Posterior Myocardial Infarct (PMI)

Myocardial infarction is usually described as anterior or inferior but a few affect the posterior wall of the left ventricle to produce true posterior myocardial infarction. 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. This is an unusual position for an infarct but when it does occur, the diagnosis may easily be missed.¹

It is difficult to be sure of the percentage of myocardial infarctions that are true posterior as there may be more than just the posterior wall involved but also because the criteria for diagnosis are less well recognised and it would seem 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.² 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

The main risk factors are as for any other type of MI although smoking³ has been suggested to be an even greater risk factor. Variations to the coronary anatomy may also be a risk but this is also difficult to assess.

The presentation in terms of symptoms and signs would seem to be very much the same as other MIs. The literature does not give any indication as to whether the distribution of pain in posterior infarction is any guide. The literature about diagnosis is mostly concerned with ECG changes. Some is about echocardiography, angiography and post mortem findings. Very scant attention is paid to what the patient says.

The other differential diagnoses associated with MI must be considered.

If the ECG changes are noted they need to be distinguished from other causes of similar changes. Right ventricular hypertrophy can cause large R waves in the early V leads. RVH is associated with lung disease and it is unsafe to diagnose RVH in its absence. Infarction of the right ventricle is rare but will produce a similar ECG.

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, in theory, 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. Right bundle branch block does not tend to affect the pattern in the same way. See internet links (below) for images.

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^4,5 with V7 to V9 going further round the chest wall. In one case these findings were validated by angioplasty.⁶ As long ago as 1976 posterior chest leads were suggested, and a single, unipolar posterior V9 lead combined with the T-wave index was found superior to the standard 12-lead ECG criteria.⁷

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

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

Non-drug management

This is as for any other type of MI. Oxygen should be given and rapid transfer to a place where thrombolysis can be given and CPR is readily available.

Drugs

Drug management is as for any other type of MI. However, there is often delay in diagnosis that can lead to delay in thrombolysis and presumably inferior outcome. However, 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 and so there is no definitive evidence for thrombolysis in these cases. Criteria for reperfusion therapy in acute myocardial infarctions require the presence of ST elevation in 2 contiguous leads.

Surgical

Coronary angiography with a view to PCTA or CABG can be performed as in other MI.

The risk of ventricular aneurysm, rupture and death may be greater than with myocardial infarctions at other sites.⁸ 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.⁹

The study from Tehran suggested that patients with posterior MI tended to be older and have more risk factors. This might, in part, account for the finding of a higher rate of complications and death in those with a posterior MI.² A study from Belfast suggested that the few patients with posterior myocardial infarction may tend to have larger infarcts with higher enzyme levels.¹⁰

As for other myocardial infarctions.

True posterior myocardial infarction is rare compared with anterior and inferior infarction and when it does occur it may not be pure but associated with infarction of other areas too. The diagnostic criteria by ECG are less clear and the absence of routine leads V7,8,9 probably means that diagnosis is often missed. An interesting research project would be to use a 15 leads ECG or at least the standard 12 leads plus V9 on a large number of patients admitted to hospital with suspected myocardial infarction. With a large study, probably with over 1,000 subjects there are a number of questions that may be answered:

• In those patients proved to have myocardial infarction, how many had pure posterior myocardial infarction?
• How many had infarction of the posterior wall as well as other sites?
• In how many was the diagnosis made by the addition of the 3 extra V leads when it would have been missed without them?
• Are there any clinical features such as the site of the pain that may indicate a posterior infarct?
• Do they differ significantly from other MI patients in such ways as age, sex, risk factors, size of infarct and prognosis?