Methods. Tel-Hashomer and Tel-Aviv, Israel

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1 506 JACC Vol. 31, No. 3 March 1, 1998: Significance of ST Segment Elevations in Posterior Chest Leads (V 7 to V 9 ) 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 (V 7 to V 9 ) 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 V 7 to V 9. 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 V 7 to V 9 was associated with a higher incidence of at least one of the following adverse clinical events: reinfarction, heart failure or death (p 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 V 7 to V 9 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 V 1 to V 3 (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 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, Address for correspondence: Dr. Hanoch Hod, Heart Institute, Sheba Medical Center, Tel-Hashomer 52621, Israel. babethr@post.tau.ac.il. 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 V 7 to V 9 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. Methods Patients and study protocol. Patients 75 years old with a first acute inferior MI in whom thrombolytic therapy could be initiated within 4hofsymptom 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 1998 by the American College of Cardiology /98/$19.00 Published by Elsevier Science Inc. PII S (97)00538-X

2 JACC Vol. 31, No. 3 MATETZKY ET AL. March 1, 1998: ST SEGMENT ELEVATION IN LEADS V 7 TO V Abbreviations and Acronyms CK creatine kinase ECG electrocardiogram, electrocardiographic IRA infarct-related artery LVEF left ventricular ejection fraction MI myocardial infarction rt-pa recombinant tissue-type plasminogen activator TIMI 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 (V 7 to V 9 ). Leads V 7 to V 9 were recorded in the same horizontal plane as lead V 6 and on the posterior axillary line (lead V 7 ), the posterior scapular line (lead V 8 ) and the left border of the spine (lead V 9 ). The ECG was obtained by a Hewlett-Packard three-channel ECG recorder with flat electrodes, so that the ECG from leads V 7 to V 9 was recorded simultaneously using standard electrodes (leads V 4 to V 6 ) 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 V 7 to V 9 and for ST segment depression 1 mm in two or more of leads V 1 to V 3. 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 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 normal; 2 mild hypokinesia; 3 severe hypokinesia; 4 akinesia; and 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 V 7 to V 9. 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 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 V 7 to V 9 (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 14 vs. 60 9, p 0.008) and 2 months later (55 10 vs.

3 508 MATETZKY ET AL. JACC Vol. 31, No. 3 ST SEGMENT ELEVATION IN LEADS V 7 TO V 9 March 1, 1998: Table 1. Baseline Characteristics Group A (n 46) Group B (n 41) p Value Age (yr) Female gender 10 (22%) 5 (12%) 0.24 Previous angina 18 (39%) 7 (17%) 0.02 Risk factors for CAD Smoking 36 (78%) 31 (76%) 0.77 Hyperlipidemia 15 (33%) 12 (29%) 0.74 Hypertension 9 (20%) 6 (15%) 0.54 Diabetes mellitus 5 (11%) 5 (12%) 0.85 Interval from onset of symptoms to initiation of rt-pa (min) PTCA 25 (54%) 21 (51%) 0.77 Data presented are mean value SD or number (%) of patients. CAD coronary artery disease; Group A patients with ST segment elevation in leads V 7 to V 9 ; Group B patients without ST segment elevation in leads V 7 to V 9 ; PTCA percutaneous transluminal coronary angioplasty; rt-pa recombinant tissue-type plasminogen activator , p 0.02). In accordance, group A had significantly higher peak CK levels than those without these changes (1, vs 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 Group A (n 46) Group B (n 41) p Value Time to cath (days) IRA RCA 29 (63%) 37 (90%) LCx 16 (35%) 2 (5%) LAD 0 1 (2.5%) 0.95 Undetermined 1 (2%) 1 (2.5%) 1.0 Patent IRA 36 (78%) 31 (76%) 0.77 Multivessel CAD 21 (46%) 17 (41%) 0.68 Data presented are mean value SD or number (%) of patients. cath catheterization; IRA infarct-related artery; LAD left anterior descending coronary artery; LCx left circumflex coronary artery; RCA right coronary artery; other abbreviations as in Table 1. Table 3. In-Hospital Clinical Course Group A (n 46) Group B (n 41) Reinfarction 10 (22%) 4 (10%) Postinfarction angina 2 (4.5%) 2 (5%) High degree AV block 2 (4.5%) 7 (17%) CHF 5 (11%) 2 (5%) CABG 1 (2%) 1 (2.5%) Mortality 3 (6.5%) 1 (2.5%) Combined adverse clinical event (CHF, reinfarction, death) 12 (26%)* 4 (10%)* *p 0.05, Group A versus Group B. Data presented are number (%) of patients. AV atrioventricular; CABG coronary artery bypass graft surgery; CHF congestive heart failure; other abbreviations as in Table 1. Clinical findings (Table 3). The patients with concomitant ST segment elevation in leads V 7 to V 9 (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 V 7 to V 9 and ST segment depression in leads V 1 to V 3. Significant ST segment depression in leads V 1 to V 3 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 V 1 to V 3 had no ST segment elevation in leads V 7 to V 9 (Fig. 1). When ST segment elevation in leads V 7 to V 9 and ST segment depression in leads V 1 to V 3 at hospital admission were compared with respect to diagnostic accuracy of posterior involvement (at least severe hypokinesia), ST segment elevation in leads V 7 to V 9 had a similar sensitivity (80% vs. 72%, p 0.34) but a higher specificity (84% vs. 57%, p 0.02) and test accuracy (82% vs. 66%, p 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 V 7 to V 9 (Group A), IRA patency resulted in a higher LVEF both at hospital discharge (56 13 vs , p 0.012) and at the 2-month follow-up visit (56 10 vs. 49 9, p 0.052). In patients without posterior ST segment elevation, LVEF was similar with or without IRA patency at hospital discharge (59 10 vs [p 0.4]) and at the 2-month follow-up visit ( vs [p 0.7]). Discussion Classically, ECG diagnosis of posterior wall infarction is based on the appearance of prominent R waves in leads V 1 and

4 JACC Vol. 31, No. 3 MATETZKY ET AL. March 1, 1998: ST SEGMENT ELEVATION IN LEADS V 7 TO V Figure 2. Flowchart illustrating distribution of patients (PTS) with and without ST segment elevation (ST 1) in leads V 7 to V 9 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 V 7 to V 9 with (left panel) and without concomitant ST segment depression in leads V 1 to V 3 (right panel). V 2, 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 V 9 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 V 7 to V 9 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 V 7 to V 9 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 V 7 to V 9 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 V 7 to V 9 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 V 7 to V 9 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 V 7 to V 9 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.

5 510 MATETZKY ET AL. JACC Vol. 31, No. 3 ST SEGMENT ELEVATION IN LEADS V 7 TO V 9 March 1, 1998: Beneficial effect of thrombolytic therapy in inferior wall infarction with and without ST segment elevation in leads V 7 to V 9. 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 V 1 to V 4. 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 V 7 to V 9 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 V 7 to V 9 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. Conclusions. We recommend routine recording of leads V 7 to V 9 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. 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