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Oesophageal pain in coronary artery disease
  1. Internal Medicine,
  2. Heilig Hartziekenhuis,
  3. Wilgenstraat 2,
  4. 8800 Roeselare, Belgium
  5. Department of Gastroenterology,
  6. University Hospital Gasthuisberg,
  7. K.U. Leuven, 3000 Leuven, Belgium

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Up to 26% of patients with angina-like chest pain sufficiently severe to necessitate more invasive examinations have normal coronary arteries on arteriography.1 Since the late 1970s, the oesophagus has gained notoriety as a possible cause of the chest pain in these patients. Depending upon the criteria used to accept an oesophageal origin of the pain, up to 50% of patients with normal coronary arteries have oesophageal pain. Gastroenterologists now widely accept that the best and possibly the only way to determine whether the oesophagus is the likely cause of the chest pain is to show a temporal correlation between the pain attack and an abnormal oesophageal event, such as acid reflux or severe motor disturbances.

Since the development of 24 hour pH and pressure measurements by the Leuven group, prolonged recordings have become a standard investigation in patients with non-cardiac chest pain.2 These measurements, which attempt to correlate symptoms with abnormal oesophageal events, led to the finding that most of the spontaneous pain attacks were reflux related, although many of these patients have a normal acid exposure on quantitative analysis of 24 hour pH monitoring. This has been called the acid hypersensitive oesophagus.3

Analogous to the use of exercise tests in cardiology to provoke myocardial ischaemia, several provocation tests have been used in an attempt to identify the oesophagus as the origin of chest pain. Provocation by acid or by motility stimulating agents, mechanical stimulation by balloon distension and other stimuli have all been used. The acid perfusion and edrophonium tests seem to be the most reliable and are able to detect most patients with non-cardiac chest pain of oesophageal origin.4

If patients have chest pain which seems to be exclusively related to acid (positive acid perfusion test or spontaneous pain related to acid reflux, or both), they are considered to have an acid sensitive oesophagus. Similarly, patients with a positive edrophonium test and/or a positive distension test and/or spontaneous pain in relation to severe dysmotility have a mechano-sensitive oesophagus. Patients who are sensitive to several stimuli are considered to have an irritable oesophagus. Acid plays a major role in these patients as those with an acid sensitive oesophagus and an irritable oesophagus are far more common than patients with a mechano-sensitive oesophagus.4

Schofield et al were the first to describe oesophageal abnormalities in patients with proven coronary artery disease. During standard oesophageal manometry, abnormalities were found in 2/20 (10%) patients with coronary artery disease and in 23/52 (44%) patients with normal coronary angiograms.5 In 1990 Bortolotti et al described oesophageal abnormalities, especially reflux, in 14/18 patients with coronary artery disease, in whom treatment with nitroderivatives and calcium antagonists had become partially ineffective.6 Lux et al compared pain related oesophageal motility, gastro-oesophageal reflux and ST segment deviation in patients with intermittent chest pain and normal (30 patients) or pathological coronary angiography (15 patients). Pain correlated abnormal motility or gastro-oesophageal reflux occurred at the same frequency in patients with normal and pathological coronary angiography. Moreover, simultaneous ECG recording revealed significant correlation of ST segment deviation and gastro-oesophageal reflux or abnormal motility in patients with coronary artery stenoses.7

The study by Cooke et al in this issue (see page 323) is the first to compare prospectively the incidence of oesophageal abnormalities in relation to chest pain in patients with normal coronary angiograms (61 patients) and in a small group of so-called controls with proven angina pectoris (25 patients). The authors concluded that oesophageal function tests (standard manometric study, acid perfusion test, 24 hour pH monitoring) were capable of implicating the oesophagus as a source of pain in patients with normal angiograms (44%) and in patients with coronary artery disease (36%). With the exception of simultaneous contractions during standard manometry (6.7v 0.8%), however, the incidence of abnormal testing (acid perfusion test, acid exposure) and in particular the correlation of gastro-oesophageal reflux with chest pain were as common in patients with normal coronary angiograms as in controls with angina (23v 24%). Neither the chest pain characteristics (duration, predictability, rest pain, typical pain) nor the presence of additional oesophageal symptoms (heartburn, dysphagia, waterbrash) were predictive of an oesophageal abnormality. However, pain characteristics (duration, predictability, rest pain) and additional symptoms (dysphagia, variable stool habits) differed significantly between patients with normal coronary arteries and patients with coronary artery disease. Apparently, chest pain of oesophageal origin does exist in patients with coronary artery disease and is as frequent as in patients with normal coronary arteries. Reflux is the key factor in both patient groups.

Some studies have suggested that reflex coronary ischaemia is the mechanism underlying acid induced pain. Acid perfusion tests in patients with coronary artery disease may induce myocardial ischaemia8 and a lower exertional angina threshold.9 It has also been shown recently that acid stimulation of the oesophagus may lead to reduced coronary blood flow.10 Simultaneous pH monitoring and ECG recordings have also shown a significant correlation between ST segment deviation and gastro-oesophageal reflux in patients with coronary artery disease.7

In conclusion, gastro-oesophageal reflux is probably responsible for a number of episodes of chest pain in patients with coronary artery disease, and this is as frequent as in patients with chest pain and normal coronary arteries. The exact mechanism by which chest pain is induced after stimulation of the oesophageal mucosa by acid remains speculative. Intermittent chest pain of cardiac and oesophageal origin cannot be differentiated on the basis of the case history or the clinical picture, or both. Further studies are needed to clarify the benefit (if any) of acid secretion blocking agents as sole or concomitant treatment in these patients.


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