ECG & Echocardiography Case Study Chronic Myocardial Infarction-Credit Cardio Rhythm Online Blogspot

ECG and echo are very useful non-invasive investigations when it comes to assessing patients with a history of myocardial infarction. In ECG terms an old (chronic) myocardial infarction may be characterised by pathological Q waves. In echo terms it may be characterised by regional wall motion abnormalities.

The ECG

Remember it is primarily the ST segments that give us information regarding acute changes, and this can be divided into two main categories: Non-ST Elevation Myocardial Infarction (NSTEMI) and ST Elevation Myocardial Infarction (NSTEMI). 

If Q waves develop this is referred to as a Q-wave infarction, and if no Q waves develop this is sometimes referred to as a non-Q wave infarction. If Q waves do develop they may however resolve due to early treatment, regress, or disappear with time. Q waves may also be electrically silent, meaning they occur in a region where the ECG cannot record the injury. Therefore, not all patients who have an MI develop or show Q waves, and not all Q waves persist. So, given that ST changes typically resolve in time, it is of course possible for someone with a history of MI to have a perfectly normal ECG some stage down the line. That said if Q waves do develop they can remain on the ECG for life. 

A Q wave is a negative deflection that precedes an R wave. Physiologic q waves or “septal” q waves represent normal depolarisation of the septum. They are usually small and commonly seen in the lateral leads. Occasionally you may also see isolated q waves as a normal variant in leads such as III, aVR, and V1. Pathologic Q waves tend to be deeper and wider, and as with ST/T wave changes should be seen in at least 2 contiguous (neighbouring) leads. The general consensus is that loss of electrical forces due to necrosis or scarring of the heart muscle result in the leads (overlying the infarcted area) recording electrical activity from the opposite ventricular wall (moving from an inner to outer direction). The electrical activity is then essentially moving away from these leads at this point and thus creates a negative deflection – the Q wave.

Depending on where the infarction is you may see a Q wave develop before the R wave. In other leads you may note that your R wave has disappeared and the complex becomes a QS wave. 

Be aware though, not all pathologic Q waves are due to MI. Of course, history is crucial. In the event that you have unexpected Q waves (i.e. there is no other evidence of MI) you’ll also need to consider a differential diagnosis such as cardiomyopathy, amyloid, altered conduction (LBBB and WPW), and ventricular enlargement. 

Echocardiography

As a cardiac sonographer I routinely see patients after the diagnosis of an MI has been made and usually after intervention i.e. establishing prognosis. Most acute MIs are apparent on history, ECG, and cardiac enzymes, but an emergency echo may be used to assess regional wall motion abnormalities (RWMAs), which can occur within seconds of a coronary artery occlusion, or to rule out other causes of chest pain (such as aortic dissection) if needed. It is also used to check for any other associated complications such as ventricular septal defect (VSD), papillary muscle rupture, ventricular aneurysms, thrombus, RV wall motion abnormalities, and free wall rupture.

A regional wall motion abnormality is when an area of the ventricle doesn’t contract as well as it should, or doesn’t contract at all. These may be scored or described as being hypokinetic (reduced movement) or akinetic (no movement) – the latter is usually associated with thinning and brightness of the wall i.e. dead muscle. In identifying any hypokinetic/akinetic areas in relation to the remaining normal regions, we can then also comment on how well the left ventricle functions and estimate the ejection fraction – this is the percentage of blood that leaves the left ventricle when it contracts. An ejection fraction of >55% is considered normal LV function. Between 45-54% is considered mildly impaired, 35-45% is moderately impaired, and less than 35% is severely impaired. As with ECG changes, regional wall motion abnormalities caused by myocardial infarction may resolve due to early treatment/reperfusion; this is the situation in what’s known as myocardial stunning.

In the same way that not all pathological Q waves are due to MI, please also bear in mind that not all regional wall motion abnormalities are due to myocardial infarction – other causes include left bundle branch block, RV overload, cardiomyopathy, and prior cardiac surgery.

Lead Groups & Wall Segments

When assessing an ECG we divide our 12-lead into four main contiguous lead groups: inferior, lateral, septal, and anterior. Regions not well represented on a standard 12-lead are the posterior region and the right ventricle; that said, both these regions can be better represented using alternative lead placements, or in the case of posterior infarction looking for reciprocal changes in the right precordial leads.

In echo we assess the left ventricle according to a 17 segment model. The left ventricle is assessed at basal level (6 segments), mid-cavity level (6 segments), and apical level (4 segments) plus the apical cap. This is a parasternal short axis view at mid cavity level – if the views are on axis the LV should appear circular in shape. Just imagine that you have sliced through the ventricles (perpendicular to the septum) and you are looking downwards into the ventricles.  

Just to confuse matters, with regards to terminology, in echo we no longer have posterior segments at all. And, we no longer have pure lateral or septal segments (except at the apex). We have pure anterior and inferior segments, but the septal region is divided into anteroseptal and inferoseptal, and the lateral region is divided into anterolateral and inferolateral (the latter used to be known as posterior). Yep, I know, you like potato and I like potahto…let’s call the whole thing off! Personally I still use the term “posterior” in echo, I tend to write it in brackets – as of yet no one has complained.

Case Study 

Ok, so these days due to primary intervention and preventative measures, life in the echo lab may be a bit lacklustre when it comes to following up myocardial infarctions. I can’t actually remember the last time I saw a ventricular aneurysm. But, signs of a good old-fashioned chronic MI do crop up from time to time – mostly from those who had their infarction some decades back or from those who have had a “silent MI” (a heart attack without any obvious symptoms, usually meaning that medical intervention wasn’t sought early enough). Not to be confused with “electrically silent”. Here is the ECG of a 65 year old male who had an MI in 1993; he has never had coronary intervention. Where do you see evidence of the MI?

Yes that’s right we can see pathological Q waves in leads III and aVF – the inferior region. I would also add that transition is late i.e. occurring after V4 (aka poor R wave progression) and there is also left axis deviation – a common finding in inferior MIs.

Here is the corresponding echo. If you are not used to looking at echo I’ve included a normally functioning LV on the left so that you can compare. The echo on the right shows thinning and akinesia of not just the inferior region, but also the inferolateral (posterior) region. There are also adjacent inferoseptal and anterolateral regions of hypokinesia. Using the Simpsons biplane method the ejection fraction was estimated at 39% - moderately impaired.

If you have trouble watching the video below, especially if you are using Internet Explorer, click  here 

I think what’s interesting about this case study is it demonstrates the limitations of the ECG if trying to estimate infarct size. We see only two Q waves in the inferior leads, and yet perhaps more RWMAs on echo than the ECG suggests. Of course, as already mentioned above, the absence of Q waves could simply imply that a non-Q wave infarction has taken place, that previous Q waves have resolved, or that infarction has occurred in areas that are electrically silent – the latter seems to be particularly true for the posterior and some of the lateral segments. Another reason may be ischaemic hibernating myocardium; this is similar to myocardial stunning in the sense that it exhibits resting wall motion abnormalities due to coronary disease, which then improves if the flow of blood is restored. I try not to get these two terms mixed up, so I always think of “stunning” as being nearer to the event [of an acute MI] lasting only for a short period of time following reperfusion, and “hibernation” as a state of persistently impaired LV function due to ongoing ischaemia. I may have oversimplified all of this somewhat, but the main point is that lack of or absence of Q waves does not rule out LV impairment.

What about RV impairment? It occurred to me whilst writing this that given RV infarction complicates around 40% of inferior MIs I rarely see old RV wall motion abnormalities. The main reason for this is quite simply that the RV is less susceptible to damage due to it being a much smaller chamber with less oxygen demand. Therefore RV function generally improves in the majority of patients even without intervention.

Of course, although echo is a more direct method for measuring the extent of myocardial damage, it too has its limitations. If image quality is poor, visualisation of the endocardium may not be adequate enough to assess all the regions by 2D alone. Contrast echo is useful in these situations. I would also add that to some (or maybe a large) extent it is operator dependent.

I hope you have enjoyed this case study. I have also included some further links below. These case studies are always written from my perspective as a cardiac physiologist and for teaching beginners, so whether you are a beginner or an ECG/echo expert, please feel free to ask questions or to add any further comments in the section below. Thanks for reading. Mx