What does atypical chest pain mean? Part 1

“I just had my dinner, this hospital food is terrible by the way, look at this, what is this?….anyway  a couple minutes later the pain just grabbed me here”, he says rubbing the back of four fat, tobacco stained fingers up and down from his throat to his epigastrium.

“And you were just sitting down in your chair, right?” – “Yeah. I get this all the time though at home though”.

You sit down to wearily write your note; ‘Impression: Atypical chest pain, probably GORD. Plan: Serial troponins to exclude cardiac’.

Of course, the pain only lasted 10 minutes, so your troponins will probably be negative. So is the pain atypical?

Atypical is another in a series of medical terms that we use all the time which don’t really mean anything- or rather mean different things for different people and should probably be abandoned (1). Some clinicians even use it in order to facilitate admitting the patient to hospital (1).

The question of what exactly is ‘typical’ for angina, or how frequent something needs to be in order to be considered typical, is an interesting one, which provides fodder for many future blog posts. Surely though, positional pain or pain related to food can’t be angina? At least this is kind of what I have been given to understand. Not so easy apparently.

We will run through 3 examples of chest pain presentations well described in the literature which are associated with severe CAD, which many people might consider to be atypical. They go to show that few patients read the medical school textbook. Or maybe the medical school textbook is incomplete.

Post-prandial angina

8.6% of patients with ischemic heart disease experience post prandial angina (angina after meals), with higher incidence of three vessel disease and left main disease, and lower ejection fractions on average. Such angina is more likely to occur after the dinner meal (2). The mechanism is unclear but is thought to be related to either redistribution of blood flow to the gut or increases in cardiac output following meals. Increases in heart rate, blood pressure and systemic vascular resistance are all observed at the onset of angina, which usually occurs within 25 minutes of the meal (2,3). Continue reading

STEMI equivalents

It is another weary on call night, where annoyingly everyone has decided to have chest pain. As you sit down to scrutinise probably your tenth ECG, some ST elevation in lead AVR catches your eye. This jolts you from your torpor. Real pathology? You get your registrar to swing by and have a look. He furrows his brow as he looks down his nose at you, saying;

“ Remember, young padawan, one lead is no lead.” He reminds you of the STEMI criteria (1), which must be present in at least 2 anatomically contiguous leads:

  1. ≥1 mm (0.1 mV) of ST segment elevation in the limb leads
  2. ≥ 2 mm elevation in the precordial leads
  3. New LBBB

It turns out this teaching is not quite complete and will eventually cause you to miss some significant coronary occlusions. For you see, the classification of MIs into STEMI and NSTEMI is not some random division based on the aesthetic s of the ECG waveform. STEMI represents total occlusion of a coronary artery, therefore high risk of cardiogenic shock and death, and therefore benefit of immediate revascularisation. NSTEMI, on the other hand, an incomplete blockage, has failed to show benefit from immediate angiography (2).

The key point is that there are other ECG patterns that are also indicative of coronary occlusion which are simply not taught, mostly because they have only been described in the last decade or two, and unfortunately medicine can be slow to catch up. These “STEMI equivalents” cannot just be sat on, waiting for the troponin.


To start with, new LBBB is not even considered a STEMI criterion anymore (3). You can however interpret ST segments in a LBBB, despite what you might have been told, by utilising the ‘Scarbossi Criteria’. These will be covered in a separate post.

De Winter’s Waves

de winter
[Image Credit: wikem.org/wiki/File:Dewinter.jpg]
ST depression indicating NSTEMI? Think again.

A decade ago, De Winter et al described the above ECG pattern consisting of  “1-to 3-mm upsloping ST-segment depression at the J point in leads V1 to V6 that continued into tall, positive symmetrical T waves. In most patients there was a 1- to 2-mm ST-elevation in lead aVR” (4). Continue reading