True posterior myocardial infarction (MI) is rare compared with anterior and inferior infarction and is usually associated with infarction of other areas too. When it does occur, the diagnosis may easily be missed.^1,2

Pathogenesis

They usually result from occlusion of the left circumflex coronary artery but the anatomy can vary a little. Occlusion of the right coronary artery may be the cause.

Epidemiology

It is difficult to be sure of the percentage of MIs that are true posterior because:

• There may be more than just the posterior wall involved.
• The criteria for diagnosis are less well recognised.
• It seems likely that many are missed.

A study from Tehran involved routinely performing more extensive ECGs, including V7, 8, 9 and right precordial leads. 9% of cases had ST elevation in the posterior leads, 3.3% as an isolated finding. ST elevation in posterior leads was detected in 10.9% of those who did not have ST elevation on the standard 12 leads.³ It may be debated how relevant these findings on Iranian patients are to the UK but they are reflected by some other papers from Europe and North America.

Risk factors

• As for any cardiovascular disease.
• Patients tend to be older and have more risk factors.³
• Smoking has been suggested to be an even greater risk.⁴
• Variations to the coronary anatomy may also be a risk but this is difficult to assess.

Presentation

The same as acute coronary syndrome (ACS).⁵

There is very scanty information in the literature about typical patient symptoms with posterior MI.

Differential diagnosis

The same as ACS.

Other causes of similar ECG changes:

• Right ventricular hypertrophy can cause large R waves in the early V leads.
• Infarction of the right ventricle is rare but will produce a similar ECG.

Investigations

The ECG does not have a lead that faces directly to the posterior wall of the heart. However, abnormalities of depolarisation will cause reciprocal or mirror changes in the anterior leads. The important leads are V1, 2, 3 - of which V2 is the most important. The 3 classical changes to be sought are:

• A tall and slightly wide R wave.
• There should be elevation of the ST segment, but in practice it is usually very slight, if at all.
• There must be a high T wave in V2. This is essential and, without it, the diagnosis is unsafe.

The diagnosis of MI on the ECG can be even more difficult in the presence of left bundle branch block.

Some authors claim that because the standard 12 lead ECG will fail to detect a posterior myocardial infarct in many cases, a 15 lead trace should be routinely used with V7 to V9 going further round the chest wall.^6,7 In one case these findings were validated by angioplasty.⁸

The blood changes of treponins and CK are as for other MI.

Associated diseases

The inferior wall or the posterior septum may also be involved.

Management

General management

This is as for ACS.⁵

Oxygen should be given and rapid transfer to a place where thrombolysis can be given and CPR is readily available.

Pharmacological

Again management is as for any type of MI.

Studies on the outcome of true posterior MI without reciprocal changes in anterior leads and not conforming to the standard indications for thrombolysis have not been done. There is no definitive evidence for thrombolysis in these cases.

Surgical

Coronary angiography with a view to percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass grafting (CABG) can be performed as in other MI.

Complications

• The risk of ventricular aneurysm, rupture and death may be greater than with myocardial infarctions at other sites.^9,10
• Rupture of chordae tendinae can lead to valve incompetence.
• Rupture of the septum appears to be a special risk with a high mortality despite surgical repair.¹¹

Prognosis

The suggestion that these patients tend to be older and have more risk factors, might account for the higher rate of complications and death in those with a posterior MI.³ Delay in diagnosis may also contribute.¹²A study from Belfast suggested that the few patients with posterior MI may tend to have larger infarcts with higher enzyme levels.¹³

Prevention

As for any ischaemic heart disease.

Document references

1. Ravakhah K; Death certificates are not reliable: revivification of the autopsy.; South Med J. 2006 Jul;99(7):728-33. [abstract]
2. Khan JN, Chauhan A, Mozdiak E, et al; Posterior myocardial infarction: are we failing to diagnose this? Emerg Med J. 2010 Oct 20. [abstract]
3. Oraii S, Maleki M, Tavakolian AA, et al; Prevalence and outcome of ST-segment elevation in posterior electrocardiographic leads during acute myocardial infarction.; J Electrocardiol. 1999 Jul;32(3):275-8. [abstract]
4. Landmark K, Abdelnoor M; Current smokers develop more posterior myocardial infarctions probably due to increased tendency to thrombosis.; Scand Cardiovasc J. 2000;34(1):73-8. [abstract]
5. Chest pain of recent onset, NICE Clinical Guideline (March 2010); Assessment and diagnosis of recent onset chest pain or discomfort of suspected cardiac origin
6. Matetzky S, Freimark D, Feinberg MS, et al; Acute myocardial infarction with isolated ST-segment elevation in posterior chest leads V7-9: "hidden" ST-segment elevations revealing acute posterior infarction.; J Am Coll Cardiol. 1999 Sep;34(3):748-53. [abstract]
7. Agarwal JB, Khaw K, Aurignac F, et al; Importance of posterior chest leads in patients with suspected myocardial infarction, but nondiagnostic, routine 12-lead electrocardiogram.; Am J Cardiol. 1999 Feb 1;83(3):323-6. [abstract]
8. Wung SF, Drew BJ; New electrocardiographic criteria for posterior wall acute myocardial ischemia validated by a percutaneous transluminal coronary angioplasty model of acute myocardial infarction.; Am J Cardiol. 2001 Apr 15;87(8):970-4; A4. [abstract]
9. Hutchins KD, Skurnick J, Lavenhar M, et al; Cardiac rupture in acute myocardial infarction: a reassessment.; Am J Forensic Med Pathol. 2002 Mar;23(1):78-82. [abstract]
10. Huang CM, Chen LW, Huang SH, et al; Acute left ventricular rupture following posterior wall myocardial infarction. Intern Med. 2010;49(14):1387-90. Epub 2010 Jul 15. [abstract]
11. Jeppsson A, Liden H, Johnsson P, et al; Surgical repair of post infarction ventricular septal defects: a national experience.; Eur J Cardiothorac Surg. 2005 Feb;27(2):216-21. [abstract]
12. Krishnaswamy A, Lincoff AM, Menon V; Magnitude and consequences of missing the acute infarct-related circumflex Am Heart J. 2009 Nov;158(5):706-12. Epub 2009 Sep 24. [abstract]
13. Menown IB, Allen J, Anderson JM, et al; Early diagnosis of right ventricular or posterior infarction associated with inferior wall left ventricular acute myocardial infarction.; Am J Cardiol. 2000 Apr 15;85(8):934-8. [abstract]

Internet and further reading

• ECG Image Index, Alan E Lindsay ECG Learning Center
• ACC/AHA Clinical Competence in ECG Diagnoses, Alan E Lindsay ECG Learning Center
• True Posterior MI and Right Ventricular MI

Acknowledgements