, and wall motion associated with the anginal state. Cardiac performance will be considered in relation to heart rate, contractile state of the muscle, preload, and afterload.' Preload can be defined as the resting fiber length as determined by end-diastolic volume, and is often expressed in terms of end-diastolic pressure. Afterload is the load that the ventricle must overcome during ejection; in the absence of aortic valve disease this is essentially a function of arterial pressure during systole. Only angina pectoris associated with coronary artery disease will be discussed.

Abnormalities of Left Ventricular Function Associated with the Anginal State