Special Feature

ECG Manifestations of Acute Posterior Wall Myocardial Infarction

By William Brady, MD

Posterior myocardial infarction (pmi) refers to infarction of the posterior wall of the left ventricle, and PMI results from acute disruption of perfusion in the left circumflex or right coronary artery with its posterior descending branches. PMI most often occurs in the setting of either acute inferior or lateral myocardial infarction—as predicted from the coronary anatomy. Acute PMI has been reported to occur in 15-21% of MIs—the vast majority occurring with acute infarction of the inferior or lateral wall of the left ventricle.1-4 Isolated acute PMI does occur, however, with a reported rate of occurrence described as "very low."1,2,5,6

The electrocardiogram (ECG), with the addition of left posterior thorax leads, has increased the rate of detection of isolated PMI from "very low" to a 3-7% range among all patients with acute MI.3,4

Detection of acute PMI is difficult in that the standard 12-lead ECG does not adequately image the posterior wall of the left ventricle.7 Further, ECG criteria suggestive of acute PMI are not widely known among practitioners. For these reasons, it is theorized that the PMI is one of the most commonly missed acute infarction ECG patterns.8 Rapid ECG recognition of acute PMI is of clinical importance for several reasons. First, patients with acute inferior or lateral MI who also have posterior wall involvement are experiencing a larger infarct, with the associated, proportionally increased risks of arrhythmia, left ventricular dysfunction, and death. Second, the use of acute therapies, including treatments aimed at urgent revascularization, may benefit patients with acute inferoposterior MI more so than patients with an isolated infarct of a single wall of the left ventricle. Finally, isolated acute PMI, if not clinically recognized as a transmural infarction, likely will not receive appropriate therapy including a thrombolytic agent or urgent angioplasty.

From the perspective of the standard 12-lead ECG, the "typical" electrocardiographic findings indicative of acute transmural MI will be reversed. This reversal results from the fact that the endocardial surface of the posterior wall faces the anterior precordial leads (V1 through V3) in the standard 12-lead ECG.9 In other words, ST segment depression (STD), prominent R waves, and upright T waves in leads V1 through V3— "when reversed"—may represent the ST segment elevation (STE), Q waves, and T-wave inversions, respectively, of acute PMI. As seen in Figure 1 below, in the setting of isolated acute PMI, the 12-lead ECG (lead V1) in the right precordial chest leads will display STD with a large R wave in the setting of acute PMI; if viewed from the posterior perspective of the thorax (lead V8), these same findings are "reversed" and indicate acute transmural infarction of the posterior wall of the left ventricle with STE.

Using the standard 12-lead ECG, numerous ECG abnormalities suggestive of acute PMI have been reported, including various features of the QRS complex, ST segment, and T-wave.6-7,10-12 STD greater than 1 mm in leads V1 through V3 may indicate acute PMI. (See Figure 2, A-D.) The presence of STD in the precordial leads, however, does not always indicate acute PMI, but it may reflect reciprocal change. Mukharji et al explored this issue in the setting of acute inferior wall MI.11 Of all patients with acute inferior MI, 80% demonstrated anterior STD in the right precordial leads. By employing standard ECG criteria for the diagnosis of PMI, they noted that only one-third of these cases actually experienced acute PMI. Using scintigraphic methods, the investigators note that posterior infarction had occurred more frequently than was expected from analysis of the standard 12-lead ECG. They demonstrate that approximately two-thirds of these patients actually had suffered a PMI.

Boden et al also note that approximately 50% of patients presenting with acute MI who demonstrated precordial STD on the 12-lead ECG were found to have had a PMI. In addition to presence of STD in the right precordial leads, the actual morphology of the STD is an important feature to consider.

Boden et al note that horizontal STD in the right precordial leads was encountered in 100% of patients experiencing PMI, as compared to patients with non-Q wave myocardial infarction (NQWMI) who presented with precordial STD described as down-sloping. (See Figure 2, A-C.) This observation on ST segment morphology may help the clinician to distinguish reciprocal change from acute PMI. Horizontal STD in leads V1 through V3, occurring in a patient with the potential for acute ischemic heart disease, should lead one to consider the diagnosis of acute PMI and employ additional investigations such as posterior thorax ECG leads.

The T wave, the R wave, and co-existing infarctions of adjacent walls of the heart provide further ECG clues when searching for acute PMI. A tall, upright T wave in leads V1 or V2 is suggestive of acute PMI. (See Figure 2, A-D.)12 A combination of horizontal STD with tall upright T waves in the right precordial leads is highly suggestive of acute PMI. (See Figure 2, A-B)6 A tall, wide R wave in leads V1 or V2 (See Figure 2, A-D) as well as an R/S wave ratio greater than 1.0 in lead V2 (See Figure 2, B) are suggestive findings.5,10

Lastly, coexistent acute infarction of either the inferior or lateral walls is another ECG feature that should raise the clinical suspicion for acute PMI, particularly if STD and/or prominent R waves are observed in the right precordial leads. Acute inferior MI, with associated STD in the leads V1, V2, and V3, represents coexisting acute PMI in approximately one-half of cases encountered.6,11

The physician may employ additional-lead ECGs in select cases, looking for involvement of the posterior wall in patients with co-existing inferior or lateral acute infarct and, therefore, identify a larger-sized infarct with the potential for increased risk of poor outcome. Alternatively, in a chest pain patient with a high clinical suspicion for acute MI with only STD noted in the right precordial leads, the additional-lead ECG may reveal PMI and, therefore, identify a patient with an acute MI, which creates the potential for alteration in the therapeutic decisions.

The use of additional-lead ECGs among all adult chest pain patients in the ED has not yielded therapeutic or diagnostic benefit.2 Unsuspected PMI was not noted in this population. Further, therapeutic and disposition decisions were not altered. When considering a higher-risk population, additional-lead ECGs did influence the rate of diagnosis of PMI.1

Greater than 1 mm ST segment elevation in the posterior leads V8 and V9 confirms the presence of PMI and is felt to be superior to the findings noted in leads V1 through V3. (See Figure 2, E.) Leads V8 and V9 are placed on the patient’s left posterior thorax at the tip of the scapula and one-half the distance between the scapular tip and the paraspinal muscles, respectively. The degree of STE is less pronounced due to the relatively larger distance between the myocardium and surface electrodes on the patient’s back.1,4,7

References

1. Zalenski RJ, et al. Assessing the diagnostic value of an ECG containing leads V4R, V8, and V9; The 15-leadECG. Ann Emerg Med 1993;22:786-793.

2. Brady WJ, et al. The 15-lead ECG in emergency department chest pain patients: Comparison to the 12-lead ECG. Ann Emerg Med Abstract. Publication pending.

3. Pollack M, et al. Emergency department diagnosis of acute posterior-wall myocardial infarction using left posterior chest leads. Acad Emerg Med 1997;34:399.

4. Melendez LJ, et al. Usefulness of three additional electrocardiographic chest leads (V7, V8, and V9) in the diagnosis of acute myocardial infarction. Can Med Assoc J 1978;119:745-748.

5. Goldberger AL. Myocardial infarction: Electrocardiographic Differential Diagnosis, 4th ed. St Louis: Mosby-Year Book; 1992.

6. Boden WE, et al. Electrocardiographic evolution of posterior acute myocardial infarction: Importance of early precordial ST-segment depression. Am J Cardiol 1978;59:782.

7. Rich MW, et al. Electrocardiographic diagnosis of remote posterior wall myocardial infarction using unipolar posterior lead V9. Chest 1989;96:489-493.

8. Perloff JK. The recognition of strictly posterior myocardial infarction by conventional scale electrocardiography. Circulation 1964;30:706-718.

9. Conover MB. Understanding Electrocardiography: Arrhythmias and the 12-lead ECG, 6th ed. St Louis: Mosby-Year Book; 1992.

10. Aufderheide TP, Brady WJ. Electrocardiography in the patient with myocardial ischemia or infarction. In: Gibler WB, Aufderheide TP, eds. Emergency Cardiac Care. St Louis: Mosby-Year Book; 1994.

11. Mukharji J, 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.

12. Eisenstein I, et al. Electrocardiographic and vectorcardiographic diagnosis of posterior wall mycardial infarction: Significance of the T wave. Chest 1985;88:409-416.