Posterior Mi

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JACC Vol. 31, No. 3 March 1, 1998:506 –11

Significance of ST Segment Elevations in Posterior Chest Leads (V7 to V9) in Patients With Acute Inferior Myocardial Infarction: Application for Thrombolytic Therapy SHLOMI MATETZKY, MD, DOV FREIMARK, MD, PIERRE CHOURAQUI, MD, BABETH RABINOWITZ, MD, FACC, SHMUEL RATH, MD, ELIESER KAPLINSKY, MD, FACC, HANOCH HOD, MD, FACC Tel-Hashomer and Tel-Aviv, Israel

Objectives. This study was designed to examine whether ST segment elevation in posterior chest leads (V7 to V9) during acute inferior myocardial infarction (MI) identifies patients with a concomitant posterior infarction and whether these patients might benefit more from thrombolysis. Background. Because the posterior wall is faced by none of the 12 standard electrocardiographic (ECG) leads, the ECG diagnosis of posterior infarction is problematic and has often remained undiagnosed, especially in the acute phase. Methods. Eighty-seven patients with a first inferior infarction who were treated with recombinant tissue-type plasminogen activator were stratified according to the presence (Group A [46 patients]) or absence (Group B [41 patients]) of concomitant ST segment elevation in posterior chest leads V7 to V9. Results. Patients in Group A had a higher incidence of posterolateral wall motion abnormalities (p < 0.001) on radionuclide

ventriculography, a larger infarct area (as evidenced by higher peak creatine kinase levels) (p < 0.02) and a lower left ventricular ejection fraction (LVEF) at hospital discharge (p < 0.008) than those in Group B. ST segment elevation in leads V7 to V9 was associated with a higher incidence of at least one of the following adverse clinical events: reinfarction, heart failure or death (p 5 0.05). Although patency of the infarct-related artery (IRA) in Group A resulted in an improved LVEF at discharge (p < 0.012), LVEF was unchanged in Group B, regardless of the patency status of the IRA. Conclusions. ST segment elevation in leads V7 to V9 identifies patients with a larger inferior MI because of concomitant posterolateral involvement. Such patients might benefit more from thrombolytic therapy. (J Am Coll Cardiol 1998;31:506 –11) ©1998 by the American College of Cardiology

Because none of the 12 standard electrocardiographic (ECG) leads face the posterior left ventricular wall, the ECG diagnosis of posterior myocardial infarction (MI) is based on mirrorimage reflection of the electrical events involving the posterior wall on the precordial leads (1–7). Although an infarction involving the posterior wall might occur as an isolated infarction, it occurs more often in association with an inferior infarction (8). During the acute phase of inferior infarction, ECG detection of posterior infarction rested on the appearance of concomitant ST segment depression in leads V1 to V3 (2–7). However, these changes are relatively insensitive and not specific (3,7,9,10) and may represent inferoseptal infarction (11) or, as suggested earlier by a number of other investigators (12–16), anterior ischemia or non–Q wave MI. Because the beneficial effect of thrombolytic therapy is proportional to the amount of jeopardized myocardium (17–

20), the early appreciation of the extent of an inferior infarction, and thus the early detection of posterior involvement (8), is gaining increasing importance in the present era of interventional therapy. Previous studies have suggested that ECG recording from the posterior chest leads might directly indicate the ECG events of the posterior wall (1,21–24), but none of these studies examined this possibility in the acute phase of MI. The present study was undertaken 1) to assess the value of ST segment elevation in posterior chest leads V7 to V9 in the early diagnosis of posterior wall involvement during the acute phase of inferior MI; and 2) to test the hypothesis that patients with an inferior MI in whom this particular ECG pattern is found might benefit more from thrombolytic therapy than those in whom this pattern is absent.

From the Heart Institute, Sheba Medical Center, Tel-Hashomer; and Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel. Manuscript received July 11, 1997; revised manuscript received October 3, 1997, accepted November 26, 1997. Address for correspondence: Dr. Hanoch Hod, Heart Institute, Sheba Medical Center, Tel-Hashomer 52621, Israel. E-mail: [email protected]. ©1998 by the American College of Cardiology Published by Elsevier Science Inc.

Methods Patients and study protocol. Patients ,75 years old with a first acute inferior MI in whom thrombolytic therapy could be initiated within 4 h of symptom onset were eligible for the study. The diagnosis of inferior MI was based on a history of chest pain suggestive of myocardial ischemia lasting .30 min and ECG ST segment elevation $1 mm in at least two of leads 0735-1097/98/$19.00 PII S0735-1097(97)00538-X

JACC Vol. 31, No. 3 March 1, 1998:506 –11

Abbreviations and Acronyms CK 5 creatine kinase ECG 5 electrocardiogram, electrocardiographic IRA 5 infarct-related artery LVEF 5 left ventricular ejection fraction MI 5 myocardial infarction rt-PA 5 recombinant tissue-type plasminogen activator TIMI 5 Thrombolysis in Myocardial Infarction

II, III and aVF. The diagnosis was confirmed in all patients by elevation of creatine kinase (CK) levels to at least twice the higher normal value at our laboratory (#90 IU/liter in men; #80 IU/liter in women), with the CK, MB fraction .6% of the highest total CK. CK levels were determined at hospital admission, every 3 h during the first 24 h and once daily thereafter. Excluded from the study were patients with an ECG pattern of complete left bundle branch block or the accepted contraindications to thrombolysis. The patients were treated with 100 mg of recombinant tissue-type plasminogen activator (rt-PA) during 4 h, intravenous infusion of heparin for at least 5 days and 250 mg of aspirin daily thereafter. Electrocardiography. A 15-lead ECG was recorded on hospital admission before initiation of rt-PA and included, in addition to the standard 12 leads, three posterior chest leads (V7 to V9). Leads V7 to V9 were recorded in the same horizontal plane as lead V6 and on the posterior axillary line (lead V7), the posterior scapular line (lead V8) and the left border of the spine (lead V9). The ECG was obtained by a Hewlett-Packard three-channel ECG recorder with flat electrodes, so that the ECG from leads V7 to V9 was recorded simultaneously using standard electrodes (leads V4 to V6) with the patient in the supine position. The ECG was reviewed for the presence of ST segment elevation of at least 0.5 mm in two or more of leads V7 to V9 and for ST segment depression $1 mm in two or more of leads V1 to V3. ST segment deviation was measured 80 ms after the J point. As suggested by previous studies (22,25), an ST segment elevation of 0.5 mm was considered significant in the posterior chest leads because of the greater distance separating the posterior chest wall from the heart. In addition, the summed ST segment elevations in the three contiguous leads demonstrating the greatest ST segment elevation were calculated on the admission ECG. A $50% decrease in the summed ST segment elevations within 2 h of thrombolytic therapy was considered early ST segment resolution, as previously proposed by other investigators (26,27). Radionuclide ventriculography. To evaluate left ventricular global and regional function, patients underwent rest gated blood pool radionuclide imaging within 24 h of hospital admission, before discharge and 2 months later. Images were acquired in the anterior and the 45° left anterior oblique (best septal) projections. Left ventricular ejection fraction (LVEF) was calculated from the 45° left anterior oblique projection. For the purpose of evaluation of segmental wall motion, the

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507

left ventricle was divided into five segments: septal, inferoapical, posterolateral, anterolateral and anterobasal. Regional wall motion in each segment was graded according to the following point scale: 1 5 normal; 2 5 mild hypokinesia; 3 5 severe hypokinesia; 4 5 akinesia; and 5 5 dyskinesia. Angiography. Patients were scheduled to undergo catheterization within 72 h of rt-PA initiation. Significant stenosis in the large diagonal or marginal branches was considered left anterior descending or circumflex coronary artery disease, respectively. The flow pattern of the infarct-related artery (IRA) was determined by Thrombolysis in Myocardial Infarction (TIMI) classification criteria. The IRA was considered patent if perfusion was TIMI grade 2 or 3 and occluded if it was TIMI grade 0 or 1. In any coronary artery, stenosis was considered significant if the lumen diameter was narrowed by $50% in any projection. Using this definition, the number of significantly diseased coronary vessels was determined. Percutaneous transluminal coronary angioplasty of the culprit lesion was attempted in all patients with significant stenosis or occlusion of the IRA. Data analysis. Because the sample size was relatively small, the study was underpowered to detect differences in specific clinical outcomes, such as heart failure, reinfarction or mortality between patients with and without ST segment elevation in leads V7 to V9. Thus, patients were compared by means of the prespecified combined clinical end point of heart failure, reinfarction or death (at least one adverse event). Results are presented as mean value 6 SD for continuous variables and as frequency for discrete variables. Continuous variables were compared by the standard t test, and discrete variables by chi-square analysis with Yates correction.

Results Patients. The study group included 87 consecutive patients with a first inferior MI. No patient was excluded because of technical problems in recording or reading the ECG from the posterior leads. Forty-six patients (53%) had significant ST segment elevation in posterior chest leads V7 to V9 (Group A), and 41 (47%) did not (Group B). Group A patients had a significantly higher incidence of previous angina pectoris (39% vs. 17%, p , 0.02); otherwise, no significant differences were noted between the two groups with respect to baseline characteristics (Table 1). Posterolateral involvement and indexes of infarct size. Group A had a significantly higher incidence of abnormal wall motion in the posterolateral segment on early ventriculogram than group B (89% vs. 46%, p , 0.001). When only severe hypokinesia or more severe wall motion abnormality was considered, the differences were even more pronounced (87% in Group A vs. 24% in Group B, p , 0.001). In other respects, the distribution of the regional wall motion abnormalities was comparable between the two groups. Patients with ST segment elevation in the posterior leads had a significantly lower LVEF than those without this ECG pattern at hospital discharge (53 6 14 vs. 60 6 9, p , 0.008) and 2 months later (55 6 10 vs.

508

MATETZKY ET AL. ST SEGMENT ELEVATION IN LEADS V7 TO V9

JACC Vol. 31, No. 3 March 1, 1998:506 –11

Table 1. Baseline Characteristics

Age (yr) Female gender Previous angina Risk factors for CAD Smoking Hyperlipidemia Hypertension Diabetes mellitus Interval from onset of symptoms to initiation of rt-PA (min) PTCA

Table 3. In-Hospital Clinical Course

Group A (n 5 46)

Group B (n 5 41)

p Value

57 6 10 10 (22%) 18 (39%)

54 6 10 5 (12%) 7 (17%)

0.17 0.24 0.02

36 (78%) 15 (33%) 9 (20%) 5 (11%) 134 6 39

31 (76%) 12 (29%) 6 (15%) 5 (12%) 124 6 48

0.77 0.74 0.54 0.85 0.29

25 (54%)

21 (51%)

0.77

Data presented are mean value 6 SD or number (%) of patients. CAD 5 coronary artery disease; Group A 5 patients with ST segment elevation in leads V7 to V9; Group B 5 patients without ST segment elevation in leads V7 to V9; PTCA 5 percutaneous transluminal coronary angioplasty; rt-PA 5 recombinant tissue-type plasminogen activator.

60 6 10, p , 0.02). In accordance, group A had significantly higher peak CK levels than those without these changes (1,254 6 673 vs. 847 6 723 IU/liter, p , 0.05). Angiography. The IRA could be identified in 85 patients (98%). In two patients (one in group A and one in group B), no significant stenosis was seen. The left circumflex coronary artery was the IRA in a significantly higher proportion of patients in group A than group B (35% vs. 5%, p , 0.001). The reverse was noted with respect to the right coronary artery, which was the IRA in 63% of patients presenting with ST segment elevation in the posterior lead and in 90% of those without this ECG pattern (p , 0.003). Despite the differences in the identity of the culprit vessel, both groups had a similar patency rate and a similar incidence of multivessel coronary artery disease (Table 2). Among the 65 patients with a patent IRA in both groups, early ST segment elevation resolution and early (within 12 h) peak CK were noted in 55 patients (82%). In comparison, the two aforementioned clinical signs of reperfusion were noted in only three patients (15%) from among those with an occluded IRA (p , 0.01). Table 2. Angiographic Findings

Time to cath (days) IRA RCA LCx LAD Undetermined Patent IRA Multivessel CAD

Group A (n 5 46)

Group B (n 5 41)

p Value

4.3 6 1.7

4.3 6 1.8

1.0

29 (63%) 16 (35%) 0 1 (2%) 36 (78%) 21 (46%)

37 (90%) 2 (5%) 1 (2.5%) 1 (2.5%) 31 (76%) 17 (41%)

0.003 0.001 0.95 1.0 0.77 0.68

Data presented are mean value 6 SD or number (%) of patients. cath 5 catheterization; IRA 5 infarct-related artery; LAD 5 left anterior descending coronary artery; LCx 5 left circumflex coronary artery; RCA 5 right coronary artery; other abbreviations as in Table 1.

Reinfarction Postinfarction angina High degree AV block CHF CABG Mortality Combined adverse clinical event (CHF, reinfarction, death)

Group A (n 5 46)

Group B (n 5 41)

10 (22%) 2 (4.5%) 2 (4.5%) 5 (11%) 1 (2%) 3 (6.5%) 12 (26%)*

4 (10%) 2 (5%) 7 (17%) 2 (5%) 1 (2.5%) 1 (2.5%) 4 (10%)*

*p 5 0.05, Group A versus Group B. Data presented are number (%) of patients. AV 5 atrioventricular; CABG 5 coronary artery bypass graft surgery; CHF 5 congestive heart failure; other abbreviations as in Table 1.

Clinical findings (Table 3). The patients with concomitant ST segment elevation in leads V7 to V9 (Group A) appeared to have a more complicated in-hospital course than those in group B, as manifested by higher occurrence rate of the combined clinical end point of at least one of the following adverse clinical events: reinfarction, heart failure or death (26% vs. 10%, p # 0.05). Comparison of ST segment elevation in leads V7 to V9 and ST segment depression in leads V1 to V3. Significant ST segment depression in leads V1 to V3 was noted in 52 patients (60%). The occurrence of ST segment depression in the precordial leads agreed only partially with the occurrence of ST segment elevation in the posterior chest leads. In 10 Group A patients (22%), ST segment depression was not present on the admission ECG, and 16 patients (31%) with ST segment depression in leads V1 to V3 had no ST segment elevation in leads V7 to V9 (Fig. 1). When ST segment elevation in leads V7 to V9 and ST segment depression in leads V1 to V3 at hospital admission were compared with respect to diagnostic accuracy of posterior involvement (at least severe hypokinesia), ST segment elevation in leads V7 to V9 had a similar sensitivity (80% vs. 72%, p 5 0.34) but a higher specificity (84% vs. 57%, p 5 0.02) and test accuracy (82% vs. 66%, p 5 0.01). Beneficial effect of an open IRA in patients with an inferior MI with and without posterior lead ST segment elevation. To assess the impact of thrombolytic therapy, LVEF was analyzed in both groups according to IRA patency (Fig. 2). In patients with ST segment elevation in leads V7 to V9 (Group A), IRA patency resulted in a higher LVEF both at hospital discharge (56 6 13 vs. 44 6 12, p , 0.012) and at the 2-month follow-up visit (56 6 10 vs. 49 6 9, p 5 0.052). In patients without posterior ST segment elevation, LVEF was similar with or without IRA patency at hospital discharge (59 6 10 vs. 61 6 9 [p 5 0.4]) and at the 2-month follow-up visit (60 6 9.5 vs. 59 6 13 [p 5 0.7]).

Discussion Classically, ECG diagnosis of posterior wall infarction is based on the appearance of prominent R waves in leads V1 and

JACC Vol. 31, No. 3 March 1, 1998:506 –11

MATETZKY ET AL. ST SEGMENT ELEVATION IN LEADS V7 TO V9

509

Figure 2. Flowchart illustrating distribution of patients (PTS) with and without ST segment elevation (ST 1) in leads V7 to V9 at hospital admission according to IRA patency and LVEF in each of the four groups that resulted.

Figure 1. ECGs from two patients with an inferior MI judged to have significant ST segment elevation in leads V7 to V9 with (left panel) and without concomitant ST segment depression in leads V1 to V3 (right panel).

V2, but these R waves might appear hours after the onset of symptoms. Previous investigators (2–7) have suggested that precordial ST segment depression during the acute stage of inferior MI might be related to posterior wall involvement. However, such precordial ST segment depression might also reflect anterior wall ischemia or non–Q wave MI (12–16). Furthermore, precordial ST segment depression might be diminished by right ventricular infarction (25) or might be masked by the development of a complete right bundle branch block pattern. Consequently, this ECG sign has low to moderate sensitivity and specificity for posterior wall infarction (3,4,7,9 –12).

Previous studies (1,21,22) have demonstrated the appearance of pathologic Q waves in posterior chest leads in patients with an old posterior infarction. However, these studies included only a small number of patients in whom posterior infarction was diagnosed by standard ECG (21,22) or vectorcardiographic criteria (1). Rich et al. (23) studied 369 patients who underwent exercise testing with thallium scintigraphy, 27 of whom met scintigraphic criteria for posterior infarction. They showed that the presence of Q waves in lead V9 was more accurate than the classic standard ECG criteria for diagnosing posterior infarction. In accordance with our results, Zalenski et al. (24) found ST segment elevation in leads V7 to V9 in 6 (50%) of 12 patients with an acute inferior MI. However, the presence of a posterior infarction in patients with ST segment elevation in leads V7 to V9 was not confirmed, and patients with and without ST segment elevation were not compared. We showed that the early diagnosis of concomitant posterolateral infarction in patients with an acute inferior MI could be made on the basis of the presence of ST segment elevation in leads V7 to V9 and that these ECG changes are more accurate than ST segment depression in precordial leads for detecting posterior involvement. Consequently, concomitant ST segment elevation in leads V7 to V9 identified a subset of patients with a larger inferior MI, as evidenced by higher peak CK levels and poorer left ventricular function. The higher incidence of a combined clinical end point (heart failure, reinfarction or mortality) in patients with ST segment elevation in leads V7 to V9 suggests that these patients might also have had a more complicated clinical course. Our results with regard to the differences in the identity of the IRA among patients with and without ST segment elevation in leads V7 to V9 concur with those of previous studies (28 –30) showing that posterior wall infarction was associated with more frequent circumflex artery disease. Complete atrioventricular block is almost entirely restricted to right coronary artery–related infarction (31), thus possibly also explaining the somewhat higher incidence of high degree atrioventricular block in Group B than in Group A patients.

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MATETZKY ET AL. ST SEGMENT ELEVATION IN LEADS V7 TO V9

Beneficial effect of thrombolytic therapy in inferior wall infarction with and without ST segment elevation in leads V7 to V9. Previous studies that evaluated the results of thrombolytic therapy for inferior MI demonstrated only an insignificant trend toward mortality reduction (17–20) and yielded conflicting conclusions with respect to the resulting improvement in left ventricular function (32–36). Nevertheless, only few studies have evaluated the beneficial effect of thrombolytic therapy in high risk subsets of patients with an inferior MI. Bar et al. (37) demonstrated a higher, enzymatically estimated infarct size limitation after successful thrombolysis in patients with an inferior MI with a summed ST segment elevation .6 mm than in those with a lower summed ST segment elevation. However, they did not extrapolate their results to terms of ventricular function. Berland et al. (38) found postreperfusion improvement in segmental contraction only in patients who had concomitant precordial lead ST segment depression on the admission ECG, but they failed to show similar differences regarding LVEF. However, Bates et al. (36) postulated an insignificant improvement in either regional or global left ventricular function in patients with an inferior MI after thrombolytic therapy, with or without ST segment depression in leads V1 to V4. In the present study, a patent IRA appeared to be more beneficial in patients with an inferior MI with ST segment elevation in posterior leads V7 to V9 at hospital admission. Previous studies (39,40) have shown that the amount of myocardial salvage by thrombolytic therapy is proportional to the initial amount of jeopardized myocardium. Thus, the concomitant posterolateral involvement in patients with ST segment elevation in leads V7 to V9 on hospital admission, which indicates a larger infarct, presumably accounts for the higher beneficial effect in these patients. Moreover, in patients with an inferior infarction, posterior involvement is associated with the development of significant mitral regurgitation, although successful thrombolysis reduces the prevalence of mitral regurgitation in conjunction with a reduction in the prevalence of posterior wall motion abnormalities (41). Study limitations. The present study is limited by its small sample size and is therefore underpowered to detect differences in specific clinical outcomes and the beneficial effects of thrombolysis in terms of clinical results between Groups A and B. We therefore suggest that the present study, which reports initial results, should be interpreted with caution. Larger studies are needed. The patients in the present study underwent catheterization on the fourth day, on average; thus, only the impact of “patency” and not “early reperfusion” could be determined. Yet the similar timing of catheterization and the similar incidence of early reinfarction (within 72 h) in both groups, as well as the much higher occurrence of clinical signs of reperfusion in patients with a patent IRA, suggest that the intergroup differences in left ventricular function response to patency reflect differences in the beneficial effects of thrombolysis.

JACC Vol. 31, No. 3 March 1, 1998:506 –11

Conclusions. We recommend routine recording of leads V7 to V9 in all patients admitted to the hospital with an acute inferior MI and suggest that ST segment elevation in these leads, because it implies a large area of jeopardized myocardium, might argue in favor of thrombolytic therapy or another form of reperfusion, such as direct coronary angioplasty.

References 1. Perloff JK. The recognition of strictly posterior myocardial infarction by conventional scalar electrocardiography. Circulation 1964;30:706 –18. 2. Goldberg HL, Borer JS, Jacobstein JG, Kluger J, Scheidt SS, Alonso DR. Anterior ST depression in acute inferior myocardial infarction: indicator of posterolateral infarction. Am J Cardiol 1981;48:1009 –15. 3. Croft CH, Woodward W, Nicod BP, et al. Clinical implications of anterior S-T segment depression in patients with acute inferior myocardial infarction. Am J Cardiol 1982;50:428 –30. 4. 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. 5. Ong L, Valdellon B, Coromilas J, Brody R, Reiser P, Morrison J. Precordial ST segment depression in inferior myocardial infarction: evaluation by quantitative thallium-201 scintigraphy and technetium-99m ventriculography. Am J Cardiol 1983;51:734 –9. 6. Haltky 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. 7. Lew AS, Weiss AT, Shah PK, et al. Precordial ST segment depression during acute inferior myocardial infarction: early thallium-201 scintigraphy evidence of adjacent posterolateral or inferoseptal involvement. J Am Coll Cardiol 1985;5:203–9. 8. Nestico PF, Hakki AH, Iskandrian AS, Anderson GJ. Electrocardiographic diagnosis of posterior myocardial infarction revisited: a new approach using a multivariate discriminant analysis and thallium-201 myocardial scintigraphy. J Electrocardiol 1986;19:33– 40. 9. Mukharji J, Murray S, Lewis SE, et al. Is anterior ST depression with acute transmural inferior infarction due to posterior infarction? A vectorcardiographic and scintigraphic study. J Am Coll Cardiol 1984;4:28 –34. 10. Cohen M, Blanke H, Karsh KR, Holt J, Rentrop P. Implications of precordial ST segment depression during acute inferior myocardial infarction: arteriographic and ventriculographic correlations during the acute phase. Br Heart J 1984;52:497–501. 11. Boden WE, Spodick DH. Diagnostic significance of precordial ST-segment depression. Am J Cardiol 1989;63:358 – 61. 12. 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. 13. Salcedo JR, Baird MD, Chambers RJ, Beanlands DS. Significance of reciprocal ST segment depression in anterior precordial leads in acute inferior myocardial infarction: concomitant left anterior descending coronary disease? Am J Cardiol 1981;48:10003– 8. 14. Haraphongse M, Jugdutt BL, Rossall RE. Significance of precordial ST segment depression in acute transmural inferior infarction: coronary angiographic findings. Cathet Cardiovasc Diagn 1983;9:143–51. 15. Billadello JJ, Smith JL, Ludbrooke PA, et al. Implications of “reciprocal” ST segment depression associated with acute myocardial infarction identified by positron tomography. J Am Coll Cardiol 1983;2:616 –24. 16. Roubin GS, Shen WF, Nicholson M, Dunn RF, Kelly DT, Harris PJ. Anterolateral ST segment depression in acute inferior myocardial infarction. Am Heart J 1984;107:1177– 82. 17. Rentrop P, Smith H, Painter L, Holt J. Changes in left ventricular ejection fraction after intracoronary thrombolytic therapy: results of Registry of the European Society of Cardiology. Circulation 1983;68:55– 60. 18. Vermeer F, Simoons M, Bar FW, et al. Which patients benefit most from early thrombolytic therapy with intracoronary streptokinase? Circulation 1986;74:1379 – 89. 19. Hackworthy RA, Vogel MB, Harris PJ. Influence of infarct artery patency on the relation between initial ST segment elevation and final infarct size. Br Heart J 1986;56:222–5.

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20. Muller DWM, Topol EJ. Selection of patients with acute myocardial infarction for thrombolytic therapy. Ann Intern Med 1990;113:949 – 60. 21. Tulloch JA. The electrocardiographic features of high posterolateral myocardial infarction. Br Heart J 1952;14:379 – 86. 22. Elek R, Herman LM, Griffith GC. A study of unipolar left back leads and their application to posterior myocardial infarction. Circulation 1953;7 Suppl VII:VII-656 – 8. 23. Rich MW, Imburgia M, King TR, Fischer KC, Kovach KL. Electrocardiographic diagnosis of remote posterior wall myocardial infarction using unipolar posterior lead V9. Chest 1989;96:489 –93. 24. Zalenski RJ, Cooke D, Rydman R, Sloan EP, Murphy DG. Assessing the diagnostic value of an ECG containing leads V4R, V8, and V9: the 15-lead ECG. Ann Emerg Med 1993;22:786 –93. 25. Lew AS, Maddahi J, Shah PK, Weiss AT, Peter T, Berman DS. Factors that determine the direction and magnitude of precordial ST-segment deviations during inferior wall acute myocardial infarction. Am J Cardiol 1985;55: 883– 8. 26. Barbash GI, Hod H, Miller HI, et al. Rapid resolution of ST elevation and prediction of clinical outcome in patients undergoing thrombolysis with alteplase (recombinant tissue-type plasminogen activator): results of the Israeli Study of Early Intervention in Myocardial Infarction. Br Heart J 1990;64:241–7. 27. Bossaert L, Conraads V, Pintens H, for the Belgian EMS Study Group. ST-segment analysis: a useful marker for reperfusion after thrombolysis with APSAC? Eur Heart J 1991;12:357– 62. 28. Huey BL, Beller GA, Kaiser DL, Gibson RS. A comprehensive analysis of myocardial infarction due to left circumflex artery occlusion: comparison with infarction due to right coronary artery and left anterior descending artery occlusion. J Am Coll Cardiol 1988;12:1156 – 66. 29. Newman NN, Dunn RF, Harris PJ, Bautovich GJ, McLaughlin AF, Kelly DT. Differentiation between right and circumflex coronary artery disease on thallium myocardial perfusion scanning. Am J Cardiol 1983;51:1052– 8. 30. Bough EW, Korr KS. Prevalence and severity of circumflex coronary artery disease in electrocardiographic posterior myocardial infarction. J Am Coll Cardiol 1986;7:990 – 6. 31. Clemmensen P, Bates ER, Califf RM, et al., for the TAMI Study Group. Complete atrioventricular block complicating inferior wall acute myocar-

MATETZKY ET AL. ST SEGMENT ELEVATION IN LEADS V7 TO V9

32. 33.

34. 35.

36.

37.

38. 39. 40. 41.

511

dial infarction treated with reperfusion therapy. Am J Cardiol 1991;67: 225–30. White HD, Norris RM, Brown MA, et al. Effect of intravenous streptokinase on left ventricular function and early survival after acute myocardial infarction. N Engl J Med 1987;317:850 –5. Bassand JP, Machecourt J, Cassagnes J, et al., for the APSIM Study Investigators. Multicenter trial for intravenous Anisoylated Plasminogen Streptokinase Activator Complex (APSAC) in acute myocardial infarction: effects on infarct size and left ventricular function. J Am Coll Cardiol 1988;13:988 –97. O’Rourke M, Baron D, Keogh A, et al. Limitations of myocardial infarction by early infusion of recombinant tissue-type plasminogen activator. Circulation 1988;77:311–5. National Heart Foundation of Australia Coronary Thrombolysis Group. Coronary thrombolysis and myocardial salvage by tissue plasminogen activator given up to 4 hours after onset of myocardial infarction. Lancet 1988;1:203–7. Bates ER, Clemmensen PM, Califf RM, et al., for the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) Study Group. Precordial ST segment depression predicts a worse prognosis of inferior infarction despite reperfusion therapy. J Am Coll Cardiol 1990;16:1538 – 44. Bar FW, Vermeer F, de Zwaan C, et al. Value of admission electrocardiogram in predicting outcome of thrombolytic therapy in acute myocardial infarction: a randomized trial conducted by The Netherlands InterUniversity Cardiology Institute. Am J Cardiol 1987;59:6 –13. Berland J, Cribier A, Behar P, Letac B. Anterior ST depression in inferior myocardial infarction: correlation with results of intracoronary thrombolysis. Am Heart J 1986;111:481– 8. Bates ER. Reperfusion therapy in inferior myocardial infarction. J Am Coll Cardiol 1988;12 Suppl A:44 –51A. Mauri F, Gasparini M, Barbonaglia L, et al. Prognostic significance of the extent of myocardial injury in acute myocardial infarction treated by streptokinase (the GISSI trial). Am J Cardiol 1989;63:1291–5. Tenenbaum A, Leor J, Motro M, et al. Improved posterobasal segment function after thrombolysis is associated with decreased incidence of significant mitral regurgitation in a first inferior myocardial infarction. J Am Coll Cardiol 1995;25:1558 – 63.

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