Abstract:

The syndromes of angina pectoris and of intermittent claudication are similar in that both are dependent upon the activity of ischemic muscular organs. For this reason, the classical work of Lewis 1 and of Katz, 2 designed to elucidate the mechanism of angina pectoris, was done primarily on striated muscles since the arm or leg muscles lent themselves admirably for study. Exercise of muscles experimentally rendered ischemic * * By ischemic muscles is meant muscles with a poor or an absent arterial blood flow. gives rise to: (1) pain within the region being exercised, 3,4 (2) a marked increase in blood pressure, 5,6 and (3) tachycardia. 7 In spite of the fact that all three phenomena probably occur with the production of ischemia in muscles, only the pain element has been properly investigated. 1-4,8-12 Incidental phenomena which occur in patients with intermittent claudication deserve an explanation. For example, hypertrophy of the heart without valvular disease was found by us in such patients, even though the blood pressure was normal at rest. The fact that many of these patients die suddenly without apparent cause also requires analysis. In order to assay the possible clinical importance of the induced rise in blood pressure and the tachycardia, we have studied the general cardiovascular reactions produced by exercise of spontaneously ischemic voluntary muscles in man. In this report, the blood pressure changes and the variations produced by several drugs following exercise of the legs in patients with intermittent claudication are described. The observations concerned with heart rate and with the origin of the pain thus produced will be reported later. 13,14 In addition, there is described a new method which permits the detection of impairment of the arterial circulation in exercising legs, even when the blood flow appears adequate at rest. © 1949.