Usefulness of ST-Segment Changes in >2 Leads on the Emergency Room Electrocardiogram in Either Unstable Angina Pectoris or Non-Q-Wave Myocardial Infarction in Predicting Outcome Marc Cohen, MD, Linda Hawkins, RN, Steven Greenberg, MD, and Valentin Fuster, MD
To determine the reliability of the admission electrocardiogram in predicting outcome in patients hospitalized for chest pain at rest, 90 patients were randomized into a trial of aspirin versus heparin in unstable angina or non-Q-wave myocardial infarction, and prospectively followed for 3 months. The emergency room admission electrocardiogram was analyzed for ST-segment deviation 21 mm/lead and T-wave changes. Unfavorable outcomes were recurrent ischemic pain, myocardial infarction and coronary revascularization with angioplasty or surgery. In patients who underwent coronary arteriography, a myocardium in jeopardy score ranging from 0 to 10 was assigned, based on the number of vessels with a diameter stenosis 170% and the location of the stenoses. Considering all 90 patients, an admission electrocardiogram with STsegment deviation in 12 leads had a positive predictive value for adverse clinical events of 79% and a negative predictive value of 64%. In the subset of patients without left ventricular hypet-trophy and whose admission electrocardiograms were recorded during chest pain (62 of 90), the positive predictive value of ST deviation in 12 leads improved to 89% and the negative value to 72%. Of the 62 patients, 53 underwent coronary arteriography. There was a positive linear correlation between the total number of leads with ST-segment deviation and the myocardium in jeopardy score (r = 0.80, p 2 leads yielded a sensitivity of 89%, but O-I the specificity was relatively low (56%). NOL WITH ST n’s Electrocardiographic correlation with extent of In the subset of 62 patients with pain during the admission electrocardiogram, the relation between the total number of leads with rzew myocardium
in jeopardy:
I I
FIGURE 2. Relation between the total number of leads (Not.) new ST changes (ST A’s) during pain (abscissa) and the myocardium in jeopardy score (ordinate).
with
ST-SEGMENT
CHANGES
IN UNSTABLE
ANGINA
1371
DISCUSSION Patients with angina at rest or with non-Q-wave myocardial infarction, especially those with electrocardiographic changes, constitute a group that is at high risk for early myocardial infarction, death, or recurrent pain requiring coronary revascularization with angioplasty or bypasssurgery.4-7Yet the outcome of an individual patient admitted with these syndromes is difficult to predict. It can range from early discharge after coronary arteriography reveals normal coronary arteries (10 to 20% of patients) to early catheterization and revascularization becauseof recurrent myocardial ischemia, or to myocardial infarction. Becauseof this variability, many physicians feel compelled.to refer all patients with angina at rest for early catheterization. The results of our study suggestthat, within certain guidelines, a simple noninvasive test-the admission electrocardiogram evaluated by the physician in the emergency room-can reliably predict an unfavorable event and help to identify which patients may benefit from early definition of their coronary anatomy and which may be continued on medical therapy and referred for early stresstesting. Prior studies of patients with unstable angina identilied several noninvasive and invasive parameters as being strong predictors of an adverseoutcome. These include recurring pain in the hospital with associated electrocardiographic changes, recurrent silent ischemia detected by Holter monitoring and the extent of tirenary artery diseasedocumented by angiography. The first noninvasive parameter to be described was recurring pain associated with electrocardiographic changes.g-ll Other studies used information derived from the admission electrocardiogram. In a study of >l,OOO patients with unstable angina, Lewis et al2 observed that ST-segment depression on admission was the most important predictor of death. They did not, however, exclude patients with left ventricular hypertrophy or left bundle branch block from their analysis. Other investigators12-l4 have focused attention on a specific pattern of electrocardiographic changesnamely, anterior T-wave inversions-as being predictive of a poor outcome and of severeproximal stenosis in the left anterior descendingartery. More recently, 2 large natural history studies,15sr6 incorporating clinical as well as coronary arteriographic data, identified an abnormal “baseline” electrocardiogram as one of the important prognostic variables in multivariate analysis. However, they did not attempt to specify which electrocardiographic abnormalities were most predictive of a poor outcome. The noninvasive technique of Holter monitoring over 24 to 48 hours has identified recurrent silent ischemia as a marker for unfavorable outcome in patients 1372
THE AMERICAN JOURNAL OF CARDIOLOC;Y VOLUME 67
with unstable angina.17-lgUsing continuous electrocardiographic monitoring, Nademanee,l8 Langer lg and their co-workers observed a significant correlation between a total duration of ischemia >60 minutes and the presenceof multivessel coronary artery disease.However, in a population of patients with unstable angina that was not preseiected,Wilcox et a12o,21 found that recurrent pain at rest was a more sensitivepredictor of serious events than was silent ischemia. Other studies, using multivariate analysis incorporating both noninvasive and invasive parameters,identified the extent of coronary artery diseaseas the most powerful predictor of adverse clinical outcome..4J6Jg,22 To avoid referring all patients with unstable angina for invasive catheterization, previous investigators attempted to correlate electrocardiographic changes with the extent of coronary artery disease.Papapietro et a123obtained a correlation betweenthe magnitude of maximal ST-segmentshifts, and,3- versus 1: or 2-vesselcoronary artery disease.Langer et all9 obtained a correlation between the duration of ST-segment shifts on Holter monitoring and the number (range 1 to 3) of vessels diseased.However, they accepteda diameter stenosisof 250% as significant. In an angioplasty model of acute transient ischemia, Cohen et a124observedthat both the sum of ST-segmentshifts and the total number of leads with ST shifts correlated well with the percentage of the left ventricular perimeter in jeopardy. Based on these investigations, the present study evaluated different electrocardiographic parameters and correlated them with a more sensitive indicator of the extent of myocardium in jeopardy. The traditional method of ranking the extent of coronary disease-namely, l-, 2or 3-vessel disease-was substituted with a coronary scoring systemthat more accurately reflected the extent of myocardium at risk. In contrast to Papapietro et al, our observationssuggestthat the total number of leads revealing ST-segmentchangeswas a more reliable indicator than either the maximal magnitude or the sum of ST-segmentdeviation. In addition, this study is the first to demonstratethat data from the admissionelectrbcardiogram are of reliable predictive value in patients with unstable angina. With data from the admissionelectrocardiogram, decisions regarding triaging of patients to intensive care unit beds25or timing of inv&siveinteiventions (early versus delayed) could be facilitated. Study iimitaths: The predictive values we observed apply only when patients are treated as ours were, with antithrombotic therapy. There are limitations in applying admissionelectrocardiographic criteria to the general population. First, a baseline pattern of left ventricular hypertrophy reduces both the predictive value and the correlation with the myocardium in jeopardy. Second, using the admission electrocardiogram in the abJUNE 15. 1991
senceof chest pain significantly reduces the sensitivity. Lastly, in the presenceof chest pain, an electrocardiogram with minimal changes does not completely preclude the presence of multivessel coronary artery disease. In conclusion, in patients with unstable angina, an admission electrocardiogram recorded during pain and revealing ischemic changesis by itself a reliable predictor of major clinical events. Conversely, a “benign” electrocardiogram recorded during pain correctly identifies patients with a benign clinical course in most cases,but does not necessarilypreclude recurrent ischemia or intervention.
REFERENCES 1. Farhi JI, Cohen M, Fuster V. The broad spectrum of unstable angina pectoris and its implications for future controlled trials. Am J Cardiol 1956;55:547-550. 2. Lewis HD Jr, Davis JW, Archibald DG, Steinke WE, Smitherman TC, Doherty JE III, Schnapcr HW, LeWinter MM, Linares E, Pouget JM, Sabharwal SC, Chesler E, DeMots H. Protective effects of aspirin against acute myocardial infarction and death in men with unstable angina. N Engl J Med 1953;309:396-403. 3. Cairns JA, Gent M, Singer J, Finnie KJ, Froggatt GM, Holder DA, Jablonsky G, Kostuk WJ, Melendez LJ, Myers MG, Sack&t DL, Sealey BJ, Tamer PH. Aspirin, sulfinpyrazone or both in unstable angina: results of a Canadian multicenter trial. N Engl J Med 1985;313:1369-1375. 4. Ouyang P, Brinker JA, Mellits ED, Weisfeldt ML, Gerstenblith G. Variables predictive of successful medical therapy in patients with unstable angina; selection by multivariate analysis from clinical, electrocardiographic, and angiographic evaluations. Circulation 1954;70:367-316. 5. Theroux P, Ouimet H, McCans J, Latour JG, Joly P, Levy G, Pelletier E, Juneau M, Stasiak J, DeGuise P, Pelletier GB, Rinzler D, Waters DD. Aspirin, hepariu, or both to treat acute unstable. angina. N Engl J Med 1958;319: 1105-1111. 6. Cohen M, Adams PC, Hawkins L, Bach M, Fuster V. Usefulness of antithrombotic therapy in rest angina pectoris or non-Q-wave myocardial infarction in preventing death and myocardial infarction (a pilot study from the Antithrombotic Therapy in Acute Coronary Syndromes Study Group). Am / Cardiol 1990;66:1287-1292. 7. Gibson RS, Bode” WE, Theroux P, Strauss HD, Pratt CM, Gheorghiade M, Capone RJ, Crawford MH, Schlant RC, Kleiger RE, Young PM, Schectman K, Perryman B, Roberts R, and the Diltiazem Reinfarction Study Group. Diltiazem and reinfarction in patients with non-Q-wave myocardial infarction: results of a double blind, randomized, multicenter trial. N Engl J Med 1956;315:423-429, 8. Califf,RM, Pillips HR III, Hindman MC, Mark DB, Lee KL, Behar VS, Johnson RA, Pryor DB, Rosati &A, Wagner GS, Harm1 FE. Prognosticvalue of a
coronary artery jeopardy score. J Am CON Curdiol 1955;5:1055-1063. 9. Gazes PC, Mobley EM, Faris HM, Duncan RC, Humphries GB. Preinfarctional (unstable) angina-a prospective study: ten year follow-up. Circulation 1973;45:331-337. 10. Olson HG, Lyons KP, Aronow WS, Stinson PJ, Kuperus J, Waters HJ. The high-risk angina patient: identification by clinical features, hospital course, electrocardiography and technetium-99m stannous pyrophosphate scintigraphy. Circulation 1951;64:67&654. 11. Demoulin TC, Bertholet M, Chevigne M, Legrand V, Renier J, Soumagne D, Soyeur D, Limet R, Kulbertus H. Prognostic significance of electrocardiographic findings-& angina at rest: therapeutic implications. Br Heart J 1951;46:320-324. 12. de Zwaan C, Bar FW, Jan&en JHA, Cheriex E, Dassen WRM, Brugada P, Penn CCKM, Wellens YJJ. Angiographic and clinical characteristics of patients with unstable aigiua showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. Am Heart J 1959;117:657-664. 13. Haines DE,‘Raabe DS, Gundel WD, Wackers FJ. Anatomic and prognostic significance of new TIwave inversion in unstable angina. Am J Cardbl 1953;52:14-15: 14. Granborg J, Grande P, Pedersen A. Diagnostic and prognostic implications of transient isolated negative T waves in suspected acute myocardial infarction. Am J Cardiol 1956;57:203-207. 15. Severi S, Orsini E, Marraccini P, Michelassi C, L’Abbate A. The basal electrocardiogram and the exercise stress test in assessing prognosis in patients with unstable angina. Eur Heart J 1955;9:441-446. 16. De Servi S, Berzuini C, Poma E, Ferrario M, Ghio S, Scire A, Cioffl P, Ardissino D, Ma&martini C, Spccchii G. Long-term survival and risk stratification in patients with angina at rest undergoing medical treatment. Znt J Card&l 1959;22:43-50. 17. Gottlieb SO, Weisfeldt ML, Ouyang P, Mellits ED, Gerstenblith G. Silent ischemia as a marker for early unfavorable outcomes in patients with unstable angina. N Engl J Med 1986;314:1214-1219. 18. Nademanee K, Intarachot V, Josephson MA, Rieders D, Mody FV, Singh BH. Prognostic significance of silent myocardial &hernia in patients with unstable angina. J Am CON Cardiol 1987;10:1-9. 19. Langer A, Freeman MR, Armstrong PW. ST segment shift in unstable angina: pathophysiology and association with coronary anatomy and hospital outcome. J Am Coil Car&l 1959;13:1495-1502, ?O. Wilcox I, Freedman SB, Kelly DT, Harris PJ. Clinical significance of silent i&hernia ;h unstable angina pectoris. Am J Cardiol 1990;65:1313-1316. 21. Wilcox I, Freedman SB, McCredie RJ, Carter GS, Kelly DT, Harris PJ. Risk of adverse outcome in patients admitted to the coronary care unit with suspected unstable angina pectoris. Am J Cardiol 1959;64:545-545. 22. Severi S, Michelassi C, Orsini E. Marraccini P, L’Abbate A. Long-term prognosis of transient acute myocardial ischemia at rest. Am J Cardiol 1959;64:559-595. 23. Papapietro SE, N&s GS, Paine TD, Mantle JA, Rackley CE, Russel RO, Rogers WJ. Transient electrocardiographic changes in patients with unstable angina: relation to coronary arterial’anatomy. Am J Cardiol 1950;46:25-32. 24. Cohen M, Scharpf SJ, Rentrop KP. Prospective analysis of electrocardiographic variables as markers for extent and location of acute wall motion abnormalities observed during coronary angioplasty in human subjects. J Am Co11 Cardiol 1957;10:17-24. 25. Selker HP. Coronary care unit triage decision aids: how do we know when they work? Am .I Med 1959;57:491-493.
ST-SEGMENT CHANGES IN UNSTABLE ANGINA
1373
To determine the reliability of the admission electrocardiogram in predicting outcome in patients hospitalized for chest pain at rest, 90 patients were randomized into a trial of aspirin versus heparin in unstable angina or non-Q-wave myocardial infarction, and prospectively followed for 3 months. The emergency room admission electrocardiogram was analyzed for ST-segment deviation 21 mm/lead and T-wave changes. Unfavorable outcomes were recurrent ischemic pain, myocardial infarction and coronary revascularization with angioplasty or surgery. In patients who underwent coronary arteriography, a myocardium in jeopardy score ranging from 0 to 10 was assigned, based on the number of vessels with a diameter stenosis 170% and the location of the stenoses. Considering all 90 patients, an admission electrocardiogram with STsegment deviation in 12 leads had a positive predictive value for adverse clinical events of 79% and a negative predictive value of 64%. In the subset of patients without left ventricular hypet-trophy and whose admission electrocardiograms were recorded during chest pain (62 of 90), the positive predictive value of ST deviation in 12 leads improved to 89% and the negative value to 72%. Of the 62 patients, 53 underwent coronary arteriography. There was a positive linear correlation between the total number of leads with ST-segment deviation and the myocardium in jeopardy score (r = 0.80, p 2 leads yielded a sensitivity of 89%, but O-I the specificity was relatively low (56%). NOL WITH ST n’s Electrocardiographic correlation with extent of In the subset of 62 patients with pain during the admission electrocardiogram, the relation between the total number of leads with rzew myocardium
in jeopardy:
I I
FIGURE 2. Relation between the total number of leads (Not.) new ST changes (ST A’s) during pain (abscissa) and the myocardium in jeopardy score (ordinate).
with
ST-SEGMENT
CHANGES
IN UNSTABLE
ANGINA
1371
DISCUSSION Patients with angina at rest or with non-Q-wave myocardial infarction, especially those with electrocardiographic changes, constitute a group that is at high risk for early myocardial infarction, death, or recurrent pain requiring coronary revascularization with angioplasty or bypasssurgery.4-7Yet the outcome of an individual patient admitted with these syndromes is difficult to predict. It can range from early discharge after coronary arteriography reveals normal coronary arteries (10 to 20% of patients) to early catheterization and revascularization becauseof recurrent myocardial ischemia, or to myocardial infarction. Becauseof this variability, many physicians feel compelled.to refer all patients with angina at rest for early catheterization. The results of our study suggestthat, within certain guidelines, a simple noninvasive test-the admission electrocardiogram evaluated by the physician in the emergency room-can reliably predict an unfavorable event and help to identify which patients may benefit from early definition of their coronary anatomy and which may be continued on medical therapy and referred for early stresstesting. Prior studies of patients with unstable angina identilied several noninvasive and invasive parameters as being strong predictors of an adverseoutcome. These include recurring pain in the hospital with associated electrocardiographic changes, recurrent silent ischemia detected by Holter monitoring and the extent of tirenary artery diseasedocumented by angiography. The first noninvasive parameter to be described was recurring pain associated with electrocardiographic changes.g-ll Other studies used information derived from the admission electrocardiogram. In a study of >l,OOO patients with unstable angina, Lewis et al2 observed that ST-segment depression on admission was the most important predictor of death. They did not, however, exclude patients with left ventricular hypertrophy or left bundle branch block from their analysis. Other investigators12-l4 have focused attention on a specific pattern of electrocardiographic changesnamely, anterior T-wave inversions-as being predictive of a poor outcome and of severeproximal stenosis in the left anterior descendingartery. More recently, 2 large natural history studies,15sr6 incorporating clinical as well as coronary arteriographic data, identified an abnormal “baseline” electrocardiogram as one of the important prognostic variables in multivariate analysis. However, they did not attempt to specify which electrocardiographic abnormalities were most predictive of a poor outcome. The noninvasive technique of Holter monitoring over 24 to 48 hours has identified recurrent silent ischemia as a marker for unfavorable outcome in patients 1372
THE AMERICAN JOURNAL OF CARDIOLOC;Y VOLUME 67
with unstable angina.17-lgUsing continuous electrocardiographic monitoring, Nademanee,l8 Langer lg and their co-workers observed a significant correlation between a total duration of ischemia >60 minutes and the presenceof multivessel coronary artery disease.However, in a population of patients with unstable angina that was not preseiected,Wilcox et a12o,21 found that recurrent pain at rest was a more sensitivepredictor of serious events than was silent ischemia. Other studies, using multivariate analysis incorporating both noninvasive and invasive parameters,identified the extent of coronary artery diseaseas the most powerful predictor of adverse clinical outcome..4J6Jg,22 To avoid referring all patients with unstable angina for invasive catheterization, previous investigators attempted to correlate electrocardiographic changes with the extent of coronary artery disease.Papapietro et a123obtained a correlation betweenthe magnitude of maximal ST-segmentshifts, and,3- versus 1: or 2-vesselcoronary artery disease.Langer et all9 obtained a correlation between the duration of ST-segment shifts on Holter monitoring and the number (range 1 to 3) of vessels diseased.However, they accepteda diameter stenosisof 250% as significant. In an angioplasty model of acute transient ischemia, Cohen et a124observedthat both the sum of ST-segmentshifts and the total number of leads with ST shifts correlated well with the percentage of the left ventricular perimeter in jeopardy. Based on these investigations, the present study evaluated different electrocardiographic parameters and correlated them with a more sensitive indicator of the extent of myocardium in jeopardy. The traditional method of ranking the extent of coronary disease-namely, l-, 2or 3-vessel disease-was substituted with a coronary scoring systemthat more accurately reflected the extent of myocardium at risk. In contrast to Papapietro et al, our observationssuggestthat the total number of leads revealing ST-segmentchangeswas a more reliable indicator than either the maximal magnitude or the sum of ST-segmentdeviation. In addition, this study is the first to demonstratethat data from the admissionelectrbcardiogram are of reliable predictive value in patients with unstable angina. With data from the admissionelectrocardiogram, decisions regarding triaging of patients to intensive care unit beds25or timing of inv&siveinteiventions (early versus delayed) could be facilitated. Study iimitaths: The predictive values we observed apply only when patients are treated as ours were, with antithrombotic therapy. There are limitations in applying admissionelectrocardiographic criteria to the general population. First, a baseline pattern of left ventricular hypertrophy reduces both the predictive value and the correlation with the myocardium in jeopardy. Second, using the admission electrocardiogram in the abJUNE 15. 1991
senceof chest pain significantly reduces the sensitivity. Lastly, in the presenceof chest pain, an electrocardiogram with minimal changes does not completely preclude the presence of multivessel coronary artery disease. In conclusion, in patients with unstable angina, an admission electrocardiogram recorded during pain and revealing ischemic changesis by itself a reliable predictor of major clinical events. Conversely, a “benign” electrocardiogram recorded during pain correctly identifies patients with a benign clinical course in most cases,but does not necessarilypreclude recurrent ischemia or intervention.
REFERENCES 1. Farhi JI, Cohen M, Fuster V. The broad spectrum of unstable angina pectoris and its implications for future controlled trials. Am J Cardiol 1956;55:547-550. 2. Lewis HD Jr, Davis JW, Archibald DG, Steinke WE, Smitherman TC, Doherty JE III, Schnapcr HW, LeWinter MM, Linares E, Pouget JM, Sabharwal SC, Chesler E, DeMots H. Protective effects of aspirin against acute myocardial infarction and death in men with unstable angina. N Engl J Med 1953;309:396-403. 3. Cairns JA, Gent M, Singer J, Finnie KJ, Froggatt GM, Holder DA, Jablonsky G, Kostuk WJ, Melendez LJ, Myers MG, Sack&t DL, Sealey BJ, Tamer PH. Aspirin, sulfinpyrazone or both in unstable angina: results of a Canadian multicenter trial. N Engl J Med 1985;313:1369-1375. 4. Ouyang P, Brinker JA, Mellits ED, Weisfeldt ML, Gerstenblith G. Variables predictive of successful medical therapy in patients with unstable angina; selection by multivariate analysis from clinical, electrocardiographic, and angiographic evaluations. Circulation 1954;70:367-316. 5. Theroux P, Ouimet H, McCans J, Latour JG, Joly P, Levy G, Pelletier E, Juneau M, Stasiak J, DeGuise P, Pelletier GB, Rinzler D, Waters DD. Aspirin, hepariu, or both to treat acute unstable. angina. N Engl J Med 1958;319: 1105-1111. 6. Cohen M, Adams PC, Hawkins L, Bach M, Fuster V. Usefulness of antithrombotic therapy in rest angina pectoris or non-Q-wave myocardial infarction in preventing death and myocardial infarction (a pilot study from the Antithrombotic Therapy in Acute Coronary Syndromes Study Group). Am / Cardiol 1990;66:1287-1292. 7. Gibson RS, Bode” WE, Theroux P, Strauss HD, Pratt CM, Gheorghiade M, Capone RJ, Crawford MH, Schlant RC, Kleiger RE, Young PM, Schectman K, Perryman B, Roberts R, and the Diltiazem Reinfarction Study Group. Diltiazem and reinfarction in patients with non-Q-wave myocardial infarction: results of a double blind, randomized, multicenter trial. N Engl J Med 1956;315:423-429, 8. Califf,RM, Pillips HR III, Hindman MC, Mark DB, Lee KL, Behar VS, Johnson RA, Pryor DB, Rosati &A, Wagner GS, Harm1 FE. Prognosticvalue of a
coronary artery jeopardy score. J Am CON Curdiol 1955;5:1055-1063. 9. Gazes PC, Mobley EM, Faris HM, Duncan RC, Humphries GB. Preinfarctional (unstable) angina-a prospective study: ten year follow-up. Circulation 1973;45:331-337. 10. Olson HG, Lyons KP, Aronow WS, Stinson PJ, Kuperus J, Waters HJ. The high-risk angina patient: identification by clinical features, hospital course, electrocardiography and technetium-99m stannous pyrophosphate scintigraphy. Circulation 1951;64:67&654. 11. Demoulin TC, Bertholet M, Chevigne M, Legrand V, Renier J, Soumagne D, Soyeur D, Limet R, Kulbertus H. Prognostic significance of electrocardiographic findings-& angina at rest: therapeutic implications. Br Heart J 1951;46:320-324. 12. de Zwaan C, Bar FW, Jan&en JHA, Cheriex E, Dassen WRM, Brugada P, Penn CCKM, Wellens YJJ. Angiographic and clinical characteristics of patients with unstable aigiua showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. Am Heart J 1959;117:657-664. 13. Haines DE,‘Raabe DS, Gundel WD, Wackers FJ. Anatomic and prognostic significance of new TIwave inversion in unstable angina. Am J Cardbl 1953;52:14-15: 14. Granborg J, Grande P, Pedersen A. Diagnostic and prognostic implications of transient isolated negative T waves in suspected acute myocardial infarction. Am J Cardiol 1956;57:203-207. 15. Severi S, Orsini E, Marraccini P, Michelassi C, L’Abbate A. The basal electrocardiogram and the exercise stress test in assessing prognosis in patients with unstable angina. Eur Heart J 1955;9:441-446. 16. De Servi S, Berzuini C, Poma E, Ferrario M, Ghio S, Scire A, Cioffl P, Ardissino D, Ma&martini C, Spccchii G. Long-term survival and risk stratification in patients with angina at rest undergoing medical treatment. Znt J Card&l 1959;22:43-50. 17. Gottlieb SO, Weisfeldt ML, Ouyang P, Mellits ED, Gerstenblith G. Silent ischemia as a marker for early unfavorable outcomes in patients with unstable angina. N Engl J Med 1986;314:1214-1219. 18. Nademanee K, Intarachot V, Josephson MA, Rieders D, Mody FV, Singh BH. Prognostic significance of silent myocardial &hernia in patients with unstable angina. J Am CON Cardiol 1987;10:1-9. 19. Langer A, Freeman MR, Armstrong PW. ST segment shift in unstable angina: pathophysiology and association with coronary anatomy and hospital outcome. J Am Coil Car&l 1959;13:1495-1502, ?O. Wilcox I, Freedman SB, Kelly DT, Harris PJ. Clinical significance of silent i&hernia ;h unstable angina pectoris. Am J Cardiol 1990;65:1313-1316. 21. Wilcox I, Freedman SB, McCredie RJ, Carter GS, Kelly DT, Harris PJ. Risk of adverse outcome in patients admitted to the coronary care unit with suspected unstable angina pectoris. Am J Cardiol 1959;64:545-545. 22. Severi S, Michelassi C, Orsini E. Marraccini P, L’Abbate A. Long-term prognosis of transient acute myocardial ischemia at rest. Am J Cardiol 1959;64:559-595. 23. Papapietro SE, N&s GS, Paine TD, Mantle JA, Rackley CE, Russel RO, Rogers WJ. Transient electrocardiographic changes in patients with unstable angina: relation to coronary arterial’anatomy. Am J Cardiol 1950;46:25-32. 24. Cohen M, Scharpf SJ, Rentrop KP. Prospective analysis of electrocardiographic variables as markers for extent and location of acute wall motion abnormalities observed during coronary angioplasty in human subjects. J Am Co11 Cardiol 1957;10:17-24. 25. Selker HP. Coronary care unit triage decision aids: how do we know when they work? Am .I Med 1959;57:491-493.
ST-SEGMENT CHANGES IN UNSTABLE ANGINA
1373
