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Editor,—Non-cardiac chest pain is a major problem in general practice, in outpatients, and on the wards. Some patients are “reassured” that their pain is not cardiac but this is of course not the end of the matter. Professor Mayou and others1-3 have demonstrated that these patients are still in trouble at follow up. Some are given the label “musculoskeletal” but this is not very convincing without a clear explanation. I suggest that this diagnosis can be supported in many cases by demonstrating reproduction of the pain by passive spinal movements. Production of symptoms by passive movements is well known to orthopaedic specialists.4 Flexion, extension, lateral flexion, and rotation of the cervical spine, and rotation of the thoracic spine are the basic movements, and sometimes the position has to be held at the extreme for a least five seconds to reproduce symptoms—but I do not know why. This method of examination is not well known. Fifteen consecutive medical senior house officers and eight casualty officers were asked how they would demonstrate that chest pain was musculoskeletal and the best that they could do was percussion or direct pressure.
In six months of cardiology outpatients there were 27 patients (16 women and eight men) with a provisional diagnosis of angina whose history indicated another diagnosis. Their discomfort was either too unpredictable, too long or too short in duration, perhaps with paraesthesia in the fingers, or did not respond appropriately to antianginal drugs. One patient seemed to have oesophageal spasm and reflux and responded to appropriate treatment. One had pain reproduced by pressure on a costochondral joint. Of the remainder all but three had their discomfort reproduced in part or completely by passive spinal movements. Two patients also had their symptoms reproduced by percussion over the spine; both had vertebral collapse, one from osteoporosis and one from a secondary deposit. Two patients said that they were pale and sweaty during the pain, and pallor and sweating were reproduced by passive thoracic rotation and relieved by return to normal; a concurrent ECG was unchanged. Seven patients had exercise tests, two of which were positive and they await catheterisation; their pain has not responded to antianginal medication so there is doubt that they have angina.
Of 20 consecutive patients with typical angina and positive exercise tests, only three had some discomfort in the chest on thoracic spinal rotation and they were clear that it was a different pain from their angina.
Review of the 27 patients with non-anginal pain at one year showed that seven had definite relief from non-steroidal anti-inflammatory drugs and one from physiotherapy. None had been admitted to hospital and those that still had pain seemed resigned to their symptoms but not anxious.
The exact origin of musculoskeletal pain remains obscure. It seems likely that the pain is referred along the intercostal nerves where it is exacerbated by inspiration, presumably from painful rib rotation.
Coronary disease and inflammatory spinal disease can co-exist and this physical sign does not exclude angina but its presence in the absence of any objective evidence of myocardial ischaemia—for example, no ECG changes during pain, is helpful in the differential diagnosis. Perhaps more important it demonstrates that the pain is mechanical, often allowing confident discharge without a backup nitroglycerin inhaler and giving the patient a fairly clear explanation of the symptoms, which does far more than negative tests to avoid chronic ill health.