bly applies to the United States. There is thus no uniformity in the torso location of the limb electrodes for exercise stress testing. We suggest that there should be since as early as 1930 Wilson9 showed that moving the limb electrodes onto the torso distorts the electrocardiogram. In 1949 he wrote, “it should be pointed out that whereas the exact location of the limb electrodes are a matter of no importance, the position of the electrodes on the trunk must be determined with considerable precision if consistent results are to be obtained in exneriments on different subjects. . .“.I0 a We have studied the effect of using 4 different torso locations for the left lea electrode, keeping the arm electrodes ii their respective infraclavicular fossae, and found that each produced a different electrocardiogram, with R-wave amplitude in the “inferior” leads increasing progressively as the left leg electrode was moved nearer to the area of the heart.* Thus, the exercise electrocardiogram recorded by 1 group using its torso-based electrode placements will be different from that recorded by another group using different torso electrode locations. This is important since recent studies have shown that the degree of exercise-induced ST-segment depression is influenced by R-wave amplitudei1J2; leads with the tallest R waves will be the most sensitive for ST-segment changes, so the sensitivity of different exercise electrocardiographic lead systems will vary. This makes comparison of data from different centers difficult. In 1938 the American Heart Association and the Cardiac Society of Great Britain and Ireland (as the British Cardiac Society was then known) first met to try to standardize the electrocardiogram, although it was another 6 years before the standard 12-lead electrocardiogram finally emerged. The exercise electrocardiogram remains unstandardized; we suggest that the time has come when it should be. Mark Papouchdo Michael A. James
Bristol, United Kingdom 9 August 1989 1. Sevilla DC, Dohrmann ML, Somelofski CA, Wawrzynski RP, Wagner NB, Wagner GS. Invalidation of the resting electrocardiogram obtained via exercise electrode sites as a standard 12-lead recording. Am J Cardiol 1989,63:3539. 2. Papouchado M, Walker PR, James MA,
Clarke LM. Fundamental differences between the standard I2-lead electrocardiograph and the modified (Mason-Likar) exercise lead system. Eur Heart J 1987;8:725-733. 3. Mason RE, Likar I. A new system of multiple-lead exercise electrocardiography. Am Heart J 1966;71:196-205. 4. Papouchado M, Culling W, James MA. ECG changes during selective percutaneous transluminal coronary artery angioplasty (letter). Lancer 1986;1:1498. 9. Diamond D, Griffith DH, Greenberg ML, Carleton RA. Torso mounted electrocardiographic electrodes for routine clinical electrocardiography. J Electrocardiol 1979:12:403406.
6. Rautaharju PM, Prineas RJ, Crow RS, Scale D, Furberg C. The effect of modified limb 1048
electrode positions on. electrocardiographic wave amnlitude. J Elecirocardiol 1980:13: 109-113: 7. Gamble P, McManus H, Jensen D, Froelither V. A comparison of the standard 12-lead electrocardiogrsm to exercise electrode placements. Chest 1984;85:616-622. 8. Kleiner JP, Nelson WP, Boland MJ. The 12lead electrocardiogram in exercise testing. Arch Intern h4ed 1978;138:1572-1573. 9. Wilson FN. The distribution of potential differences uroduced bv the heart within the bodv and at iis surfaces.- Am Heart J 1929-l 936; 5: 599-619. _._. _ __.. 10. Wilson FN, Bryant JM, Johnston FD. On the possibility of constructing an Einthoven triangle for a given subject. Am Heart J 1949; 37:493-522.
il. Hakki A-H, Iskandrian AS, Kutalek S, Hare TW, Sokoloff NS. R wave amplitude: a new determinant of failure of patients-with coronary heart disease to manifest ST segment depression during exercise. JACC 1984;3:11551160. 12. Holler&erg M, Go M, Massie BM, Wisneski JA, Gertz EW. Influence of R-wave amplitude on exercise-induced ST depression: Need for a “gain factor” correction when interpreting stress electrocardiograms. Am J Cardiol 1985;56:13-17.
Panic Disorder and Depression in Patients with Chest Pain Not Due to Coronary Artery Disease We are concerned that the article by Beitman et al’ has substantially underestimated the importance of psychiatric disorders in patients with chest pain and angiographically normal coronary arteries. They have concluded that about 25% of these patients have panic disorder, 25% have microvascular angina, 25% have esophageal disorders and the remaining 25% have chest discomfort resulting from a variety of other conditions. The data, in our opinion, argue that panic disorder and major depressive disorder often coexist with most of the other diagnoses established in these patients. Colgan et al2 have reported that 59% of their patients who had chest pain and esophageal disorders with normal coronary arteries also had a current psychiatric disorder, most commonly depression or anxiety (p