Author + information
- Received July 11, 1997
- Revision received October 3, 1997
- Accepted November 26, 1997
- Published online March 1, 1998.
- Shlomi Matetzky, MDAB,
- Dov Freimark, MDAB,
- Pierre Chouraqui, MDAB,
- Babeth Rabinowitz, MD, FACCAB,
- Shmuel Rath, MDAB,
- Elieser Kaplinsky, MD, FACCAB and
- Hanoch Hod, MD, FACCAB,* ()
- ↵*Dr. Hanoch Hod, Heart Institute, Sheba Medical Center, Tel-Hashomer 52621, Israel.
Objectives. This study was designed to examine whether ST segment elevation in posterior chest leads (V7to 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 V7to 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 V7to V9was 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 V7to V9identifies patients with a larger inferior MI because of concomitant posterolateral involvement. Such patients might benefit more from thrombolytic therapy.
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 mirror-image 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 . During the acute phase of inferior infarction, ECG detection of posterior infarction rested on the appearance of concomitant ST segment depression in leads V1to V3[2–7]. However, these changes are relatively insensitive and not specific [3, 7, 9, 10]and may represent inferoseptal infarction 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 , 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 V7to V9in 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.
1.1 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 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.
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 (V7to V9). Leads V7to V9were recorded in the same horizontal plane as lead V6and 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 V7to V9was recorded simultaneously using standard electrodes (leads V4to 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 V7to V9and for ST segment depression ≥1 mm in two or more of leads V1to 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].
1.3 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.
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 patentif perfusion was TIMI grade 2 or 3 and occludedif 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.
1.5 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 V7to 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 ± SD for continuous variables and as frequency for discrete variables. Continuous variables were compared by the standard ttest, and discrete variables by chi-square analysis with Yates correction.
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 V7to 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).
2.2 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. 60 ± 10, p < 0.02). In accordance, group A had significantly higher peak CK levels than those without these changes (1,254 ± 673 vs. 847 ± 723 IU/liter, p < 0.05).
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).
2.4 Clinical Findings (Table 3)
The patients with concomitant ST segment elevation in leads V7to 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).
2.5 Comparison of ST Segment Elevation in Leads V7to V9and ST Segment Depression in Leads V1to V3
Significant ST segment depression in leads V1to V3was 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 V1to V3had no ST segment elevation in leads V7to V9(Fig. 1).
When ST segment elevation in leads V7to V9and ST segment depression in leads V1to V3at hospital admission were compared with respect to diagnostic accuracy of posterior involvement (at least severe hypokinesia), ST segment elevation in leads V7to V9had 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).
2.6 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 V7to V9(Group A), IRA patency resulted in a higher LVEF both at hospital discharge (56 ± 13 vs. 44 ± 12, 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. 61 ± 9 [p = 0.4]) and at the 2-month follow-up visit (60 ± 9.5 vs. 59 ± 13 [p = 0.7]).
Classically, ECG diagnosis of posterior wall infarction is based on the appearance of prominent R waves in leads V1and 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 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 . Rich et al. 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 V9was more accurate than the classic standard ECG criteria for diagnosing posterior infarction. In accordance with our results, Zalenski et al. found ST segment elevation in leads V7to V9in 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 V7to V9was 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 V7to V9and 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 V7to V9identified 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 V7to V9suggests 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 V7to V9concur 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 , thus possibly also explaining the somewhat higher incidence of high degree atrioventricular block in Group B than in Group A patients.
3.1 Beneficial Effect of Thrombolytic Therapy in Inferior Wall Infarction With and Without ST Segment Elevation in Leads V7to 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. 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. 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. 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 V1to 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 V7to V9at 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 V7to V9on 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 .
3.2 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.
We recommend routine recording of leads V7to V9in 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.
- creatine kinase
- electrocardiogram, electrocardiographic
- infarct-related artery
- left ventricular ejection fraction
- myocardial infarction
- recombinant tissue-type plasminogen activator
- Thrombolysis in Myocardial Infarction
- Received July 11, 1997.
- Revision received October 3, 1997.
- Accepted November 26, 1997.
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