Posterior Myocardial Infarct

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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

See also: Acute Coronary Syndrome written for patients

Posterior myocardial infarction 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]

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.

It is difficult to be sure of the percentage of myocardial infarctions that are posterior because it seems likely that many are missed.[3] The risk factors are the same for any cardiovascular disease, such as smoking, hypertension, diabetes, hyperlipidaemia, etc.

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See separate Cardiac-type Chest Pain Presenting in Primary Care, Acute Coronary Syndrome and Acute Myocardial Infarction articles.[4] However, posterior myocardial infarctions may be difficult to diagnose and the diagnosis is thought to be frequently missed. There is very scanty information in the literature about typical patient symptoms with posterior myocardial infarction.

See the separate Acute Coronary Syndrome article. Other causes of similar ECG changes include:

  • 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.

Posterior myocardial infarction is difficult to recognise because the leads of the standard 12-lead electrocardiogram are not a direct representation of the area involved. 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 three classical changes to be sought are:

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

Diagnosis of posterior myocardial infarction may be facilitated by using the posterior leads V(7) to V(9), leading to easier and faster recognition with consequences for treatment and improved prognosis.

The blood changes of troponins and creatine kinase are as for other areas of myocardial infarction. See the separate Cardiac Enzymes and Markers for Myocardial Infarction article.

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

General management

See the separate Acute Coronary Syndrome article.[4]

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 myocardial infarction.

Studies on the outcome of posterior myocardial infarction 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 myocardial infarction.

  • The risk of ventricular aneurysm, rupture and death may be greater than with myocardial infarctions at other sites.[5]
  • 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.[6]

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 myocardial infarction. Delay in diagnosis may also contribute.[7] 

See the separate Prevention of Cardiovascular Disease article.

Further reading & references

  1. Ravakhah K; Death certificates are not reliable: revivification of the autopsy. South Med J. 2006 Jul;99(7):728-33.
  2. Khan JN, Chauhan A, Mozdiak E, et al; Posterior myocardial infarction: are we failing to diagnose this? Emerg Med J. 2010 Oct 20.
  3. van Gorselen EO, Verheugt FW, Meursing BT, et al; Posterior myocardial infarction: the dark side of the moon. Neth Heart J. 2007 Jan;15(1):16-21.
  4. Chest pain of recent onset; NICE Clinical Guideline (March 2010)
  5. 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.
  6. 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.
  7. Krishnaswamy A, Lincoff AM, Menon V; Magnitude and consequences of missing the acute infarct-related circumflex artery. Am Heart J. 2009 Nov;158(5):706-12. Epub 2009 Sep 24.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Huw Thomas
Current Version:
Peer Reviewer:
Dr Adrian Bonsall
Document ID:
1716 (v24)
Last Checked:
11/02/2016
Next Review:
09/02/2021

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