Editor,—I enjoyed the prospective study by Cooke et al (Gut1998;42:323–329) on the relation between oesophageal abnormalities and chest pain in patients with normal coronary angiograms and with angina pectoris. This study confirms the findings of previous studies1 ,2 that the oesophagus is responsible for chest pain in a high percentage of patients with coronary artery disease, and that an episode of gastro-oesophageal reflux nearly always triggers this pain.

However, no explanation for this unexpected finding has been given. The tentative proposition that it is the result of a decreased angina threshold3 and a reflex coronary ischaemia, both induced by the contact of acid with the oesophageal mucosa, is not acceptable for two reasons: firstly, because this oesophagocardiac reflex may be the basis for linked angina but not for oesophageal angina and, secondly, because the patients should have shown simultaneous electrocardiographic (ECG) abnormalities during the pain induced by the acid perfusion test. Unfortunately, a concurrent ECG was not performed during pH monitoring. This intriguing finding gives rise to two questions: why do these patients have such a high incidence of gastro-oesophageal reflux and why does this so frequently cause them pain?

I believe that the first question can be answered by the fact that patients with angina pectoris are usually prescribed long term medication such as nifedipine or nitroderivatives; these drugs are potent inhibitors of lower oesophageal sphincter tone, which is the main antireflux barrier. It would be interesting to know whether the patients with angina from Cooke and colleagues’ study had taken this type of medication for long periods, and whether their lower oesophageal sphincter tone was below normal at the time of the study. In a previous study, we measured manometrically the lower oesophageal sphincter tone in patients with angina after a drug washout, and found a significantly lower value than normal.5 It seems probable that the chronic consumption of spasmolytic drugs may have reduced this tone, giving patients with coronary artery disease the appearance of pathological gastro-oesophageal reflux. Furthermore, it is possible that the absence of oesophageal spastic disorders, such as nutcracker oesophagus, could be attributed to the long term pharmacological suppression of oesophageal contractile activity.

With regard to the second question, it is very odd that patients with angina and gastro-oesophageal reflux complain mainly of retrosternal pain instead of the more common symptoms of gastro-oesophageal reflux—for example, heartburn, acid regurgitation, etc.6Previous studies have shown that there is a decrease in the pain perception threshold of patients with oesophageal angina and normal coronary angiograms,7 but we do not know whether pain perception in patients with oesophageal angina and coronary artery disease is similarly altered. I would expect a positive result from research on this matter, because it is not unreasonable to suppose that chronic cardiac pain may have sensitised the nociceptive neurones of the dorsal horn of the spinal cord,8 where the nociceptive fibres coming from the oesophageal mucosa also converge, thus developing a secondary hyperalgesia allodynia.9Should spinal hyperalgesia be present, episodes of gastro-oesophageal reflux that are generally not perceived to cause pain, could simulate the pain of angina.