SciELO - Scientific Electronic Library Online

vol.96 número9Diagnóstico de la infección por Helicobacter pylori mediante el test rápido de la ureasa en pacientes con hemorragia por úlcera duodenal: influencia de los signos endoscópicos de sangrado y de la obtención simultánea de biopsias de cuerpo y antro gástrico índice de autoresíndice de materiabúsqueda de artículos
Home Pagelista alfabética de revistas  

Servicios Personalizados




Links relacionados


Revista Española de Enfermedades Digestivas

versión impresa ISSN 1130-0108

Rev. esp. enferm. dig. vol.96 no.9 Madrid sep. 2004




Chest pain of esophageal origin


Chest pain of non-coronary origin is a commonly difficult to solve clinical issue. Once coronary causes have been ruled out, many other origins still remain to be investigated regardless of clinical presentation. First, cardiac (mitral valve prolapse, pericarditis, hypertrophic cardiomyopathy, aortic stenosis, aortic dissecting aneurysm), pulmonary (pleuritis, pneumothorax, tracheobronchitis), mediastinal (mediastinitis), musculoskeletal (rupture, muscle distension and overload, osteochondritis -Tietze's syndrome-, intercostal neuritis, cervical or dorsal spine osteoarthritis), and psychogenic (stress, panic disorders) causes should be excluded. Thence we may consider potential gastrointestinal origins, among which esophageal conditions clearly predominate in both their most common modalities: gastroesophageal reflux with or without lesions, and motor disorders. Other causes such as gastroduodenal ulcer, functional dyspepsia, and biliary lithiasis are not so frequent, but pancreatitis may sometimes present with chest pain events.

The reason why so many clinical conditions may result in a common complaint should be sought in the pathophysiologic grounds of chest pain, where various types of pain may exist - local visceral pain, which is felt as a poorly-localized, deep pain around the esophagus that may be referred to the sternal area, and referred visceral pain, which is felt on the body surface in association with skin hyperalgesia. The latter is mainly seen in conditions involving the lower esophagus, and may be referred to the back, upper chest, neck, maxillary angles, and even arms, thus simulating heart ischemia. There is also secondary visceral pain, where a stimulus from a different viscus travels a reflex path to result in a functional disorder here. This secondary pain becomes particularly relevant through cardiac-esophageal vago-vagal reflexes, a fact that already drew considerable attention many years ago (1). More recent studies even suggested the role spinal trapezium muscle stimulation may play, inducing similar situations for both the esophagus and the heart (2).

As far as the esophagus is concerned, the presence of thermoreceptors, mechanoreceptors, and chemoreceptors should be born in mind. The role of the former is poorly understood (cold, warm, and mixed receptors), not so the role of the remaining two. Mechanoreceptors may be either vagal or spinal, with spinal receptors being nociceptors that still fail to be spotted at the mucosa. Within the esophageal smooth muscle neural structures (intraganglionic laminar endings) have been found that are identified as mechanoreceptors. As regards chemoreceptors, they have not been precisely located at the mucosa; however, they are not apparently superficial since many local anesthetics fail to modify acid-induced pain responses, a fact that has been acknowledged for more than 40 years now (3).

An important aspect is pain perception, as pain responses are not always alike for equal stimuli. Pain threshold varies among subjects, and factors are believed to exist that may play a role in pain perception. More recent studies conclude that chest pain of esophageal origin results from abnormal nociception. This has been demonstrated using evoked tests such as edrophonium provocation and balloon distension, but it is also true that selected patients with heart disease, as is the case with microvascular angina, exhibit a similar behavior.

Chest pain affects 12.4% of the Spanish population according to a recent epidemiologic study performed by us (4,5), and 22% in association with characteristic heartburn symptoms. This means that this clinical condition is much more frequent than previously thought. Studies performed to this day, particularly in the United States, show that 10-30% of patients with angina have normal coronary arteries in angiographic studies (6). No explaining causes can be detected in 40% of such patients, and most studies consistently point out that 18-58% of cases result from esophageal causes. Such cases (7,8) should be searched for a mechanic etiology (achalasia, diffuse esophageal spasm, nutcracker esophagus, hypertensive lower esophageal sphincter), or for a chemical effect, as is the case with gastroesophageal reflux, which back in 1982 DeMeester (9) estimated was responsible for 40% of patients with chest pain and normal coronaries. Many of these cases simply exhibit hypersensitivity to acid and are labeled hypersensitive esophagus (10,11). Lastly, one should search for a mixed effect, which is much more common than previously estimated. One should not forget that a number of complex patients may have intricate causes and exhibit, say, both esophageal changes and ischemic heart disease. These are rare, often difficult-to-manage cases. Many cardiologists prescribe PPIs to patients undergoing procedures for coronary obstruction whose pain persists, with good results. An in-depth study of such patients -who are usually referred to us at specialized units- should be carried out with a careful work-out and recourse to all those specialized tests a modern motility unit should have access to.

No single technique should be discarded since cases are all distinct; pain should be ideally evoked or induced in every test. In such cases esophageal manometry -either stationary or ambulatory- as well as 24-hour pH-metry, and evoked tests are mandatory. For other patients endoscopy is required, as less commonly is radiography or radionuclide testing.

The study by Ciriza de los Ríos et al. (12) published in this issue deals with the role of stationary esophageal manometry in patients with non-cardiac chest pain, reflux, and dysphagia. The authors report that 42.2% of patients with non-cardiac CP had normal manometry results, whereas the remaining 57.8% had abnormal results. Amongst the latter 19.2% had symptomatic peristalsis, 53.8% had a hypotensive LES, and the rest had nonspecific changes. Patients with a hypotensive LES may be thought of as having reflux, and 24-hour pH-metry might have well clarified a relevant number of painful events. These same authors reject stationary manometry as a single test in the diagnosis of such patients, but they also claim it provides truly valuable information that is even conclusive on occasion. When this or a similar test is not available, testing with omeprazole (13,14) or any other PPI at high doses may solve doubts and yield a diagnosis of GERD-induced CP.

Anyway, CP of esophageal origin is sometimes a difficult-to-manage condition. Even GER cases responding to PPI therapy resemble so much an angina event in a patient with coronary heart disease that a number of affected individuals remain doubtful, and are thus apt to seek help more frequently in clinics, or even in hospital emergency rooms. Management will depend on the existing cause, and PPIs will be naturally of choice for GERD; unresponsive patients may have recourse to surgery or other reconstructive endoscopic procedures. For motor disorders nifedipine and diltiazem may be effective, and selected psychodrugs such as trazodone may come in handy on occasion. Pain improvement has been recently reported in patients with motor disorders following an injection of botulinum toxin at the gastro-esophageal junction (15), but further studies are needed to confirm this option. Patient follow-up is sometimes complex and should be performed on a rigorously monitored tailored basis (16), since chest pain bears a strong cultural link with the heart; making the patient understand that his or her pain may be due to non-cardiac causes is therefore not always an easy task.

M. Díaz-Rubio

Service of Digestive Diseases.
Hospital Clínico de San Carlos. Madrid. Spain



1. Rasmussen K, Funch-Jensen P, Ravnsbaek J, Bagger JP. Oesophageal spasm in patients with coronary artery spasm. Lancet 1986; 1: 174-6.

2. Jou CJ, Farber JP, Oin C, Foreman RD. Convergent pathways for cardiac - and esophageal- somatic motor reflexes in rats. Auton Neurosci 2002; 99: 70-7.

3. Hoockman P, Siegel CL, Heindrix TR. Failure of oxethazine to alter acid-induced esophageal pain. Dig Dis Sci 1966; 11: 811-3.

4. Díaz-Rubio M, Moreno Elola-Olaso C, Rey E, Locke GR III, Rodríguez-Artalejo F. Simptoms of gastro-oesoghageal reflux: prevalence, severity, duration and associated factors in a Spanish population. Aliment Pharmacol Ther 2004: 19: 95-105.

5. Rey E, Moreno C, Rodríguez-Artalejo F, Locke GR, Díaz-Rubio M. Association between typical and atypical symptoms of gastroesophageal reflux: a population-based study in Spain. Gastroenterology 2003; 124: A166.

6. Van Dorpe A, Piessens J, Willems JL, De Geest H. Unexplained chest pain with normal coronary arteriograms. A follow-up study. Cardiology 1987; 74: 436-43.

7. Richter JE. Oesophageal motility disorders. Lancet 2001; 358: 823-8.

8. DeMeester TR, O'sullivan GC, Bermúdez G, Midell AI, Cimochowski CE, O'Drobinak J. Esophageal function in patients with angina-type chest pain and normal coronary angiograms. Ann Surg 1982; 196: 488-98.

9. Dekel R, Pearson T, Wendel C, De Garmo P, Fennerty MB, Fass R. Assessment of oesophageal motor function in patients with dysphagia or chest pain - the Clicical Outcomes Research Initiative experience. Aliment Pharmacol Ther 2003; 18: 1083-9.

10. Álvarez Sánchez A, Rey E, Alba C, Díaz-Rubio M. Association between gastro-oesophageal reflux and chest pain. Is acid chemosensitivity the underlying mechanism? GUT 2003; 52 (Supl. VI): A99.

11. Rao SS, Hayek B, Mundipalli R, Gregersen H. Does esophageal function vary at the striated and smooth muscle segments in functional chest pain? Am J Gastroenterol 2002; 97: 2201-7.

12. Ciriza de los Ríos C, García Menéndez L, Díez Hernández, Delgado Gómez M, Fernández Eroles AL, Vega Fernández A, et al. Papel de la manometría esofágica estacionaria en la práctica clínica. Resultados manométrico en pacientes con reflujo gastroesofágico, disfagia y dolor torácico no cardiaco. Rev Esp Enferm Dig 2004; 96: 606-11.

13. Fass R, Fennerty MB, Ofman JJ, Gralnek IM, Johnson C, Camargo E, et al. The clinical and economic value of a short course of omeprazole in patients with noncardiac chest pain. Gastroenterology 1998; 115: 42-9.

14. Bautista J, Fullerton H, Briseno M, Cui H, Fass R. The effect of an ampirical trial of high-dose lansoprazole on symtom response of patients whith non-cardiac chest pain- a randomized, double-blind, placebo-controlled, crossover trial. Aliment Pharmacol Ther 2004; 19: 1123-30.

15. Miller LS, Pullela SV, Parkman HP, Schiano TD, Cassidy MJ, Cohen Fisher RS. Treatment of chest pain in patient with noncardiac, nonreflux, nonacalasia spastic esophageal motor disorders using botulinum toxin injection into the gastroesophageal junction. Am J Gastroenterol 2002; 97: 1640-6.

16. Rey Díaz-Rubio E, Roncero García-Escribano O, Álvarez Sánchez A, Díaz-Rubio M. Evolución a largo plazo del dolor torácico no cardiaco. Rev Esp Enferm Dig 2002; 94: 25-9.

Creative Commons License Todo el contenido de esta revista, excepto dónde está identificado, está bajo una Licencia Creative Commons