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Prognostic significance of precordial ST segment depression on admission electrocardiogram in patients with inferior wall myocardial infarction
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JACC Vol. 28, No. 2 August 1996:313-8
Prognostic Significance of Precordial ST Segment Depression on Admission Electrocardiogram in Patients With Inferior Wall Myocardial Infarction YOCHA|
BIRNBAUM,
MD, IZHAK HERZ, MD, SAMUEL SCLAROVSKY,
BRURIA
ZLOTIKAMIEN,
MD, ANGELA
MD,
C H E T R I T , MSc,* L I R A Z O L M E R , BSc,*
G A B R I E L I. B A R B A S H , M D , M P H t Petah-Tiqva, Tel-Hashomer and Tel Aviv, Israel
Objectives. This study assessed retrospectively the correlation between the pattern of precordial ST segment depression on the admission electrocardiogram (ECG) and hospital mortality in patients with an inferior myocardial infarction treated with intravenous thrombolytic therapy. Background. Previous studies have shown that in acute inferior myocardial infarction, ST segment depression in the precordial leads is associated with increased hospital mortality. However, the significance of the different patterns of precordial ST segment depression has been evaluated in only two previous studies. Methods. The study included 1,321 patients (1,020 men) who enrolled in the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO-I) trial in Israel and received intravenous thrombolytic therapy. Patients with an ST segment elevation >0.1 mV in at least two of the inferior leads were included. Patients were classified into four groups on the basis of their admission ECG: group I = patients with no precordial ST segment depression (n = 346); group II = those for
whom the sum of ST segment depression in leads Vl to V3 was greater than that in leads ¥4 to V6 (n = 700); group III = those for whom the sum of ST depression in leads Vmto V3 was equal to that in leads V4 to V6 (n = 162); group 1V = those with maximal ST depression in leads V4 to V6 (n = 113). Results. The overall hospital mortality rate was 3.6% (48 patients): for groups I, II, III and IV it was 2.9%, 2.8%, 4.3% and 9.7%, respectively. Multivariable logistic regression analysis confirmed that hospital mortality was independently associated with the pattern of precordial ST segment depression. The odd ratios in group IV relative to group I was 2.78 (95% confidence interval 1.26 to 6.13, p = 0.007). Conclusions. The risk of mortality is higher in patients with an inferior myocardial infarction and maximal ST segment depression in precordial leads V4 to V6 versus precordial leads V1 to V3 on the admission ECG. (JAm CoU Cardiol 1996;28:313-8)
In the era of thrombolytic therapy and various forms of invasive revascularization, it is increasingly important to identify patients with an acute myocardial infarction who are likely to develop complications during the early phase of infarction. This is especially true for inferior myocardial infarction, which is considered to have a more favorable prognosis than anterior myocardial infarction but includes high risk subgroups with increased mortality and morbidity (1). Because of its widespread availability and low cost, the 12-lead electrocardiogram (ECG) remains one of the most cost-effective and noninvasive ways to confirm myocardial infarction. Abundant published reports associate various ECG patterns of inferior myocardial infarction with high morbidity and mortality (1-14). In particular, ST segment depression in
precordial leads has been associated with a larger infarction (2-6), worse wall motion abnormalities (3-7), lower ejection fraction (3-8) and a higher rate of short- and long-term complications and mortality (2,5,6,8-11), even with reperfusion therapy (12-14). However, most previous studies of the prognostic significance of precordial ST segment depression in inferior myocardial infarction have not differentiated among the various patterns of ST segment depression. Ishikawa et al. (15), studying 92 patients with an acute inferior wall myocardial infarction, found that patients with precordial ST segment depression in leads V 1 to V 4 had higher peak creatine kinase (CK) values than patients without precordial ST segment depression. They reported higher complication rates among 17 patients with ST segment depression in leads V t to V 4 than in 27 patients without precordial ST segment depression, 10 patients with ST segment depression in leads V 2 to V 5, 13 patients with ST segment depression in V 3 to V6 or 25 patients with ST segment depression in leads V1 to V6. Recently, a retrospective study of 213 patients with an inferior wall myocardial infarction (113 patients were treated
From the BeilinsonMedical Center, Petah-Tiqva;*Sheba MedicalCenter, Tel-Hashomer; and tTel Aviv Sourasky Medical Center, Tel Aviv Sackler Facultyof Medicine,Tel AvivUniversity,Tel Aviv,Israel. Manuscript received September 19, 1995; revised manuscript received February 21, 1996,acceptedApril 2, 1996. Address for correspondence:Dr. Gabriel 1. Barbash, Tel Aviv Sourasky Medical Center, 6 WeizmanStreet,Tel Aviv64239, Israel.
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BIRNBAUM ET AL. ST DEPRESSION IN I N F E R I O R INFARCTION
w " A__ II
JACC Vol. 28, No. 2 August 1996:313-8
+ + + , + _c
-V',-
" - k " " V " --"k- -,,r~ --,w- ..,.v% -,7.,.
"w -4~ .&_ -t-- _~
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Figure 1. Representative admission electrocardiogram of patients with an inferior acute myocardial infarction in each of the four groups: group I = no precordial leads with ST segment depression; group II = ST segment depression in leads V 2 and V3; group I I I = ST segment depression in leads V 2 to V6; group IV = ST segment depression mainly in leads V4 to V 6.
with thrombolytic therapy) demonstrated that patients with maximal ST segment depression in leads V4 to V6 are at higher risk for hospital mortality than patients with maximal ST segment depression in leads V1 to V3 (16). The current retrospective analysis assessed the prognostic significance of the various patterns of precordial ST segment depression on the admission ECG in 1,321 patients with an inferior myocardial infarction treated with thrombolytic therapy.
Methods Patients. All patients with an inferior myocardial infarction who enrolled in the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO-I) trial in 25 medical centers in Israel were included in the analysis. Patients were admitted within 6 h of onset of symptoms, with chest pain lasting at least 20 rain accompanied by ECG signs ->0.1-mV ST segment elevation in at least two leads (II, III or aVF). Patients with intraventricular conduction defects, ventricular rhythm, ventricular pacing or ECG evidence of left ventricular hypertrophy were excluded. All patients received either streptokinase, front-loaded tissue-type plasminogen activator (t-PA) or a combination of streptokinase and t-PA according to the GUSTO-I protocol (17). All patients received oral aspirin, 160 to 325 mg/day, and either intravenous or subcutaneous heparin for at least 48 h. The following data were recorded: gender, age, history of diabetes mellitus, hypertension, previous infarction, angina pectoris, smoking status, Killip score on admission, time elapsed from onset of symptoms to thrombolytic therapy, type of thrombolytic therapy, worst Killip score, peak serum CK levels, occurrence of reinfarction and hospital mortality. Electrocardiographic evaluation. The number of leads in the entry ECG with ST segment elevation (---0.1 mV for limb leads and ->0.2 mV for precordial leads) was recorded. The degree of ST depression was determined for all precordial leads (measured manually to the nearest 0.05 mV, 0.06 s after the J point). Patients were classified into the following four groups on the basis of the admission ECG (Fig. 1): group I =
no precordial ST segment depression (ST segment depression <0.1 mV in each of the precordial leads); group II = ST segment depression ->0.1 mV in more than one precordial lead with maximal ST segment depression in leads V 1 to V3; group I I I = ST segment depression >--0.1 mV in more than one precordial lead with the sum of ST segment depression in VI to V3 equal to that in V 4 to V6; and group IV : ST segment depression ->0.1 mV in more than one precordial lead with maximal ST segment depression in leads V4 to V6. Statistical analysis. Mean values + SD were calculated for continuous variables (age, time from onset of symptoms and serum CK levels), and absolute and relative frequencies were measured for discrete variables. For continuous variables, differences between groups were analyzed statistically by oneway analysis of variance. The chi-square test was applied to compare differences between discrete variables. A logistic regression model was fitted. The dependent variable was hospital mortality, and the independent variables were gender, age, history of diabetes mellitus, hypertension, previous myocardial infarction, angina pectoris, smoking status, time from onset of symptoms to therapy, Killip score on admission, number of leads with ST segment elevation and type of ST segment depression in the precordial leads. Odds ratio and 95% confidence intervals were calculated from the estimate variables of the logistic regression model. All tests of significance were two-tailed; p values <0.05 were considered statistically significant.
Results Baseline characteristics of patients. The study cohort included 1,321 patients (1,020 men; mean age 59.6 - 11.9 years). The baseline characteristics of the patients in the four groups are presented in Table 1. The average age was slightly lower in group I and higher in group IV. The proportion of men was lower in group II and highest in group IV. Patients in group IV had the highest rates of hypertension, previous angina pectoris and previous myocardial infarction. There was no difference in the location of the first myocardial infarction among patients with previous myocardial infarction among the four patient groups. The proportion of patients assigned to the various thrombolytic strategies and the time elapsed from onset of symptoms to thrombolytic therapy did not differ significantly among the groups. The mean number of leads with ST segment elevation was highest in group II and lowest in group IV. Clinical outcome is presented in Table 2. Group IV patients more frequently had hypotension, second- and third-degree atrioventricular block, ventricular fibrillation episodes and asystole. The incidence of decompensated left ventricular function (Killip score III and IV) was greater in groups III and IV than in groups I and II. Peak serum CK levels were maximal in group II and relatively low in group IV. A total of 48 patients (3.6%) died. The hospital mortality rate was lowest in patients without precordial ST segment depression (2.9%) and in those with maximal ST depression in leads V 1 to V3 (2.8%). The mortality rate was higher in groups III and IV (4.3% and 9.7%,
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BIRNBAUM ET AL. ST DEPRESSION IN INFERIOR INFARCTION
315
Table 1. Baseline Characteristics of the F o u r Patient G r o u p s
Men Age (yr) Previous infarction Previous angina Hypertension Diabetes mellitus Current smoking Time from onset of pain to thrombolysis (rain) Killip score on admission >I No. of leads with ST elevation Therapy SK+ SQ Hep SK+ IV Hep t-PA+ IV Hep SK+ t-PA
Group I (n - 346)
Group II (n = 700)
Group III (n = 162)
Group IV (n - 113)
Total (n - 1,321)
p Value
80.5 58.3 _+ 12.0 16.4 34.8 35.6 26.7 41.7 190 ± 126 13.2 3.2 + 0.9
73.6 59.6 + 11.8 15.0 32.1 30.7 16.1 43.3 186 _+ 130 13.2 3.6 _+ 1.1
79.6 60.5 + 11.9 15.4 32.7 34.6 16.7 51.2 171 _+ 79 I6.7 3.0 _+ 0.4
84. l 62.1 + 12.4 29.2 41.6 40.7 15.0 47.8 189 + 87 15.9 2.9 _+ 0.3
77.1 59.6 + 11.9 16.6 33.7 33.3 18.9 44.2 185 + 120 13.9 3.4 + 1.0
0.01 0.02 0.002 NS NS 0.0002 NS NS NS < 0.0001
22.5 29.4 23.1 25.1
26.1 25.6 25.9 22.4
23.5 29.0 26.5 21.0
26.5 23.0 24.8 25.7
26.8 24.9 25.1 23.2
NS
Data presented are mean value ± SD or percent of patients. Hep = heparin; IV - intravenous; SK = streptokinase; SQ = subcutaneous; t-PA = tissue-type plasminogen activator.
respectively). The mortality rate from cardiac causes was 2.6%, 2.6%, 3.7% and 9.7% for groups I, II, III and IV, respectively (Table 2). The hospital and cardiac mortality rates in patients without prior acute myocardial infarction were 2.4% and 2.1%, 1.8% and 1.7%, 3.6% and 2.9% and 5.0% and 5.0% for groups I, II, III and IV, respectively (group IV vs. groups I and II, p = 0.1 and p = 0.08 for total and cardiac mortality, respectively), whereas for patients with a prior myocardial infarction, the hospital and cardiac mortality rates were 5.3% and 5.3%, 7.6% and 6.7%, 8.0% and 8.0% and 21.2% and 21.2%, respectively (group IV vs. groups I and II, p = 0.016 and p = 0.01 for total and cardiac mortality, respectively). The incidence of reinfarction did not differ among the four groups. Multivariable logistic regression analysis (Table 3) confirmed that hospital mortality was independently associated with the pattern of precordial ST segment depression on the
entry ECG. Thus, odds ratio in group IV relative to group I was 2.78 (95% confidence interval [CI] 1.26 to 6.13, p = 0.007). Because the mortality rate in patients without left precordial ST depression (groups I and II) was similarly low, multivariable analysis examined hospital mortality in group III and group IV separately, versus groups I and II combined. The odds ratio for mortality was 1.61 (95% CI 0.66 to 3.96) in group III versus groups I and II and 3.02 (95% CI 1.34 to 6.81) for group IV versus groups I and II (p = 0.01). Discussion The present study confirms earlier reports (1-16) showing that among patients with an inferior myocardial infarction, prognosis, especially among patients with a prior infarction, is worse for those with precordial ST segment depression, even
Table 2. Outcome by Patient G r o u p
Hypotension 2nd or 3rd degree AVB Ventricular fibrillation Asystole Reinfarction Worst Killip class I II IIl IV Hospital mortality Total
Cardiac Peak CK (IU)
Group I (n = 346)
Group II (n = 700)
Group II1 (n = 162)
Group IV (n = 113)
2.9 8.3 3.2 3.2 4.3
4.1 9.0 3.4 3.1 4.0
3.1 10.5 4.3 4.3 3.1
8.0 15.0 8.8 6.2 4.4
5.3 9.5 3.9 3.5 4.0
82.7 13.0 1.7 2.6
79.2 16.7 2.1 2.0
72.2 17.9 6.8 3.1
76.1 10.6 5.3 8.0
79.0 15.3 2.9 2.8
2.9 2.6 630 ± 967
2.8 2.6 1,320 _+ 1,472
4.3 3.7 1,074 + 1,157
9.7 9.7 902 + 1,251
3.6 3.3 1,074_+ 1,332
(n
Total 1,321)
p Value* 0.03 0.06 0.02 NS NS 0.0001 ---0.003 0.001 < 0.0001
*Group IV versus group I. Data presented are mean value _+ SD or percent of patients. AVB = atrioventricular block; CK = creatine kinase.
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BIRNBAUM ET AL. ST DEPRESSION IN I N F E R I O R INFARCTION
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Table 3. Baseline Characteristics Independently Associated With Hospital Mortality
Gender (female vs. male) Age 60-69 vs. <60 yr >70 vs. <60 yr Previous AMI Killip score on admission (>I vs. I) Pattern of precordial ST segment depression, group IV vs. group I
Odds Ratio
95% CI
p Value
2.21
1.12-4.37
0.016
2.32 8.83 2.96 2.87 2.78
0.75-7.16 3.26-23.9 1.53-5.73 1.46-5.61 1.26-6.13
0.0001 0.0007 0.0001 0.007
AMI ~ acute myocardial infarction; CI = confidence interval.
with thrombolytic therapy. In particular, the mortality rate is increased among those with maximal ST depression in leads V4 to V 6. Although the difference in mortality between patients with predominantly V 1 to V 3 versus those with predominantly V4 to V 6 precordial ST depression was more prominent among patients with a previous infarction, a similar trend also existed among patients without a previous infarction. The lack of significance of this difference among the patients without a previous infarction was probably related to the small number of patients in group IV (80 patients) and the overall low mortality rate in patients with a first inferior myocardial infarction. The admission ECG offers an immediate prognostic evaluation tool, irrespective of the success of the thrombolytic therapy initiated after it is recorded. Also, ST segment depression on precordial leads V4 to V6 in patients treated with thrombolytic therapy is also prognostically significant for patients with an inferior myocardial infarction who do not receive thrombolytic therapy (16). Etiology of precordial lead ST segment depression. The etiology of precordial lead ST segment depression during the acute phase of an inferior myocardial infarction has been extensively investigated, with conflicting results (2-14,18,19). The magnitude of ST segment deviation in precordial leads is influenced by many factors including the size (2-6,9,19,20) and exact location of the infarct and the presence of left anterior descending coronary artery disease (20-22) or three-vessel disease (21,22). However, most studies have focused only on ST segment changes in leads V1 to V4 (12,14,18). More pronounced ST segment depression in precordial leads V 1 to V 3 has been associated with posterior, inferoseptal and lateral left ventricular involvement (23-25), whereas right ventricular involvement attenuates ST segment depression in leads V 1 to V3, or may even cause precordial ST segment elevation (26). Persistence of ST segment depression in leads V 1 to V 3 over 24 h after admission has been reported to signify a larger infarct size and higher 1-year mortality rate (27). It is possible that patients with persistent ST segment depression in leads V 1 to V3 have a larger ischemic area as a result of posterior wall involvement and lack of efficient reperfusion. Although ST segment depression confined to leads V1 to V 3
is not associated with left anterior descending coronary artery stenosis or three-vessel disease (7,18,21), ST segment depression in leads V 5 and V 6 is usually associated with multivessel coronary disease, especially with concomitant left anterior descending artery stenosis (21,22,28). Moreover, Sclarovsky et al. (28,29) have shown that ST segment depression in leads V4 and V s in patients with unstable angina suggests significant left main or left main equivalent coronary artery disease and signifies an ominous prognosis. Prognostic significance of different patterns of preeordial ST segment depression. The hospital mortality rate in patients with an inferior myocardial infarction in our Israeli study group (3.6%) was lower than that reported for the total inferior infarction study population (4.7% to 5.3%) (17). This finding of lower mortality among the Israeli patients is similar to our observation in an earlier large-scale multinational study (30). Patients without precordial ST segment depression (group I) had a smaller infarction (as manifested by the lower peak serum CK levels) and a low hospital mortality rate (2.9%). Patients with predominantly precordial lead V 1 to V 3 ST segment depression (group II) had higher peak CK levels and more leads with ST segment elevation than those of group I, probably because of larger infarctions resulting from additional posterior and lateral wall involvement (14,23-25). However, development of heart failure or cardiac and total hospital mortality did not differ between these groups. These findings contradict previous reports that early mortality is higher in patients with ST segment depression in leads Va to V 3 than in those without precordial ST depression (1-14). However, ST segment depression in leads V 4 to V 6 was not measured in those studies, and thus, patients with maximal ST segment depression in leads V4 to V6 may have been included (as in groups III and IV). Ishikawa et al. (15) found that the complication rates in the 17 patients with ST segment depression in leads V 1 to V 4 were higher than those in patients with other types of precordial ST segment depression (leads V2 to Vs, V 3 to V6 and V1 to V6). However, in that relatively small study, ST segment depression was not classified according to the specific leads where ST segment depression was maximal in our study. It is also possible that early rapid washout of CK, especially among patients treated with thrombolytic therapy, may have influenced the level of its peak. The potential etiologic differences in coronary anatomy among the four patient groups may have also contributed to different reperfusion responses and thus to differences in CK peak levels. Our data corroborate the results of Hasdai et al. (16), although the overall mortality rate in the latter study (which included patients not treated with thrombolytic therapy) was higher than that in our study. Patients without prccordial ST segment depression and patients in whom the sum of ST segment depression in precordial leads V 1 to V 3 equaled or exceeded the sum in precordial leads V 4 to V 6 had a similar mortality rate (11.6% and 9.7%, respectively). ST segment depression predominantly in precordial leads V 4 to V 6 was
JACC Vol. 28, No. 2 August 1996:313-8
BIRNBAUM ET AL. ST DEPRESSION IN INFERIOR INFARCTION
associated with an increased mortality rate (41%) and decompensated left ventricular function. Multivariable logistic regression analysis confirmed that ST segment depression in the left precordial leads (V4 to V6) was significantly associated with a higher mortality (odds ratio 4.86, 95% CI 1.93 to 12.26) (16). The comparatively lower mortality rate found in the present study in patients with ST segment depression predominantly in precordial leads V4 to V6 (9.7%) is probably related to the difference in case mix; 47% of the patients in the earlier study were not treated with thrombolytic therapy because of cardiogenic shock, resuscitation or other contraindications. The increased hospital mortality associated with ST segment depression in precordial leads V4 to V 6 may reflect more severe coronary artery disease in these patients (21,22,28). Unfortunately, routine coronary angiography was not performed; therefore, we cannot substantiate this assumption. Study limitations. Right ventricular infarction was reported to be an independent predictor of hospital mortality after inferior myocardial infarction (31). Because neither routine echocardiographic evaluation nor right ECG recording (leads V3R and V4R) on admission was required in our study, concomitant right ventricular infarction was not consistently recorded and was therefore not part of the multivariable analysis. Because right ventricular infarction is expected to attenuate ST segment depression in leads VI to V3 (25,32), or even to cause ST segment elevation in these leads (26), patients with right ventricular infarction could have been included in group I or IV (the groups without ST segment depression in leads Va to V3). However, we found that for patients both with and without ST segment depression in precordial leads Vt to V3, the mortality rate was relatively low in those without ST segment depression in precordial leads V4 to V6. However, it is possible that adding right ventricular infarction to the model might have increased the accuracy of the risk estimation by the admission ECG even further. Conclusions. Patients with an inferior wall acute myocardial infarction and maximal ST segment depression in the left precordial leads (V 4 to V6) on the admission ECG are at particularly high risk for heart failure and death. Because the prognosis is poor despite intravenous thrombolytic therapy, more aggressive therapeutic measures, including primary or rescue mechanical revascularization, may be indicated. References 1. Berger PB, Ryan YJ. Inferior myocardial infarction: high risk subgroups. Circulation 1990;81:401-11. 2. Gelman JS, Saltrups A. Precordial ST depression in patients with inferior infarctions: clinical implications. Br Heart J 1982;48:560-5. 3. Shah PK, Pichler M, Berman DS, et al. Noninvasive identification of a high-risk subset of patients with acute inferior myocardial infarction. Am J Cardiol 1980;46:915-21. 4. Goldberg HL, Borer JS, Jacobstein JG, Kluger J, Scheidt SS, Alonso DR. Anterior ST-segment depression in acute inferior myocardial infarction: indicator of posterolateral infarction. Am J Cardiol 1981;48:1009-15. 5. Ong L, Valdellon B, Coromilas J, Brody R, Reiser P, Morrison J. Precordial S-T segment depression in inferior myocardial infarction: evaluation by quantitative thallium-201 scintigraphy and technetium-99m ventriculography. Am J Cardiol 1983;51:734-9.
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6. Gibson RS, Crampton RS, Watson DD, et al. Precordial ST-segment depression during acute inferior myocardial infarction: clinical, scintigraphic and angiographic correlations. Circulation 1982;66:732-41. 7. Berland J, Criber A, Letac B. Anterior ST depression in inferior myocardial infarction: correlation with results of intracoronary thrombolysis. Am Heart J 1986;111:481-8. 8. Roubin GS, Shen WF, Nicholson M, Dunn RF, Kelly DT, Harris PJ. Anterolateral ST segment depression in acute inferior myocardial infarction: angiographic and clinical implications. Am Heart J 1984;107:117782. 9. Hlatky MA, Califf RM, Lee KL, Pryor DB, Wagner GS, Rosati RA. Prognostic significance of precordial ST-segment depression during inferior acute myocardial infarction. Am J Cardiol 1985;55:325-9. 10. Nasmith J, Marpole D, Rahal D, Homan J, Stewart S, Sniderman A. Clinical outcomes after inferior infarction. Ann Intern Med 1982;96:22-6. 11. Krone RJ, Greenberg H, Dwyer EM, Kleiger RE, Boden WE. Long-term prognostic significance of ST segment depression during acute myocardial infarction. The Multicenter Diltiazem Postinfarction Trial Research Group. J Am Coil Cardiol 1993;22:361-7. 12. Bates ER, Clemmensen PM, Califf RM, et al. Precordial ST segment depression predicts a worse prognosis in inferior infarction despite reperfusion. J Am Coll Cardiol 1990;16:1538-44. 13. Willems JL, Willems R J, Willems GM, Arnold AER, Van de Werf F, Verstraete M. Significance of initial ST segment elevation and depression for the management of thrombolytic therapy in acute myocardial infarction. Circulation 1990;82:1147-58. 14. Lundergan CF, Reiner JS, Deychak YA, et al., for the GUSTO Investigators. Mortality stratification in acute inferior myocardial infarction by surface ECG [abstract]. Circulation 1994;90 Suppl I:I-500. 15. Ishikawa K, Kanamasa K, Morishita M, et al. Clinical characteristics of precordial ST-segment depression in acute inferior myocardial infarction. J Cardiol 1991;21:203-14. 16. Hasdai D, Sclarovsky S, Solodky A, Sulkes J, Strasberg B, Birnbaum Y. Prognostic significance of maximal precordial ST-segment depression in right (VI-V3) versus left (V4-V6)leads in patients with inferior wall acute myocardial infarction. Am J Cardiol 1994;74:1081-4. 17. The GUSTO Investigators. An international randomized trial comparing four thrombolytic strategies for acute myocardial infarction. N Engl J Med 1993;329:673-82. 18. Becker RC, Alpert JS. Electrocardiographic ST segment depression in coronary artery disease. Am Heart J 1988;115:862-8. 19. Camara EJN, Chandra N, Ouyang P, Gottlieb SH, Shapiro EP. Reciprocal ST change in acute myocardial infarction: assessment by electrocardiography and echocardiography. J Am Coil Cardiol 1983;2:251-7. 20. Gibelin P, Gilles B, Baudouy M, Guarino L, Morand P. Reciprocal ST segment changes in acute myocardial infarction: clinical, haemodynamic and angiographic implications. Eur Heart J 1986;7:133-9. 21. Strasberg B, Pinchas A, Barbash GI, et al. Importance of reciprocal ST segment depression in leads V 5 and V 6 as an indicator of disease of the left anterior descending coronary artery in acute inferior wall myocardial infarction. Br Heart J 1990;63:339-41. 22. Mongiardo R, Schiavoni G, Mazzari M, et al. Significance of electrocardiographic abnormalities in the "lateral" leads in patients with acute inferior myocardial infarction. Cardiologica 1988;33:681-90. 23. Sclarovsky S, Topaz O, Rechavia E, Strasberg B, Agmon J. lschemic ST segment depression in V2-V3 as the presenting electrocardiographic feature of posterolateral wall myocardial infarction. Am Heart J 1987; 113:1085-90. 24. Lew AS, Weiss T, Shah PK, et al. Precordial ST segment depression during acute inferior myocardial infarction: early thallium-201 scintigraphic evidence of adjacent posterolateral or inferoseptal involvement. J Am Coil Cardiol 1985;5:203-9. 25. Lew AS, Maddahi J, Shah PK, et al. Factors that determine the direction and magnitude of precordial ST-segment during inferior wall acute myocardial infarction. Am J Cardiol 1985;55:883-8. 26. Gelf IL, Shah PK, Rodriguez L, et al. ST elevation in lead V1 to V5 may be caused by right coronary artery occlusion and acute right ventricular infarction. Am J Cardiol 1984;53:991-6. 27. Lembo NJ, Starling MR, Dell'Italia LJ, Crawford MH, Chaudhuri TK, O'Rourke RA. Clinical and prognostic importance of persistent precordial (V1-V4) electrocardiographic ST segment depression in patients with inferior transmural myocardial infarction. Circulation 1986;74:56-63.
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28. Sclarovsky S, Davidson E, Strasberg B, et al. Unstable angina: the significance of ST segment elevation or depression in patients without evidence of increased myocardial oxygen demand. Am Heart J 1986;112:463-7. 29. Sclarovsky S, Davidson E, Lewin RF, Strasberg B, Arditti A, Agmon J. Unstable angina pectoris evolving to acute myocardial infarction. Am Heart J 1986;112:459-62. 30. Barbash GI, Modan M, Goldbourt U, White HD, van der Weft F, for the Investigators of the International Tissue Plasminogen Activator/ Streptokinase Mortality Trial. Comparative case fatality analysis of the
JACC Vol. 28, No. 2 August 1996:313-8 International Tissue Plasminogen Activator/Streptokinase Mortality Trial: variation by country beyond predictive profile. Am Coll of Cardiol 1993;21: 281-6. 31. Zehender M, Kasper W, Kauder E, et al. Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction. N Engl J Med 1993;328:981-8. 32. Pierard I_A, Sprynger M, Gilis F, Carlier J. Significance of precordial ST segment depression in inferior acute myocardial infarction as determined by echocardiography. Am J Cardiol 1986;57:82-5.
JACC Vol. 28, No. 2 August 1996:313-8
Prognostic Significance of Precordial ST Segment Depression on Admission Electrocardiogram in Patients With Inferior Wall Myocardial Infarction YOCHA|
BIRNBAUM,
MD, IZHAK HERZ, MD, SAMUEL SCLAROVSKY,
BRURIA
ZLOTIKAMIEN,
MD, ANGELA
MD,
C H E T R I T , MSc,* L I R A Z O L M E R , BSc,*
G A B R I E L I. B A R B A S H , M D , M P H t Petah-Tiqva, Tel-Hashomer and Tel Aviv, Israel
Objectives. This study assessed retrospectively the correlation between the pattern of precordial ST segment depression on the admission electrocardiogram (ECG) and hospital mortality in patients with an inferior myocardial infarction treated with intravenous thrombolytic therapy. Background. Previous studies have shown that in acute inferior myocardial infarction, ST segment depression in the precordial leads is associated with increased hospital mortality. However, the significance of the different patterns of precordial ST segment depression has been evaluated in only two previous studies. Methods. The study included 1,321 patients (1,020 men) who enrolled in the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO-I) trial in Israel and received intravenous thrombolytic therapy. Patients with an ST segment elevation >0.1 mV in at least two of the inferior leads were included. Patients were classified into four groups on the basis of their admission ECG: group I = patients with no precordial ST segment depression (n = 346); group II = those for
whom the sum of ST segment depression in leads Vl to V3 was greater than that in leads ¥4 to V6 (n = 700); group III = those for whom the sum of ST depression in leads Vmto V3 was equal to that in leads V4 to V6 (n = 162); group 1V = those with maximal ST depression in leads V4 to V6 (n = 113). Results. The overall hospital mortality rate was 3.6% (48 patients): for groups I, II, III and IV it was 2.9%, 2.8%, 4.3% and 9.7%, respectively. Multivariable logistic regression analysis confirmed that hospital mortality was independently associated with the pattern of precordial ST segment depression. The odd ratios in group IV relative to group I was 2.78 (95% confidence interval 1.26 to 6.13, p = 0.007). Conclusions. The risk of mortality is higher in patients with an inferior myocardial infarction and maximal ST segment depression in precordial leads V4 to V6 versus precordial leads V1 to V3 on the admission ECG. (JAm CoU Cardiol 1996;28:313-8)
In the era of thrombolytic therapy and various forms of invasive revascularization, it is increasingly important to identify patients with an acute myocardial infarction who are likely to develop complications during the early phase of infarction. This is especially true for inferior myocardial infarction, which is considered to have a more favorable prognosis than anterior myocardial infarction but includes high risk subgroups with increased mortality and morbidity (1). Because of its widespread availability and low cost, the 12-lead electrocardiogram (ECG) remains one of the most cost-effective and noninvasive ways to confirm myocardial infarction. Abundant published reports associate various ECG patterns of inferior myocardial infarction with high morbidity and mortality (1-14). In particular, ST segment depression in
precordial leads has been associated with a larger infarction (2-6), worse wall motion abnormalities (3-7), lower ejection fraction (3-8) and a higher rate of short- and long-term complications and mortality (2,5,6,8-11), even with reperfusion therapy (12-14). However, most previous studies of the prognostic significance of precordial ST segment depression in inferior myocardial infarction have not differentiated among the various patterns of ST segment depression. Ishikawa et al. (15), studying 92 patients with an acute inferior wall myocardial infarction, found that patients with precordial ST segment depression in leads V 1 to V 4 had higher peak creatine kinase (CK) values than patients without precordial ST segment depression. They reported higher complication rates among 17 patients with ST segment depression in leads V t to V 4 than in 27 patients without precordial ST segment depression, 10 patients with ST segment depression in leads V 2 to V 5, 13 patients with ST segment depression in V 3 to V6 or 25 patients with ST segment depression in leads V1 to V6. Recently, a retrospective study of 213 patients with an inferior wall myocardial infarction (113 patients were treated
From the BeilinsonMedical Center, Petah-Tiqva;*Sheba MedicalCenter, Tel-Hashomer; and tTel Aviv Sourasky Medical Center, Tel Aviv Sackler Facultyof Medicine,Tel AvivUniversity,Tel Aviv,Israel. Manuscript received September 19, 1995; revised manuscript received February 21, 1996,acceptedApril 2, 1996. Address for correspondence:Dr. Gabriel 1. Barbash, Tel Aviv Sourasky Medical Center, 6 WeizmanStreet,Tel Aviv64239, Israel.
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w " A__ II
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+ + + , + _c
-V',-
" - k " " V " --"k- -,,r~ --,w- ..,.v% -,7.,.
"w -4~ .&_ -t-- _~
lII
~v
-'U" l
II
VII
aVR aVL aVF
V1 V2
V3 V 4
V5
V6
Figure 1. Representative admission electrocardiogram of patients with an inferior acute myocardial infarction in each of the four groups: group I = no precordial leads with ST segment depression; group II = ST segment depression in leads V 2 and V3; group I I I = ST segment depression in leads V 2 to V6; group IV = ST segment depression mainly in leads V4 to V 6.
with thrombolytic therapy) demonstrated that patients with maximal ST segment depression in leads V4 to V6 are at higher risk for hospital mortality than patients with maximal ST segment depression in leads V1 to V3 (16). The current retrospective analysis assessed the prognostic significance of the various patterns of precordial ST segment depression on the admission ECG in 1,321 patients with an inferior myocardial infarction treated with thrombolytic therapy.
Methods Patients. All patients with an inferior myocardial infarction who enrolled in the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO-I) trial in 25 medical centers in Israel were included in the analysis. Patients were admitted within 6 h of onset of symptoms, with chest pain lasting at least 20 rain accompanied by ECG signs ->0.1-mV ST segment elevation in at least two leads (II, III or aVF). Patients with intraventricular conduction defects, ventricular rhythm, ventricular pacing or ECG evidence of left ventricular hypertrophy were excluded. All patients received either streptokinase, front-loaded tissue-type plasminogen activator (t-PA) or a combination of streptokinase and t-PA according to the GUSTO-I protocol (17). All patients received oral aspirin, 160 to 325 mg/day, and either intravenous or subcutaneous heparin for at least 48 h. The following data were recorded: gender, age, history of diabetes mellitus, hypertension, previous infarction, angina pectoris, smoking status, Killip score on admission, time elapsed from onset of symptoms to thrombolytic therapy, type of thrombolytic therapy, worst Killip score, peak serum CK levels, occurrence of reinfarction and hospital mortality. Electrocardiographic evaluation. The number of leads in the entry ECG with ST segment elevation (---0.1 mV for limb leads and ->0.2 mV for precordial leads) was recorded. The degree of ST depression was determined for all precordial leads (measured manually to the nearest 0.05 mV, 0.06 s after the J point). Patients were classified into the following four groups on the basis of the admission ECG (Fig. 1): group I =
no precordial ST segment depression (ST segment depression <0.1 mV in each of the precordial leads); group II = ST segment depression ->0.1 mV in more than one precordial lead with maximal ST segment depression in leads V 1 to V3; group I I I = ST segment depression >--0.1 mV in more than one precordial lead with the sum of ST segment depression in VI to V3 equal to that in V 4 to V6; and group IV : ST segment depression ->0.1 mV in more than one precordial lead with maximal ST segment depression in leads V4 to V6. Statistical analysis. Mean values + SD were calculated for continuous variables (age, time from onset of symptoms and serum CK levels), and absolute and relative frequencies were measured for discrete variables. For continuous variables, differences between groups were analyzed statistically by oneway analysis of variance. The chi-square test was applied to compare differences between discrete variables. A logistic regression model was fitted. The dependent variable was hospital mortality, and the independent variables were gender, age, history of diabetes mellitus, hypertension, previous myocardial infarction, angina pectoris, smoking status, time from onset of symptoms to therapy, Killip score on admission, number of leads with ST segment elevation and type of ST segment depression in the precordial leads. Odds ratio and 95% confidence intervals were calculated from the estimate variables of the logistic regression model. All tests of significance were two-tailed; p values <0.05 were considered statistically significant.
Results Baseline characteristics of patients. The study cohort included 1,321 patients (1,020 men; mean age 59.6 - 11.9 years). The baseline characteristics of the patients in the four groups are presented in Table 1. The average age was slightly lower in group I and higher in group IV. The proportion of men was lower in group II and highest in group IV. Patients in group IV had the highest rates of hypertension, previous angina pectoris and previous myocardial infarction. There was no difference in the location of the first myocardial infarction among patients with previous myocardial infarction among the four patient groups. The proportion of patients assigned to the various thrombolytic strategies and the time elapsed from onset of symptoms to thrombolytic therapy did not differ significantly among the groups. The mean number of leads with ST segment elevation was highest in group II and lowest in group IV. Clinical outcome is presented in Table 2. Group IV patients more frequently had hypotension, second- and third-degree atrioventricular block, ventricular fibrillation episodes and asystole. The incidence of decompensated left ventricular function (Killip score III and IV) was greater in groups III and IV than in groups I and II. Peak serum CK levels were maximal in group II and relatively low in group IV. A total of 48 patients (3.6%) died. The hospital mortality rate was lowest in patients without precordial ST segment depression (2.9%) and in those with maximal ST depression in leads V 1 to V3 (2.8%). The mortality rate was higher in groups III and IV (4.3% and 9.7%,
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315
Table 1. Baseline Characteristics of the F o u r Patient G r o u p s
Men Age (yr) Previous infarction Previous angina Hypertension Diabetes mellitus Current smoking Time from onset of pain to thrombolysis (rain) Killip score on admission >I No. of leads with ST elevation Therapy SK+ SQ Hep SK+ IV Hep t-PA+ IV Hep SK+ t-PA
Group I (n - 346)
Group II (n = 700)
Group III (n = 162)
Group IV (n - 113)
Total (n - 1,321)
p Value
80.5 58.3 _+ 12.0 16.4 34.8 35.6 26.7 41.7 190 ± 126 13.2 3.2 + 0.9
73.6 59.6 + 11.8 15.0 32.1 30.7 16.1 43.3 186 _+ 130 13.2 3.6 _+ 1.1
79.6 60.5 + 11.9 15.4 32.7 34.6 16.7 51.2 171 _+ 79 I6.7 3.0 _+ 0.4
84. l 62.1 + 12.4 29.2 41.6 40.7 15.0 47.8 189 + 87 15.9 2.9 _+ 0.3
77.1 59.6 + 11.9 16.6 33.7 33.3 18.9 44.2 185 + 120 13.9 3.4 + 1.0
0.01 0.02 0.002 NS NS 0.0002 NS NS NS < 0.0001
22.5 29.4 23.1 25.1
26.1 25.6 25.9 22.4
23.5 29.0 26.5 21.0
26.5 23.0 24.8 25.7
26.8 24.9 25.1 23.2
NS
Data presented are mean value ± SD or percent of patients. Hep = heparin; IV - intravenous; SK = streptokinase; SQ = subcutaneous; t-PA = tissue-type plasminogen activator.
respectively). The mortality rate from cardiac causes was 2.6%, 2.6%, 3.7% and 9.7% for groups I, II, III and IV, respectively (Table 2). The hospital and cardiac mortality rates in patients without prior acute myocardial infarction were 2.4% and 2.1%, 1.8% and 1.7%, 3.6% and 2.9% and 5.0% and 5.0% for groups I, II, III and IV, respectively (group IV vs. groups I and II, p = 0.1 and p = 0.08 for total and cardiac mortality, respectively), whereas for patients with a prior myocardial infarction, the hospital and cardiac mortality rates were 5.3% and 5.3%, 7.6% and 6.7%, 8.0% and 8.0% and 21.2% and 21.2%, respectively (group IV vs. groups I and II, p = 0.016 and p = 0.01 for total and cardiac mortality, respectively). The incidence of reinfarction did not differ among the four groups. Multivariable logistic regression analysis (Table 3) confirmed that hospital mortality was independently associated with the pattern of precordial ST segment depression on the
entry ECG. Thus, odds ratio in group IV relative to group I was 2.78 (95% confidence interval [CI] 1.26 to 6.13, p = 0.007). Because the mortality rate in patients without left precordial ST depression (groups I and II) was similarly low, multivariable analysis examined hospital mortality in group III and group IV separately, versus groups I and II combined. The odds ratio for mortality was 1.61 (95% CI 0.66 to 3.96) in group III versus groups I and II and 3.02 (95% CI 1.34 to 6.81) for group IV versus groups I and II (p = 0.01). Discussion The present study confirms earlier reports (1-16) showing that among patients with an inferior myocardial infarction, prognosis, especially among patients with a prior infarction, is worse for those with precordial ST segment depression, even
Table 2. Outcome by Patient G r o u p
Hypotension 2nd or 3rd degree AVB Ventricular fibrillation Asystole Reinfarction Worst Killip class I II IIl IV Hospital mortality Total
Cardiac Peak CK (IU)
Group I (n = 346)
Group II (n = 700)
Group II1 (n = 162)
Group IV (n = 113)
2.9 8.3 3.2 3.2 4.3
4.1 9.0 3.4 3.1 4.0
3.1 10.5 4.3 4.3 3.1
8.0 15.0 8.8 6.2 4.4
5.3 9.5 3.9 3.5 4.0
82.7 13.0 1.7 2.6
79.2 16.7 2.1 2.0
72.2 17.9 6.8 3.1
76.1 10.6 5.3 8.0
79.0 15.3 2.9 2.8
2.9 2.6 630 ± 967
2.8 2.6 1,320 _+ 1,472
4.3 3.7 1,074 + 1,157
9.7 9.7 902 + 1,251
3.6 3.3 1,074_+ 1,332
(n
Total 1,321)
p Value* 0.03 0.06 0.02 NS NS 0.0001 ---0.003 0.001 < 0.0001
*Group IV versus group I. Data presented are mean value _+ SD or percent of patients. AVB = atrioventricular block; CK = creatine kinase.
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Table 3. Baseline Characteristics Independently Associated With Hospital Mortality
Gender (female vs. male) Age 60-69 vs. <60 yr >70 vs. <60 yr Previous AMI Killip score on admission (>I vs. I) Pattern of precordial ST segment depression, group IV vs. group I
Odds Ratio
95% CI
p Value
2.21
1.12-4.37
0.016
2.32 8.83 2.96 2.87 2.78
0.75-7.16 3.26-23.9 1.53-5.73 1.46-5.61 1.26-6.13
0.0001 0.0007 0.0001 0.007
AMI ~ acute myocardial infarction; CI = confidence interval.
with thrombolytic therapy. In particular, the mortality rate is increased among those with maximal ST depression in leads V4 to V 6. Although the difference in mortality between patients with predominantly V 1 to V 3 versus those with predominantly V4 to V 6 precordial ST depression was more prominent among patients with a previous infarction, a similar trend also existed among patients without a previous infarction. The lack of significance of this difference among the patients without a previous infarction was probably related to the small number of patients in group IV (80 patients) and the overall low mortality rate in patients with a first inferior myocardial infarction. The admission ECG offers an immediate prognostic evaluation tool, irrespective of the success of the thrombolytic therapy initiated after it is recorded. Also, ST segment depression on precordial leads V4 to V6 in patients treated with thrombolytic therapy is also prognostically significant for patients with an inferior myocardial infarction who do not receive thrombolytic therapy (16). Etiology of precordial lead ST segment depression. The etiology of precordial lead ST segment depression during the acute phase of an inferior myocardial infarction has been extensively investigated, with conflicting results (2-14,18,19). The magnitude of ST segment deviation in precordial leads is influenced by many factors including the size (2-6,9,19,20) and exact location of the infarct and the presence of left anterior descending coronary artery disease (20-22) or three-vessel disease (21,22). However, most studies have focused only on ST segment changes in leads V1 to V4 (12,14,18). More pronounced ST segment depression in precordial leads V 1 to V 3 has been associated with posterior, inferoseptal and lateral left ventricular involvement (23-25), whereas right ventricular involvement attenuates ST segment depression in leads V 1 to V3, or may even cause precordial ST segment elevation (26). Persistence of ST segment depression in leads V 1 to V 3 over 24 h after admission has been reported to signify a larger infarct size and higher 1-year mortality rate (27). It is possible that patients with persistent ST segment depression in leads V 1 to V3 have a larger ischemic area as a result of posterior wall involvement and lack of efficient reperfusion. Although ST segment depression confined to leads V1 to V 3
is not associated with left anterior descending coronary artery stenosis or three-vessel disease (7,18,21), ST segment depression in leads V 5 and V 6 is usually associated with multivessel coronary disease, especially with concomitant left anterior descending artery stenosis (21,22,28). Moreover, Sclarovsky et al. (28,29) have shown that ST segment depression in leads V4 and V s in patients with unstable angina suggests significant left main or left main equivalent coronary artery disease and signifies an ominous prognosis. Prognostic significance of different patterns of preeordial ST segment depression. The hospital mortality rate in patients with an inferior myocardial infarction in our Israeli study group (3.6%) was lower than that reported for the total inferior infarction study population (4.7% to 5.3%) (17). This finding of lower mortality among the Israeli patients is similar to our observation in an earlier large-scale multinational study (30). Patients without precordial ST segment depression (group I) had a smaller infarction (as manifested by the lower peak serum CK levels) and a low hospital mortality rate (2.9%). Patients with predominantly precordial lead V 1 to V 3 ST segment depression (group II) had higher peak CK levels and more leads with ST segment elevation than those of group I, probably because of larger infarctions resulting from additional posterior and lateral wall involvement (14,23-25). However, development of heart failure or cardiac and total hospital mortality did not differ between these groups. These findings contradict previous reports that early mortality is higher in patients with ST segment depression in leads Va to V 3 than in those without precordial ST depression (1-14). However, ST segment depression in leads V 4 to V 6 was not measured in those studies, and thus, patients with maximal ST segment depression in leads V4 to V6 may have been included (as in groups III and IV). Ishikawa et al. (15) found that the complication rates in the 17 patients with ST segment depression in leads V 1 to V 4 were higher than those in patients with other types of precordial ST segment depression (leads V2 to Vs, V 3 to V6 and V1 to V6). However, in that relatively small study, ST segment depression was not classified according to the specific leads where ST segment depression was maximal in our study. It is also possible that early rapid washout of CK, especially among patients treated with thrombolytic therapy, may have influenced the level of its peak. The potential etiologic differences in coronary anatomy among the four patient groups may have also contributed to different reperfusion responses and thus to differences in CK peak levels. Our data corroborate the results of Hasdai et al. (16), although the overall mortality rate in the latter study (which included patients not treated with thrombolytic therapy) was higher than that in our study. Patients without prccordial ST segment depression and patients in whom the sum of ST segment depression in precordial leads V 1 to V 3 equaled or exceeded the sum in precordial leads V 4 to V 6 had a similar mortality rate (11.6% and 9.7%, respectively). ST segment depression predominantly in precordial leads V 4 to V 6 was
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associated with an increased mortality rate (41%) and decompensated left ventricular function. Multivariable logistic regression analysis confirmed that ST segment depression in the left precordial leads (V4 to V6) was significantly associated with a higher mortality (odds ratio 4.86, 95% CI 1.93 to 12.26) (16). The comparatively lower mortality rate found in the present study in patients with ST segment depression predominantly in precordial leads V4 to V6 (9.7%) is probably related to the difference in case mix; 47% of the patients in the earlier study were not treated with thrombolytic therapy because of cardiogenic shock, resuscitation or other contraindications. The increased hospital mortality associated with ST segment depression in precordial leads V4 to V 6 may reflect more severe coronary artery disease in these patients (21,22,28). Unfortunately, routine coronary angiography was not performed; therefore, we cannot substantiate this assumption. Study limitations. Right ventricular infarction was reported to be an independent predictor of hospital mortality after inferior myocardial infarction (31). Because neither routine echocardiographic evaluation nor right ECG recording (leads V3R and V4R) on admission was required in our study, concomitant right ventricular infarction was not consistently recorded and was therefore not part of the multivariable analysis. Because right ventricular infarction is expected to attenuate ST segment depression in leads VI to V3 (25,32), or even to cause ST segment elevation in these leads (26), patients with right ventricular infarction could have been included in group I or IV (the groups without ST segment depression in leads Va to V3). However, we found that for patients both with and without ST segment depression in precordial leads Vt to V3, the mortality rate was relatively low in those without ST segment depression in precordial leads V4 to V6. However, it is possible that adding right ventricular infarction to the model might have increased the accuracy of the risk estimation by the admission ECG even further. Conclusions. Patients with an inferior wall acute myocardial infarction and maximal ST segment depression in the left precordial leads (V 4 to V6) on the admission ECG are at particularly high risk for heart failure and death. Because the prognosis is poor despite intravenous thrombolytic therapy, more aggressive therapeutic measures, including primary or rescue mechanical revascularization, may be indicated. References 1. Berger PB, Ryan YJ. Inferior myocardial infarction: high risk subgroups. Circulation 1990;81:401-11. 2. Gelman JS, Saltrups A. Precordial ST depression in patients with inferior infarctions: clinical implications. Br Heart J 1982;48:560-5. 3. Shah PK, Pichler M, Berman DS, et al. Noninvasive identification of a high-risk subset of patients with acute inferior myocardial infarction. Am J Cardiol 1980;46:915-21. 4. Goldberg HL, Borer JS, Jacobstein JG, Kluger J, Scheidt SS, Alonso DR. Anterior ST-segment depression in acute inferior myocardial infarction: indicator of posterolateral infarction. Am J Cardiol 1981;48:1009-15. 5. Ong L, Valdellon B, Coromilas J, Brody R, Reiser P, Morrison J. Precordial S-T segment depression in inferior myocardial infarction: evaluation by quantitative thallium-201 scintigraphy and technetium-99m ventriculography. Am J Cardiol 1983;51:734-9.
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28. Sclarovsky S, Davidson E, Strasberg B, et al. Unstable angina: the significance of ST segment elevation or depression in patients without evidence of increased myocardial oxygen demand. Am Heart J 1986;112:463-7. 29. Sclarovsky S, Davidson E, Lewin RF, Strasberg B, Arditti A, Agmon J. Unstable angina pectoris evolving to acute myocardial infarction. Am Heart J 1986;112:459-62. 30. Barbash GI, Modan M, Goldbourt U, White HD, van der Weft F, for the Investigators of the International Tissue Plasminogen Activator/ Streptokinase Mortality Trial. Comparative case fatality analysis of the
JACC Vol. 28, No. 2 August 1996:313-8 International Tissue Plasminogen Activator/Streptokinase Mortality Trial: variation by country beyond predictive profile. Am Coll of Cardiol 1993;21: 281-6. 31. Zehender M, Kasper W, Kauder E, et al. Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction. N Engl J Med 1993;328:981-8. 32. Pierard I_A, Sprynger M, Gilis F, Carlier J. Significance of precordial ST segment depression in inferior acute myocardial infarction as determined by echocardiography. Am J Cardiol 1986;57:82-5.