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Corresponding AuthorProfessor Mohammad BadiuzzamanProfessor, Department of Cardiology National Heart Foundation Hospital & Research Institute

IntroductionPosterior wall myocardial infarction (MI) refers to infarctionof the dorsal area of the left ventricle and, in most cases, patho-physiologically involves either the left circum-flex artery (or one of its larger branches) in apatient with a left dominant system or the posterior left ventricular branch of the right coronaryartery in a patient with a right dominant system1. As predicted from the coronary anatomy, posterior-wall MI most often occurs along with acute inferior or lateral MI. Acute posterior wall MI has been reported to represent 15% to 21% of acute MIs, the vast majority occur-ring wit hacute infarction of the inferior or lateral wall of the left ventricle2-4. Isolated acute posterior wall MI, however, doesoccur; the rate of isolated occurrence of posterior wall MI isbelieved to be very low2. The additional-lead ECG using left posterior thorax leads has increasedthe reported rate of isolated posterior wall MI occurrence from "very low" to a 3% to 7% range among all patients with acute MI (AMI)3,4.

True posterior myocardial infarction (PMI), the ‘dead angle infarction’ of the electrocardiogram (ECG), is often misjudged and this may be the reasonfor under-treatment5. It is suggested to be one of the most commonly missed types

of acute myocardial infarction electrocardiographic patterns6. Theclinical presentation of PMI is not different from other myocardial infarctions, but the absence of ‘traditional’ electrocardiographic infarct signs such as ST- segment elevation can lead to errors or delay in the diagno-sis. Correct interpretation and use of the ECG using the additional leads V7 to V9 can establish the electrocardio-graphic diagnosis of PMI5. This case highlights the use of posterior ECG leads (15-lead ECG) in enhancing the diagnostic yield of a conventional ECG in patients present-ing with symptoms suspicious for an acute coronary syndrome by disclosing a posterior myocardial infarction and guiding reperfusion therapy.

Case reportA 62 year-old man presented to Emergency Department of National Heart Foundation Hospital & RI with acute chest pain with radiation to the back, dyspnoea, sweating and nausea for 20 hours. On physical examination his blood pressure was 130/70 mmHg and pulse 84 beats/min. On auscultation normal heart soundsand a midsystolic murmur grade II/VI were heard. Complete physical examination revealed no further abnormalities.

The ECG showed sinus rhythm with a tall R wavein lead V1-3, ST-segment depression with upright T waves in leads V1 to V5(Figure 1A).With the working diagnosis of an acute coronary syndrome the patient was informed about the

Case ReportAcute Posterior Myocardial Infarction- rare but easily

misdiagnosed: Case ReportBadiuzzaman M, Kalimuddin M, Malik F, Ahmed N, Ahmed MN, Dutta AK, Banik D, Kabiruzzaman M,

Rahman MH, Huq TS, Jamal MF, Khandaker M

Department of Cardiology, National Heart Foundation Hospital & Research Institute, Mirpur, Dhaka.

Abstract:Posterior wall myocardial infarction (PMI) refers to infarction of the dorsal area of the left ventricle. Diagnosing acute PMI from the 12-lead electrocardiogram (ECG) is often difficult, but in the reperfusion (Thrombolytic or Primary Percutaneous Coronary Intervention-PPCI) era it is important. This is particularly true in the acute stage when prompt and accurate diagnosis of acute myocardial infarction (AMI) is critical in determining the initiation of reperfusion therapy. The additional- lead electrocardiogram using left posterior thorax leads is potentially helpful; ST segment elevation greater than 1 mm in this distribution suggests an acute PMI. We report a case of a 62-year-old man whose first manifestation of coronary artery disease was anacute isolated posterior myocardial infarction (IPMI), which will highlight the electrocardiographic fine-tuned diagnosis of posterior myocardial infarction by using the posterior leadsV7 to V9 leading to easier and faster recognition with consequences for treatment and improved prognosis.

Key words: Posterior myocardial infarction Posterior ECG leads, diagnosis. (JNHFB 2017; 6 : 16-20)

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Badiuzzaman M et al.Acute Posterior Myocardial Infarction

Figure 1A

necessity of urgent coronary angiography but he initially refused. His ECG was reviewed by Registrar after admis-sion in CCU & subsequently, additional leads were obtained in posterior positions (V7, V8, V9), which demonstrated pathological Q (Figure 1B) suggesting cute myocardial infarction of the posterior wall. Laboratory results confirmed the diagnosis of AMI as elevated cardiac markers (troponin-I: 38.91ngm/ml& CK-MB: 185 U/L).

His Random Blood sugar was 7.05 mmol/L; Serum cretinine 1.4 mg/dl; Total Cholesterol 164 mg%; LDL 96 mg%; HDL 34 mg% and Triglyceride 165 mg%. Echocardi-ography showed akinesia of posterior wall with ejection fraction of 40% and moderate mitral regurgitation.

He finally consented and was taken to the cardiac catheter-ization laboratory with minor symptoms, almost 24 hours after his admission. Coronary angiography disclosed a complete occlusion of the left circumflex coronary artery (LCX) after its origin (Figure 2A). The left main coronary artery was patent, the left anterior descending (LAD) free of significant disease (Figure 2B) and the right coronary (RCA) arteries were free of disease (Figure 2C).

Figure 2: Total occlusion of LCX from its origin (A). LAD free of significant disease(B). Non dominant RCA free of disease (C).

Figure 1B

2A

2B

2C

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Badiuzzaman M et al.JNHFB Jan 2017

While waiting for angioplasty, patient suddenly developed acute left ventricular failure and patient shifted to CCU. One day later angioplasty was done. The culprit lesion was successfully crossed with an angioplasty wire and pre dilated. Thereafter lesion was stented with DES ( 3.5 x 23 mm). Post dilatation was done and the artery was fully recanalized with TIMI 3 distal flow (Figure 3).

Figure 3: Guide-wire passed through LCX with faint antegrade flow (A). Stent deployment (B). Final result-no residual stenosis with TIMI-3 distal flow(C).

Patient was discharged three days after PCI with good control of left ventricular failure.

DiscussionThe term PMI is used for necrosis of the dorsal, infra a trial part of the left ventricle located beneath the atrio ventricular sulcus5. The majority of patients withthe typical electrocar-diographic abnormalities for PMI have a stenosis or occlu-sion of the LCX6-8. Some patients have a stenosis or occlu-sion of the RCA. In 10%of the population the RCX is the dominant vessel. Itis the least commonly infarcted coronary artery8.Numerous electrocardiographic abnormalities using the standard 12-lead ECG suggestive of acute posterior wall MIhave been reported (Table 1).

Table 1. ECG Criteria of AMI of the Posterior Wall of the Left Ventricle Using Standard 12-Lead ECG and Additional- Lead ECG1.

*Limited to leads V1, V

2, and/or V

3

Detection of acute posterior wall MI is difficult in that the standard 12-lead ECG does not adequately image the poste-rior wall of the left ventricle9. Further, ECG criteria sugges-tive of acute posterior wall MI are not widely known among practitioners. For these reasons, it istheorized that posterior wall MI is one of the most commonly missed acute infarction electrocardiographic patterns6.

Thrombolysis is not recommended for patients with chest pain and ST-segment depression. Many such patients have unstable angina, sub endocardial acute myocardial infarction, and other causes of ST-segment depression that have not been shown tobenefit from thrombolysis10. In some patients, however, precordial ST-segment depression is a reciprocal change indicating true posterior wall acute myocardial infarction and leads V

7 to V

9 will show

ST-segment elevation10. In the setting of stable symptoms, the cause of tall R waves in leads V

1 or V

2 should be

determined (Table 2). Often this pattern is a normal variant, andthe prognosis in such persons differs markedly fromthat in other patients with tall R waves in the right precordial leads. Recording leads V

7 to V

9 will help inthis differential

diagnosis10.

3A

3B

3C

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Table 2 Causes and Diagnosis of Tall R Waves in V110.Diagnosis Confirmatory Clues

LVH= left ventricular hypertrophy; RAD=right-axis deviation; RAE= rightatrial enlargement.

Figure 1 depicts the correct placement of the posterior thoracic leads. Lead V8 is placed on the patient’s left back at the tip of the scapula. Lead V9 is placed half way between lead V8 and the left paraspinal muscles. Lead V7 is used by some clinicians and is placed at the level of lead V6 at the posterior axillary line.

Figure 1 : Posterior lead placement. Lead V7 lies in the posterioraxillary line, V8, is in the midscapular line, and V9, is 3 cm to the leftof the spinous processes9.

Figure 2. From the perspective of the standard 12-lead

ECG, the “typical” electrocardiographic findings indicative of acute transmural myocardial infarction will be reversed. This reversal results because the endocardial surface of the posterior wall faces the anterior precordial leads (V

1 through

V3) in the standard 12-lead ECG. In other words, ST depres-

sion (STD), prominent R waves, and upright T waves in leads V

1 through V

3 “when reversed” may represent STE, Q

waves, and T wave inversions, respectively, of acute PMI. If one considers the “reversed nature” of these electrocardio-graphic abnormalities when applied to the posterior wall, the findings assume a more recognizable, ominous meaning. In the setting of acute PMI, the 12-lead ECG in the right precordial chest leads (V

1 and V

2) will display STD with a

large R wave in the setting of acute PMI; if viewed from the posterior perspective of the thorax, these same findings are “reversed” and indicate acute transmural infarction of the posterior wall of the left ventricle11.

Rapid recognition of acute PMI is of clinical importance for several reasons. Firstly, patients with acute inferior or lateral wall myocardial infarction who also have posterior involve-ment are experiencing a larger sized infarct. With increasing infarct size, the risk of dysrhythmia, left ventricular dysfunction, and death is proportionally increased11. Secondly, the use of acute therapies including treatments aimed at urgent revascularization may benefit patients with acute infero-PMI more so than patients withan isolated infarct of a single wall. Lastly, isolated, acute PMI, if not clinically recognized as a transmural infarction, likely will not receive appropriate therapy, including thrombolytic agent or urgent angioplasty11.

The clinical consequences of PMIs are often serious and disproportionate to their relatively low myocardial mass loss.This may be a result of the potential for PMI to cause mitral regurgitation (MR). Matetzky and colleagues illustrated that MR was present in 69% of patients with isolated PMI, and was moderate or severe in one third of these12. Successful thrombolysis reduces the prevalence of mitral regurgitation in conjunction with ar eduction in the prevalence of posterior wall motion abnormalities13.

Reperfusion therapy has potential complications. The use of posterior leads could avoid the inappropriate use of reperfu-sion therapy where PMI is merely suspected on the basis of ST-depression in leads V

1-V

2, and where the diagnosis is in

fact anterior-wall ischaemia14.

In a recent internet-based survey, more than 20% of ED physicians did not request posterior chest leads inpatients with isolated posterior MI and the corresponding percentage for posterior plus inferior MI increased to 40%15.

Conclusion

PMI is responsible for subtle changes on the ECG. For the diagnosis of PMI it is important to recognize the clinical signs at presentation, combined with subtle manifestations on the ECG in order to start reperfusion therapy early.

Badiuzzaman M et al.Acute Posterior Myocardial Infarction

True posterior infarct

Right ventricular hypertrophy

Ventricular septal hypertrophy

Right bundl branch block

Wolff-Parkinson-White syndrome

Normal variant

ST ↓, T in V1 - V

2 Q waves and ST ↑ V

7 - V

9RAD, RAE; Secondary ST-Ts;V

7 - V

9 Normal

Associated Q waves; LVH;V

7-V

9 Normal or deep

narrow Q wavesWide QRS; broad S in V

1,

V6; R peaks late in V

1;

V7 - V

9 normal or broad S

wavesShort PR; delta wave;V

7 - V

9 Normal or delta

waveNo other abnormalities

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Cardiologists should be able to interpretelectro cardiographic signs such as ST-segment depression with upright T waves and prominent tall R waves in leads V

1 to V

3.

Posterior leads (V7-V

9,) should be assessed in all patients

presenting with chest pain and ST-depression in leads V1-V

2

on arrival to the emergency department.

They would be helpful to differentiate NSTEMI from isolated posterior AMI in suspicious cases. Increased use of posteri-or leads and recognition of changes indicating PMI will reveal more patients with PMI who will benefit from prompt reperfusion. ST in leads V7 through V9 identify infarctions that are potentially harmful, out of proportion totheir size owing to their special location in the left ventricle and there-by their potential to cause MR.

References:

1. Brady WJ. Acute posterior wall myocardial infarction: electrocar-diographicmanifestations. Am J Emerg Med 1998;16:409–413.

2. Zalenski R J, Cooke D, Rydman R, et al: Assessing the diagnos-ticvalue of an ECG containing leads V4R, V8, and V9: The 15-leadECG. Ann Emerg Med 1993;22:786-793.

3. Pollack M, Thomason G, Williams M, et al: Emergency department-diagnosis of acute posterior-wall myocardial infarction using leftposterior chest leads. AcadEmerg Med 1997;34:399 (abstr).

4. Melendez L J, Jones DT, Salcedo JR: Usefulness of three additional electrocardiographic chest leads (V7, V8, and V9) in thediagnosis of acute myocardial infarction. Can Med Assoc J 1978;119:745-748.

5. van Gorselen EOF, Verheugt FWA, Meursing BTJ, Oude Ophuis AJM. Posterior myocardial infarction: the dark side ofthe moon. Neth Heart J 2007; 15:16-21.

6. Perloff J. The recognition of strictly posterior myocardial infarction by conventional scalar electrocardiography. Circulation 1964;30:706-718.

7. Agarwal J, Khaw K, Aurignac F, Lo Curto A. Importance of posteri-or chestleads in patients withsuspected myocardial infarction, but nondiagnostic, routine 12-lead electrocardiogram. Am J Cardio l1999;83:323-326.

8. Bough E, Korr K. Prevalence and severity of circumflex coronaryar-tery disease in electrocardiographic posterior myocardial infarction. J Am Coll Cardiol1986;7:990-996.

9. Rich MW, Imburgia M, King TR, et al: Electrocardiographicdiagno-sis of remote posterior wall myocardial infarction using unipolarpos-terior lead V9. Chest 1989;96:489-493

10. Casas R, Marriott H, Glancy L. Value of leads V7-V9 in diagnosing-posterior wall acute myocardial infarction and other causes of tallR waves in V1-V2. Am J Cardiol 1997;80:508-509.

11. Brady JW, Erling B, Pollack M, Chan TC. Electrocardiographic manifestations:acute Posteriorwall myocardial infarction. J Emerg Med 2001;20:391-401.

12. Matetzky S, Freimark D, Feinberg MS, Novikov I, Rath S, Rabinowitz, Kaplinsky E, Hod H. Acute myocardial infarction withisolated ST-segment elevation in posterior chest leads V7-9. J Am CollCardiol1999;34:748-753.

13. Tenenbaum A, Leor J, Motro M, et al. Improved postero-basal segmental functionfollowing thrombolysis is associated with decreased incidence of significant mitralregurgitation in first inferior myocardial infarction. J Am CollCardi-ol1995;25:1558-1563.

14. Khan JN, Chauhan A, Mozdiak E, Khan JM, Varma C. Posterior myocardial infarction: are we failing todiagnose this?Emerg Med J 2012;29:15-18.

15. Somers MP, Pines JM, Brady WJ, Caovan D. Internet-based survey onthe use of additional lead electrocardiograms and fibrinolysis of posteriorand right ventricular acute myocardial infarctions. Am J EmergMed 2007;25:258 –261.

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