7

Angina-like chest pain of oesophageal origin

JOZEF JANSSENS GASTON VANTRAPPEN

THE OESOPHAGUS AS A POSSIBLE CAUSE OF CHEST PAIN OF NON-CARDIAC ORIGIN

Angina-like chest pain of non-cardiac origin constitutes a major diagnostic and therapeutic problem. It is also a frequent problem; up to 20% of coronarographies performed in patients with chest pain that was sufficiently alarming to warrant such an invasive examination show neither organic lesions that can account for the patients’ symptoms, nor coronary artery spasm during ergometrine (ergonovine USP) provocation (Likoff et al, 1967 ; Waxler et al, 1971; Kemp et al, 1973; Heupler et al, 1978; Wilcox et al, 1981). This indicates that the clinical history of the chest pain or the routine technical examinations or both are not always equivocal.

As cardiac and oesophageal pain can mimic each other quite closely it is not surprising that the oesophagus is considered to be a frequent cause of non- cardiac chest pain (Blackwell and Castell, 1984). Depending on the criteria set to prove the oesophageal origin of the pain, the oesophagus is considered in the literature to be the source of the chest pain in 20-60% of cases (Bennett and Atkinson, 1966; Roberts et al, 1975; Henderson et al, 1978; Svensson et al, 1978; Benjamin et al, 1979; Ferguson et al, 1981; Kline et al, 1981; Davies et al, 1982a). According to Brand et al (1977), however, a positive identification for the oesophageal origin of the pain can only be made when the patient has a similar attack of chest pain during manometry or pH-monitoring, and if, at the same time, a characteristic and reproducible abnormal motor pattern appears on manometry or if the patient has pH-proven reflux at the time of pain. Unfortunately this is only rarely the case due to the intermittent nature of the pain and because of the limited duration of conventional examinations.

Therefore, even if a cardiac origin of the pain can virtually be excluded by a negative coronary arteriography (and ergometrine provocation testing) or, in the more lucky patient, by a normal electrocardiogram obtained during a pain attack, as stated by Rapaport in a recent editorial, the real cause of pain is not firmly established in many of these patients [‘It is reasonable to assume that in

Baillike’s Clinical Gastroenterology-Vol. 1, No. 4, October 1987 843

844 J. JANSSENS AND ‘3. VANTRAPPEN

the absence of a conduction disturbance or other electrocardiographic causes that may obscure a detectable ischemic response, the failure of ST segment changes to occur in a patient complaining of chest discomfort at rest suggests an extra-cardiac source. When this is coupled with a normal resting ECG and no prior history of coronary heart disease, nor any major risk factor, the likelihood approaches a high probability’ (Rapaport, 1986)].

Nevertheless it is important to positively identify the oesophagus (or other organs) as the origin of the patient’s chest pain, because simply reassuring him about the non-cardiac nature of the pain only rarely results in definitive relief of his concern; in the absence of a positive diagnosis, the patient may be inclined to believe that the physician failed to establish the cardiac origin of his pain or that because of a poor prognosis the physician had preferred not to tell the truth (Ockene et al, 1980).

MECHANISM OF OESOPHAGEAL PAIN

Painful sensations of oesophageal origin can be categorized into three different symptoms: heartburn, odynophagia and central or angina-like chest pain.

Heartburn is felt moving from the low substernal or high epigastric region upward to the mid- or high substernal region, and may or may not be accompanied by regurgitation of acid or bitter tasting fluid. However, gastro- oesophageal reflux does not necessarily produce this typical heartburn complex. Reflux-induced pain may be cramp-like, may radiate to the neck, shoulder or arm, and may even be induced by physical exertion or emotional stress, thus closely mimicking angina-like chest pain (Bernstein et al, 1962; Bennett and Atkinson, 1966). Reflux as a cause of angina-like chest pain has probably been underestimated in the past, as recent studies indicate that over 60% of patients with angina-like chest pain of oesophageal origin experience their chest pain in association with reflux episodes (Peters et al, 1986; Vantrappen et al, 1986). In these instances, oesophageal motor abnormalities secondary to reflux may or may not be involved in the initiation of the pain (Corazziari et al, 1978; Richter et al, 1985; Vantrappen et al, 1986).

Odynophagia, or pain on swallowing, usually occurs in diseases which cause severe mucosal damage such as ulceration or severe oesophagitis (peptic, herpetic, monilial etc.). It may occur in the absence of organic lesions in the tender-oesophagus syndrome, described by Edwards (1974). Odyno- phagia is not usually a diagnostic problem in patients with angina-like chest pain because the clear association of the pain with deglutition in these instances clearly points to the oesophagus as the cause of the pain.

Oesophageal motility disorders may cause chest pain that closely mimics pain of oesophageal origin. In the early stages of achalasia, pain may occur without any relation to meals and may precede the onset of dysphagia by several months (Vantrappen and Hellemans, 1974a). Pain may also be the major problem in patients with vigorous achalasia, but in most instances the presence of dysphagia points to the probable oesophageal origin of the pain. Diffuse oesophageal spasm is characterized by attacks of central chest pain

CHEST PAIN OF OESOPHAGEAL ORIGIN 845

frequently at night and lasting for minutes or hours; dysphagia is usually not a predominant symptom and may only be revealed by close questioning (Vantrappen and Hellemans, 197417). Apart from achalasia and diffuse oesophageal spasm other more recently defined motor disturbances may also cause chest pain, such as symptomatic peristalsis (or the nutcracker oesopha- gus), hypertensive lower oesophageal sphincter and severe non-specific oesophageal motility disorders (Code, 1960; Pope, 1976; Benjamin et al, 1979; Benjamin et al, 1983; Herrington et al, 1984; Castell, 1985a; Castell, 1985b). Symptomatic peristalsis is characterized by the presence of peristaltic contractions of very high amplitude [mean peristaltic amplitude in the distal oesophagus of more than 24 kPa (180 mmHg) or peak pressures above 267 kPa (200 mmHg)] and often of abnormally long duration (more than 7.5 seconds) and is probably the single most frequent motor disorder in patients with angina-like chest pain of non-cardiac origin.

The anatomical substrate responsible for these pain sensations is only partially known. Chemoreceptors have not yet been identified in the oesophageal mucosa but they must exist, as acid perfusion of the oesophagus is able to induce heartburn and even pain in the absence of any discernible motor abnormalities. It is possible that the intra-epithelial nerve endings that extend from the subepithelial plexus and terminate at various levels between the epithelial cells constitute these chemoreceptors (Christensen, 1984). Mechanoreceptors have recently been identified in the oesophagus of several animal species (Clerc and Mei, 1983a; Clerc and Mei, 1983b). Vagal mechanoreceptors are concentrated at both ends of the oesophagus. They are located not only in the muscular wall and the mucosa but also in the adventitial layer. The sympathetic mechanoreceptors are found mainly among the muscles while some lie in the adventitial layer. Richly innervated muscle spindles, as described in the canine oesophagus, probably represent the mechanoreceptors of the striated muscle layer; the intraganglionic nerve endings (Rodrigo et al, 1975) are the most likely candidates in the smooth oesophageal muscle. Other mechanisms besides reflux and motor distur- bances may have a role in the production of pain of oesophageal origin. Rodrigo et al (1970) described the existence of non-varicose nerve fibers forming a series of laminar structures on the surface of blood vessels in the submucosa of the mid-oesophagus ofcats and monkeys. It cannot be excluded that they transmit an ischaemic-like type of pain which could occur during prolonged muscle contractions. Obviously much work remains to be done before the mechanism of chest pain of oesophageal origin is fully understood.

DIAGNOSTIC PROCEDURES

From the above data it is obvious that the main conditions held responsible for angina-like chest pain of oesophageal origin are gastro-oesophageal reflux and oesophageal motor disorders, especially those that result in peristaltic or non-peristaltic contraction waves of high amplitude and long duration.

Gastro-oesophageal reflux, however, is such a common finding and does not provoke any pain in many patients, that its mere presence can hardly be

846 .I. JANSSENS AND G. VANTRAPPEN

accepted as a proof of the oesophageal origin of the pain. Also oesophageal motor disorders are often not associated with chest pain. Therefore, most authors will only accept the oesophagus as the likely cause of pain if the familiar chest pain can be shown to coincide with a reflux episode, or with a period of severe motor abnormalities or with a combination of both (Brand et al, 1977). As this will only rarely be the case during conventional pH-probe or manometric examinations because of the limited duration of these tests, several investigators have used provocation tests to induce the familiar chest pain. Prolonging the recording to a 24-hour period is another way of increasing the chance of recording pH and pressure during a spontaneous pain episode. This does not mean that conventional examinations have no value in the diagnosis of chest pain of oesophageal origin.

Conventional examinations

Endoscopy Oesophageal carcinoma is a rare but the only life-threatening cause of angina- like chest pain of oesophageal origin. Oesophageal ulceration or even a duodenal ulcer may present with an unusual pain pattern. It seems therefore wise to start the investigation with an upper gastrointestinal endoscopy. The main reason, however, for beginning the investigation with endoscopy is that the finding of erosive oesophagitis implies that the oesophagus may be regarded as the probable cause of the angina-like chest pain and that the effect of medical treatment may be awaited before proceeding to other investiga- tions. In a study of 60 patients with non-cardiac chest pain 15 patients were found to have erosive oesophagitis. Twenty-four hour recording of oeso- phageal pressure and pH showed the oesophagus to be the definite cause of the pain in 60% of these patients and a probable cause of the pain in another 27% (Janssens et al, 1986).

Conventional manometry

If conventional manometry reveals classical achalasia, vigorous achalasia or severe diffuse spasm, it is highly probable that the angina-like chest pain is of oesophageal origin. Unfortunately these motor disorders are found in only 20% of patients with chest pain of oesophageal origin. Other motor abnormalities such as symptomatic peristalsis (nutcracker oesophagus), hypertensive lower oesophageal sphincter and severe but non-specific motor disturbances, although more frequently present, can only be considered as an oesophageal cause of chest pain if a typical pain attack has been observed to coincide in time with the occurrence of motor abnormalities. However, this will only rarely occur during short-lasting conventional manometry.

Conventional pH-monitoring

A conventional pH measurement and any other acid reflux testing, and even a 24-hour pH measurement with construction of a 24-hour pH plot and a

CHEST PAIN OF OESOPHAGEAL ORIGIN 847

numerical analysis of the data is of limited value for the diagnosis of chest pain of oesophageal origin, because the mere presence of pathological reflux does not prove that this reflux is the cause of the angina-like chest pain.

Oesophagoscopy, conventional manometry and conventional pH-monitor- ing can only rarely prove the oesophageal origin of the pain. If grossly abnormal, they suggest further examinations. However, even a completely normal endoscopy, conventional manometry and pH-monitoring do not exclude an oesophageal origin of the pain (Janssens et al, 1986).

Provocation tests

Acid perfusion test The Bernstein acid perfusion test is a simple and safe provocation test that mimics endogenous reflux by infusion of 0.1 N HCl at a rate of 6-8 ml/min in the middle third of the oesophagus via an intra-oesophageal catheter (Bernstein et al, 1962). The test is called positive-related if acid perfusion but not saline provokes the familiar angina-like chest pain. Most authors accept a positive-related acid perfusion test as a proof of the oesophageal origin of the pain. If the test provokes a sensation that is different from the familiar pain (e.g. heartburn) it is called positive-unrelated and makes the oesophagus, at best, suspect of being the cause of the pain. A negative test (acid not inducing pain or pain induced by saline) has no diagnostic value and does not exclude an oesophageal origin of the pain. In a series of 50 patients with angina-like chest pain of non-cardiac origin studied by Caste11 (1985b), the acid perfusion test was positive-related in 10% of the patients. Of the 60 patients with non- cardiac chest pain which we have studied, 27% had a positive-related acid perfusion test (Janssens et al, 1986).

Edrophonium test

Several pharmacological agents have been used to provoke oesophageal motility abnormalities. Pentagastrin and betanechol, which are known to increase the motor abnormalities in patients with diffuse oesophageal spasm (Mellow, 1977; Wexler and Kaye, 1981) have only a limited value in patients with angina-like chest pain of non-cardiac origin since these drugs were reported by Benjamin et al (1983) to induce chest pain in only 3% and 6% of these patients respectively. Ergometrine is probably the best provocative agent to induce oesophageal chest pain and motor abnormalities, with success rates reported from 22% to 60% (Dart et al, 1980; Dalal et al, 1981; Eastwood et al, 1981; London et al, 1981; Davies et al, 198221; Koch et al, 1982). However, the cardiac risks of this drug limit its use as a diagnostic test in patients suspected of having a non-life-threatening condition (Gravino et al, 1981).

Edrophonium may yield equivalent results and is much safer to use than ergometrine. Edrophonium 8&200 ,ug/kg injected intravenously was reported to induce oesophageal motor abnormalities and chest pain in 20-30% of patients (London et al, 1981; Benjamin et al, 1983; Lee et al, 1984). The test

848 J. JANSSENS AND G. VANTRAPPEN

Figure 1. Twenty-four hour pH and pressure recording system.

can safely be performed in the office. The response occurs within five minutes and ceases quickly as the drug is rapidly metabolized. Although a positive edrophonium test (motor abnormalities and symptoms) is accepted by most investigators as proof of the oesophageal origin of the pain, the intravenous administration of a relatively high dose of a cholinergic agent can hardly be considered to be a physiological provocation (in contrast with the acid perfusion test which mimics endogenous reflux).

Balloon distension

Richter et al (1986a) studied the response to intra-oesophageal balloon distension in 30 patients with non-cardiac chest pain and in 30 controls. The balloon (length = 30 mm, maximum diameter after 10 ml distension = 25 mm) was positioned 10 cm above the lower oesophageal sphincter and inflated with a progressively larger volume of air. Sixty per cent of the patients but only 20% of the controls experienced chest pain. Patients were more sensitive to a smaller volume of balloon distension. Fifty per cent of the patients had chest pain at a volume of 8 ml or less while the controls noted chest pain only at a volume of 9 ml or above. This non-pharmacological provocative test obviously warrants further study.

Prolonged recording of intra-oesophageal pressure and pH

Prolonged recording of intra-oesophageal pressure and pH is another way (besides provocation tests) to increase the chances of recording chest pain concomitantly with an episode of gastro-oesophageal reflux or oesophageal motor disorders. Therefore, our group (Vantrappen et al, 1982) has developed a new sensing, recording and analysing system that allows the continuous recording’over a 24 hour period of intra-oesophageal pH and pressures in ambulatory patients (Figure 1). The sensing probe comprises a pH glass

CHEST PAIN OF OESOPHAGEAL ORIGIN 849

electrode, an intraluminal reference electrode and three solid state pressure transducers. The probe is passed via the nose and is positioned under manometric control in such a way that pressures are measured at 3, 10 and 17 cm and pH at 5 cm above the lower oesophageal sphincter. The external diameter of the probe is 5 mm and its length 120 cm. Pressures and pH are recorded on a four-track magnetic tape of a cassette recorder that consists of pH and pressure amplifiers, a system for pulse-width modulation of the pH and for frequency modulation of the pressure signals. The magnetic tape of a commercial audio-minicassette is sufficiently long to allow a 24-hour registration period. Time multiplexing is used to record several signals on one track, i.e. the pH signal, the event-marker, an automatic calibration and a quartz clock. The sensitivity of the pH recording is 0.15 pH units. The system allows a correct registration of pressure variations up to 10 Hz. The size of the recorder is 15.5 x 9.5 x 4.5 cm and its weight is low enough (8 15 g) to be easily portable during the 24 hours of the patient’s daily routine. The patient is asked to indicate in a diary the periods of meals and sleep and to use the push button on the recorder in case of chest pain. The replay system of the recorder constructs, via a computer program, a 24-hour plot and a numerical analysis of several pH parameters. The replay system can also drive a polygraph using the pain marker as a trigger to reproduce at normal paper speed (5 mm/s) both the pH and pressure tracings, starting 10 minutes before and lasting for 15 minutes after the trigger. In this way parts of the 24-hour recording of special interest can be studied in detail.

Using this technique we have studied a group of 60 patients with angina-like chest pain of non-cardiac origin and have compared the results of this study with those obtained by conventional methods such as X-rays, endoscopy with biopsy, conventional oesophageal manometry and the acid perfusion test, using the following criteria (Janssens et al, 1986). The oesophagus was considered to be the source of the chest pain if the familiar pain sensation was reproduced by the acid perfusion test or if the pain occurred during an episode of gastro-oesophageal reflux, severe motor disorders (not occurring elsewhere on the 24-hour tracing) or both (Figure 2). The chest pain was considered to be probably of oesophageal origin when severe motor abnormalities such as achalasia, diffuse spasm or a nutcracker oesophagus were observed on conventional manometry. The mere presence of pathological reflux was considered to be of less importance for the diagnostic scoring and made the oesophageal origin of the pain only suspected. Applying these criteria to conventional investigations, the oesophagus was found to be the cause of the chest pain in 27%, a probable cause in 28% and a possible cause of the pain in 25% of the 60 patients. Analysis of the 24-hour intra-oesophageal combined pH and pressure measurement showed that episodes of chest pain were accompanied by severe motor disturbances, an episode of reflux or a combination of both in 21 of the 60 patients (35%). Eight of these 21 patients had also a positive-related acid perfusion test. When the results of the 24-hour recording were combined with those of the more conventional investigations, the final diagnostic score was as follows: the oesophagus was suspected to be the cause of the pain in 14 patients (25%) it was a probable cause ofthe pain in 10 patients (17%) and it was a likely cause in 29 patients (48%). Analogous

850 J. JANSSENS AND G. VANTRAPPEN

(b)

EVENT MARKER I

10

(cl -7

PH-1

EVENT MARKER I L

I I

P.W.

Figure 2. Replay of three short periods of 24 hour pH and pressure recordings triggered on pain (event marker). The oesophagus is considered to be the likely cause of the chest pain. (a) if the chest pain is accompanied by severe oesophageal motor disorders without reflux; (b) if the chest pain is accompanied by an episode of gastro-oesophageal reflux without motor disorders; (c) if the chest pain is accompanied by both gastro-oesophageal reflux and severe motor disorders. (The oesophageal pH was measured 5 cm above the lower oesophageal sphincter. Pressure tracings at 3, 10 and 17 cm above the lower oesophageal sphincter.)

CHEST PAIN OF OESOPHAGEAL ORIGIN 851

results have recently been published in a preliminary report by Peters et al (1986).

The 24-hour recording of intra-oesophageal pH and pressure is a physiolo- gical test and thus far the only one that allows one to decide whether the chest pain of oesophageal origin is due to motor disorders or to reflux. This distinction could be of major importance in determining the appropriate therapy.

THE IRRITABLE OESOPHAGUS

Recent observations in our laboratory suggest that there is a group of patients in whom the sensitivity of the oesophagus to various stimuli seems to be more important in the production of oesophageal pain than the disordered pathophysiological mechanism itself (Vantrappen et al, 1986; Vantrappen et al, 1987). In a group of 33 patients shown to have angina-like chest pain of oesophageal origin by the simultaneous occurrence of pain with severe motor disorders and/or gastro-oesophageal reflux on a 24-hour intra-oesophageal combined pH and pressure recording, the pain attacks were due to a spectrum of disorders varying from oesophageal motor disorders without reflux to gastro-oesophageal reflux without motor disorders. In between these two extremes was a group of 10 patients in whom the pain attacks were accompanied by the combined occurrence of motor disorders and reflux. In seven of the 10 patients the pain attacks were at times accompanied by reflux, at other times by motor disorders and at still other times by a combination of both. This indicates that an identical type of chest pain in some patients is associated with motor disorders, in others with reflux, but also that there is a group of patients in whom the similar pain attacks are associated with, and presumably due to, different disorders, i.e. reflux alone, motor disorders alone or a combination of reflux and motor disorders. Therefore, identical angina- like chest pain of oesophageal origin can be induced in the same subject by a variety of stimuli. This corresponds to our finding that a positive-related acid perfusion test is as likely to produce the typical familiar pain in patients having motor disorders only as in the group of patients having reflux (either reflux only or reflux combined with motor disorders) at the time of their spontaneous pain. It also corresponds to our observation that edrophonium may produce oesophageal motor disorders accompanied by the familiar angina-like chest pain in patients having gastro-oesophageal reflux without motor disorders at the time of their spontaneous pain. All these observations strongly suggest that there is a group of patients in whom irritability of the oesophagus plays an important role in the production of chest pain. We have called this condition irritable oesophagus.

That the oesophagus of patients with chest pain of oesophageal origin may be hypersensitive is also suggested by the work of Edwards (1974) and of Richter et al (1986a) who showed that these patients were more sensitive to smaller volumes of intra-oesophageal balloon distension than controls, in the same way as the sigmoid colon in patients with irritable bowel syndrome was

852 J. JANSSENS AND G. VANTRAPPEN

shown to be more sensitive to balloon distension than in controls (Ritchie, 1973; Whitehead et al, 1980; Kullmann and Fielding, 1981). These findings, and the observation that patients with a nutcracker oesophagus share many psychological similarities with patients with the irritable bowel syndrome, suggest that the irritable oesophagus may just be one aspect of the ‘irritable gut syndrome’ (Richter et al, 1986b).

PROVOCATION TESTS OR PROLONGED RECORDING OF INTRA-OESOPHAGEAL PRESSURE AND pH

We have recently analysed the preliminary results of a study in which 31 patients with chest pain of non-cardiac origin underwent intra-oesophageal 24-hour pH and pressure measurements as well as provocation tests with acid infusion (Bernstein test), edrophonium (80 hg/kg, i.v.) and vasopressin (2 x 20 units infused intraluminally in the oesophagus in an attempt to induce local ischaemia and chest pain. A positive test was obtained with 24-hour measurements in 13 patients (42%), with acid infusion in 11 (35%), with edrophonium in 11 (35%) and with vasopressin in five patients (16%). Twenty-one of the 3 1 patients (68%) had at least one positive examination and 16 (52%) had at least one positive provocation test. Nine of the 13 patients (69%) with a positive 24-hour measurement test also had at least one positive provocation test. However, a positive acid infusion test could be found in patients with a positive edrophonium test (a test which is accepted to specifically induce motor disturbances), a positive edrophonium test could be found in patients having only reflux without motor abnormalities at the time of their spontaneous pain, and a positive vasopressin test could be present with a positive or a negative edrophonium test and with a positive or a negative acid infusion test.

Therefore, a 24-hour pH and pressure measurement is not only the most physiological but also the most sensitive test for the diagnosis of chest pain of oesophageal origin. Moreover, it is the only test which provides reliable information on the underlying mechanism of the pain. This information may have important implications in the determination of the appropriate therapy. The fact that the angina-like chest pain of oesophageal origin was found to be related to oesophageal motor disorders in no more than 24% of the patients (Vantrappen et al, 1987) probably explains the poor results obtained with motor-blocking agents (long-acting nitrates and calcium-entry blockers) in the treatment of patients with chest pain of oesophageal origin. The chest pain of 76% of our patients was related to reflux, either alone or in combination with motor disturbances, or inducible by exogenous acid. In these patients motor-blocking agents may aggravate reflux. It would seem logical to use long-acting motor-blocking agents only in patients with pure motor disorders. In the group of patients having reflux only, treatment should be directed against acid reflux. More difficult is the treatment of the irritable oesophagus. Perhaps psychotropic drugs to decrease the visceral pain threshold may have to be combined with chronic treatment of acid reflux and short-acting motor- blocking agents for pain attacks not relieved by antacids. Further studies are

CHEST PAIN OF OESOPHAGEAL ORIGIN 853

needed to prove the value of such a therapy. Twenty-four hour combined pH and pressure measurements may well be the best method to determine the appropriate treatment.

ABOUT THE FUTURE

At present, oesophageal tests are usually only performed in patients with angina-like chest pain after a cardiac cause of the pain has been convincingly excluded, often by invasive investigations such as coronary arteriography and ergometrine provocation tests of coronary spasm.

Therefore, if a 24-hour ambulatory recording system could be developed (and work is in progress) which allows the patient to indicate pain episodes on a simultaneous recording of intra-oesophageal pressure and pH and of a multichannel electrocardiogram (ECG) with reliable ST-T segment regis- tration, it is to be expected that many unnecessary coronarographies could be avoided. At the same time, a positive diagnosis of the oesophageal origin of the angina-like chest pain would be provided.

SUMMARY

Angina-like chest pain of non-cardiac origin is a major diagnostic and therapeutic problem. The oesophagus is frequently suspected to be the cause of the chest pain in these patients. However, a positive statement for the oesophageal origin of the pain can only be made when during manometry or pH-monitoring the familiar pain attack appears to be accompanied by reflux, severe motor disorders or a combination of both. Due to the intermittent nature of the pain this is only rarely the case during short-listing conventional examinations. Provocation tests have been used to induce the familiar chest pain. The Bernstein acid perfusion test and the edrophonium test yield the best results. Prolonged (24-hour) ambulatory recording of intra-oesophageal pressure and pH to increase the chances of recording chest pain concomitantly with an episode of reflux and/or motor disorders appears to be the most sensitive and also the most physiological test. It is the only test that provides reliable information on the underlying mechanism of the pain, especially in patients with the syndrome of irritable oesophagus, thus contributing in establishing the appropriate therapy for these patients.

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