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Man With Persistent Chest Pain and ST-Segment Depression


A 54-year-old man with a history of type 2 diabetes, hypertension, and coronaryartery disease with angina presents to the physician’s office withchest pain. The pain began 3 hours earlier and is associated with diaphoresisand dyspnea. Examination results are unremarkable, except for diaphoresis.A 12-lead ECG reveals normal sinus rhythm with large R waves and horizontalST-segment depression in leads V1 through V3. The patient is given nitroglycerin,aspirin, heparin, morphine, and a &#946-blocker for noninfarction acutecardiac ischemia and transferred to the local emergency department (ED).

A 54-year-old man with a history of type 2 diabetes, hypertension, and coronaryartery disease with angina presents to the physician's office withchest pain. The pain began 3 hours earlier and is associated with diaphoresisand dyspnea. Examination results are unremarkable, except for diaphoresis.A 12-lead ECG reveals normal sinus rhythm with large R waves and horizontalST-segment depression in leads V1 through V3. The patient is given nitroglycerin,aspirin, heparin, morphine, and a β-blocker for noninfarction acutecardiac ischemia and transferred to the local emergency department (ED).On arrival at the ED, he continues to have chest pain. The examinationresults and ECG findings are unchanged. Anti-ischemic therapy is continued;laboratory studies, a chest film, and another ECG are ordered.Which of the following is best supported by the initial ECG findings?A. Acute anterior wall ischemia (noninfarction).B. Right bundle branch block (RBBB).C. Acute posterior wall myocardial infarction (MI).D. Wolff-Parkinson-White (WPW) syndrome.DISCUSSION
The ST-segment depression inthe right precordial leads of this patient'sECG suggests either anteriorwall ischemia (A) or posterior wallMI (PMI) (C). However, the patient'sclinical presentation--which includesdiaphoresis--is more commonly associatedwith infarction than with ischemia.In addition, the presence ofprominent R waves in V1 and V2 makesanterior wall ischemia less likely.The prominent R waves in leadsV1 and V2 are a notable feature ofthis ECG. The differential diagnosisof a prominent R wave in V1 and V2includes RBBB (B) and WPW syndrome(D), as well as PMI.Although a prominent R wave inV1 can suggest RBBB, a widenedQRS complex (greater than 0.12 seconds)is required to make the diagnosis.The QRS complex here is narrow,which rules out RBBB.The classic ECG triad of shortenedPR interval, delta wave, andwidened QRS complex is the hallmarkof WPW syndrome. These findingsare not evident in this tracing.Thus, review of the ECG (Figure1) suggests an acute PMI. PMIrefers to infarction of the posteriorwall of the left ventricle. PMIs represent15% to 20% of acute MIs.1-4 Inmost instances, the coronary obstructionis located in either the circumflexor the right coronary artery(posterior descending branch). Ascan be predicted from the coronaryanatomy, PMI most often occurs inthe setting of acute inferior or lateralMI. Isolated PMI is encountered inclinical practice; however, it is reportedto be "uncommon."1-6Diagnosis of acute PMI is challengingbecause the standard 12-leadECG does not directly image the posteriorwall of the left ventricle.7,8Moreover, the ECG criteria that suggest acute PMI are not widely known.However, rapid recognition ofacute PMI is of clinical importancefor several reasons. First, an acutePMI is an infarction of a major portionof the left ventricle. Patients withacute inferior or lateral wall MI whoalso have posterior involvement areexperiencing an even larger infarct,since at least 2 walls of the left ventricleare involved. As infarct size increases,the risk of arrhythmia, leftventricular dysfunction, and deathincreases proportionally.9-11Second, the use of urgent revascularizationmay benefit patients withacute inferoposterior MI more so thanpatients with an infarct in a single segmentof the left ventricle. Finally, if isolatedacute PMI is not clinically recognizedas a transmural infarction, itlikely will not receive appropriate therapy,which should include a fibrinolyticagent or urgent angioplasty.12-Lead ECG clues to acutePMI. The "typical" ECG findings thatindicate an ST-segment elevationacute MI on a standard 12-lead ECGare reversed in a patient with acutePMI (Figure 2). This results from thefact that the endocardial surface of theposterior wall faces the anterior precordialleads. In other words, ST-segmentelevation, Q waves, and T-waveinversions when "reversed" becomeST-segment depression, prominent R waves, and upright T waves in leadsV1 through V3, respectively, and suggestacute PMI.Numerous ECG findings onstandard 12-lead tracings suggestacute PMI, including abnormalitiesof the ST segment, T wave, andQRS complex (R and S waves)(Figure 3).6,7,12-14 ST-segment depressiongreater than 1 mm in leadsV1 through V3 suggests acute PMI.The presence of ST-segment depressionin the precordial leads,however, does not always indicateacute PMI. Mukharji and colleagues13investigated the cause ofright precordial ST-segment depressionin patients with ST-segment elevationinferior wall acute MI. Ofall patients with inferior wall acuteMI, 80% demonstrated anterior STsegmentdepression (in leads V1, V2,or V3). When the investigators usedstandard ECG criteria to diagnosePMI, they noted that only one thirdof the patients who had anterior STsegmentdepression in the precordialleads experienced PMI. However,when they used scintigraphicmethods, the percentage of patientsin whom PMI was diagnosed increasedmarkedly--to approximatelytwo thirds. Boden and colleagues6found that approximately 50% ofpatients who presented with chestpain and right precordial ST-segmentdepression had sustained aPMI.It is also important to considerthe morphology of the ST-segmentdepression. Boden and colleagues6noted that horizontal ST-segment depressionin the right precordial leadswas seen in 100% of patients who experiencedPMI, unlike in patientswith non-ST-segment elevation acuteMI presenting with precordial ST-segmentdepression, in whom it wasdescribed as down-sloping. Othersources support the predictive valueof horizontal ST-segment depressionin leads V1 through V3; however,there is also evidence that both downandup-sloping ST-segment depressionin the right precordial leads maybe associated with acute PMI.8,12,13While ST-segment depression isperhaps the most significant findingin acute PMI, other ECG abnormalitieswarrant review. The T wave, theassociation of the T wave and the STsegment, the R wave, and coexistinginfarctions are other ECG featuresthat can point to PMI.A tall, upright T wave in lead V1or V2 points to PMI.14 A combinationof horizontal ST-segment depressionand tall, upright T waves in the rightprecordial leads strongly suggestsacute PMI.6Various abnormalities of the Rwave in leads V1or V2 are also reportedto be associated with PMI. A tall,wide R wave in lead V1or V2 and anR:S wave ratio greater than 1.0 in leadV2 are both suggestive findings.5,12Certain authorities suggest that aprominent R wave in the right precordialleads--when associated withPMI--may not represent simple "reverse"change; rather, such QRS complexmorphology may reflect an intraventricularconduction disturbancethat has resulted from the ischemicmyocardial insult.Finally, coexistent acute infarctionof either the inferior or lateralwall is another ECG feature thatshould raise clinical suspicion ofPMI, particularly if ST-segment depressionand/or prominent R wavesare observed in the right precordialleads. Acute inferior wall MI withST-segment depression in anteriorleads V1, V2, and V3 representscoexisting PMI in approximately onehalf of patients who present withthese findings.Use of posterior ECG leads todiagnose acute PMI. In certain settings,additional ECG leads may beused to detect involvement of the posteriorwall in a patient with a coexistinginferior or lateral wall acute in farct, or to confirm isolated PMI in apatient with chest pain and ST-segmentdepression in the right precordialleads. These additional leads--V8and V9--directly visualize the posteriorwall of the left ventricle (see Figure2). They are placed as shown inFigure 4.ST-segment elevation of morethan 1 mm in the posterior leads confirmsthe presence of acute PMI andis thought to be superior to the findingsin leads V1 through V3, describedabove, as a criterion for the diagnosis.1,4,7 When ECGs that include theposterior leads are used, the reportedrate of isolated PMI among all patientswith acute MI ranges from"very low" to approximately 7%.3,4Brady and colleagues2 demonstratedthat the use of additional leads in alladult ED patients with chest pain didnot produce significant therapeutic ordiagnostic benefit. Unsuspected PMIwas not noted in the patients studied;moreover, therapeutic and dispositiondecisions were not altered. However,the population included in the Bradystudy was generally low risk.Zalenski and colleagues1 studieda higher-risk group of patients andfound that use of additional leads didaffect the rate at which acute PMIwas diagnosed and led to alterationsin management. A National Heart AttackAlert Program Working Grouphas suggested that the use of posteriorthorax leads may be helpful in certaincircumstances.15Non-evidence-based criteria foruse of additional leads include:

  • ST-segment depression in leads V1, V2, and V3.
  • ST-segment elevation acute MI ofinferior wall.
  • ST-segment elevation acute MI oflateral wall.

Outcome of this case.

Becauseof the patient's recurrent chest painand suspicious 12-lead ECG, posteriorECG leads were placed (

Figure 5

).These revealed ST-segment elevationin leads V


and V


, consistent withacute PMI (

Figure 6

). An intravenousfibrinolytic agent was administered.This resolved the patient'schest discomfort and reduced the abnormalityin the ST segment. Bedsideechocardiography demonstrated posteriorwall hypokinesis. Serum troponinvalues were elevated, consistentwith acute MI. Urgent cardiaccatheterization revealed markedstenosis of the mid and distal rightcoronary arteries with an acutethrombus in the distal right coronaryartery. Placement of an intracoronarystent successfully opened this occlusion.The patient had no further chestdiscomfort.




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R, V


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Brady WJ, Chang N, Hwang V, et al. The 15-leadECG in emergency department chest pain patients:comparison to the 12-lead ECG.

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Eur Heart J

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Stark ME, Vacek JL. The initial electrocardiogramduring admission for myocardial infarction:use as a predictor of clinical course and facility utilization.

Arch Intern Med

. 1987;147:843-846.


Aufderheide TP, Brady WJ. Electrocardiographyin the patient with myocardial ischemia or infarction.In: Gibler WB, Aufderheide TP, eds.

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Mukharji J, Murray S, Lewis SE, et al. Is anteriorST depression with acute transmural inferior infarctiondue to posterior infarction? A vectorcardiographicand scintigraphic study.

J Am Col Cardiol



Eisenstein I, Sammarco ME, Madrid WL,Selvester RH. Electrocardiographic and vectorcardiographicdiagnosis of posterior wall myocardial infarction.Significance of the T wave.




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. 1997;29:28-33.

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