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).

Decubitis angina

In the supine position there is increased venous return to the heart which increases the filling pressures of the ventricle (end diastolic pressure). Through the law of La Place, increased filling pressure leads to increased wall tension which will increase oxygen demand and therefore may provoke angina (4). Such patients tend to have elevated left ventricular diastolic pressures at baseline and disease in two or three coronary arteries (5).

Nocturnal angina

Occurs as a result of increased sympathetic tone in the early hours of the morning upon waking, or during dreaming. In fact MIs are more common in the early hours of the morning. Co-existent obstructive sleep apnoea with a drop in oxygen saturation during the night can also provoke cardiac ischemia (6). While sleep seems relaxing to us, there are still important autonomic nervous system changes that occur.


Cardiac ischemia can present in a variety of ways that you might at first glance consider ‘atypical’. Most people with these ‘atypical’ episodes seem to have pretty bad CAD, therefore they may get other manifestations of ischemia also; in fact most patients with decubitis angina also get exertional angina (5).

However, for the patients you are seeing on the ward, most of them are doing very little exertional activity while in hospital and their presenting illness may often place a larger baseline oxygen demand on the heart, so it is important to recognise these ‘atypical’ presentations.

  1. Herbert L. Fred, MD, MACP. Atypical Chest Pain; A Typical Humpty Dumpty Coinage. Tex Heart Inst J. 2009; 36(5): 373–374.
  2. Rubin Berlinerblau, Jacob Shani. Clinical study. Postprandial angina pectoris: Clinical and angiographic correlation. Journal of the American College of Cardiology. Volume 23, Issue 3, 1 March 1994, Pages 627-629
  3. Haemodynamic and electrocardiographic accompaniments of resting postprandial angina. J Figueras, BN Singh, W Ganz, HJ Swan – Heart, 1979 – heart.bmj.com
  4. Chronic cardiac chest pain . Ann-Katrin Fritz, FRCA Peter Faber, MD PhD FRCA. Continuing Education in Anaesthesia Critical Care & Pain, Volume 12, Issue 6, 1 December 2012, Pages 302–306, https://doi.org/10.1093/bjaceaccp/mks038
  5. Allen D Johnson, Hilary A Stroud, MD, CDR W. V. R Vieweg, MC, USN, John Ross Jr, M.D Variant Angina Pectoris Clinical Presentations, Coronary Angiographic Patterns, and the Results of Medical and Surgical Management in 42 Consecutive Patients. Chest. June 1978 Volume 73, Issue 6, Pages 786–794.
  6. Nocturnal angina: precipitating factors in patients with coronary artery disease and those with variant angina. AA Quyyumi, J Efthimiou, A Quyyumi, LJ Mockus… – Heart, 1986 – heart.bmj.com

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