Angina pectoris. II. Observations on the classic form of angina pectoris; preliminary report.

1. 1. Surgical procedures for the treatment of arteriosclerotic heart disease has made the recording of direct epicardial electrocardiograms possible in 15 patients with severe classic angina pectoris. Numerous “islands” of S-T segment depression widely scattered over all epicardial surfaces of both ventricles have been demonstrated. Areas other than these “islands” showed isoelectric S-T segments. “Islands” with epicardial S-T depression were not found in control patients. 2. 2. The “islands” with S-T segment depression could not be distinguished by virtue of pallor or cyanosis from the areas with isoelectric S-T segments. 3. 3. The occurrence of S-T segment depression in standard leads in classic angina is explained by the diffuse distribution of these “islands” of S-T segment depression. Standard leads face the “islands” of depression. 4. 4. The absence of reciprocal S-T segment elevation in other standard leads in classic angina is also explained. Reciprocal S-T elevation in standard leads is not manifest since the primary areas of S-T depression are located all over the ventricles. The occurrence of primary S-T segment elevation in the variant form of angina is noted, together with its restriction to a large discrete area supplied by a large coronary artery. In the variant form of angina the S-T segment depression is reciprocal in nature, in contrast to classic angina pectoris, in which reciprocal S-T segment changes are not noted in standard leads. 5. 5. Diffuse “islands” of epicardial S-T segment depression were produced experimentally in dogs by bleeding to markedly hypotensive levels. These “islands” of S-T segment depression in dogs could not be distinguished visually from areas with isoelectric S-T segments. Similar findings were noted in human beings with angina pectoris. 6. 6. Ligation of a large branch of the anterior descending coronary artery in dogs produced a large discrete area in which only epicardial S-T segment elevation was recorded. This area with S-T elevation was distinctly cyanotic, in contrast to the previously described “islands” with S-T depression which were not visually distinguishable. These findings were similar to those in patients with the variant form of angina pectoris. 7. 7. The similarity of local hypotension at the distal end of partially constricted coronary arteries, to generalized hypotension in the presence of normal coronary arteries is noted. 8. 8. The frequent persistence of classic angina following a myocardial infarction is explained by the diffuse location of the “islands” with S-T depression. Following infarction, many such “islands” remain. The disappearance of the variant form of angina following a myocardial infarction also is explained as being due to the localization of the changes to the single area which has been infarcted. 9. 9. The occurrence of S-T elevation in the variant form of angina makes prediction of the site of future infarction possible. The occurrence of S-T depression in classic angina does not permit prediction of the site of future infarction. 10. 10. The appearance of epicardial cyanosis in areas with S-T segment elevation on temporary ligation of a coronary artery suggests that coronary artery hypertonus may precipitate the variant form of angina with its S-T segment elevation. The absence of epicardial cyanosis in patients with classic angina, and in dogs with hypotension, suggests that coronary artery hypertonus is not the usual cause of classic angina. 11. 11. Ventricular arrhythmias are noted frequently in the clinical and simulated variant form of angina. They occur after the pain has been present awhile and has risen to a certain intensity. Arrhythmias are rare in the simulated form of classic angina, except for terminal ventricular fibrillation. Sudden deaths in classic angina probably occur as a result of ventricular fibrillation developing suddenly. 12. 12. Several clinical conditions are presented in which S-T segment depression is found in the absence of changes limited to the subendocardium. A number of experiments are presented indicating that the subendocardium does not contribute in significant degree to S-T segment deviations. These experiments indicate that S-T segment depressions are due to disturbances in the outer myocardial layers. 13. 13. The marked difference between S-T changes in classic angina pectoris (with S-T depression) and those in the variant form of angina or early myocardial infarction (with S-T elevation) suggests different chemical changes within the myocardium.7