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The incidence of oesophageal dysfunction (OD) is higher in patients with coronary heart disease (CHD) than in a population sample. The hypothesis was raised that this finding is the result of a cardio-oesophageal reflex in which afferent pain impulses from the heart trigger dysfunction in the oesophagus. Twenty-three patients with CHD were examined before and 14+/-5(S.D.) months after coronary bypass surgery. Total relief of angina pectoris was attained in 6 patients and improvement in 16. One patient deteriorated. The incidence of OD was 52% before operation and 65% at the follow-up investigation (no significant difference). Symptoms related to the oesophagus, other than chest pain, were as frequent before as after operation. The findings do not support the contention that OD in patients with CHD is caused by a cardio-oesophageal reflex.

Oesophageal dysfunction (OD) is a common finding in patients discharged from a coronary care unit without definite diagnosis. Of 55 patients investigated with oesophageal manometry, acid perfusion test and exercise ECG, 32 had signs of OD and 19 signs of ischaemic heart disease (IHD). Symptoms such as heart burn, acid regurgitations, feeling of a lump in the throat, surfeitness after meals, chest pain at night, and relief of chest pain when lying with the head raised were significantly more common in patients with OD than in patients with normal oesophageal function. Chest pain was significantly more often provoked by effort, emotions or cold and more often relieved by nitroglycerine in patients with signs of IHD than in those without. These pain-provoking factors were, however, also common in patients with OD. A careful case history with specific inquiry directed at not only cardiac but also oesophageal symptoms is important in the differential diagnosis of chest pain.

Oesophageal function and symptoms were investigated in 52 male patients 2-6 months after an acute myocardial infarction. Oesophageal function was tested by manometry, pH recording and acid perfusion test. Signs of oesophageal dysfunction (OD) were found in 17 patients (33%). This frequency did not differ significantly from that in a random male population sample, but was lower than in a group of male coronary care unit patients with no signs of a new or earlier myocardial infarction at discharge from hospital (p less than 0.05). All but two patients affirmed chest pain by questionnaire. At a verbal interview, 38 patients (73%) had a history of angina pectoris after discharge from hospital. Thirty-five (92%) of these patients had an ischaemic ECG reaction and/or recurrence of their anginal chest pain during the exercise test, one of them also had evidence of oesophageal origin of his chest pain. There were no signs of OD in the remaining three patients with a history of angina pectoris. Therefore, OD does not constitute a common problem in the differential diagnosis of anginal chest pain in patients with recent myocardial infarction.

Twenty-eight male patients referred to work ECG due to chest pain, all with a positive oesophageal symptom questionnaire believed to detect oesophageal dysfunction (OD), have been subjected to a graded work test and an oesophageal manometry test and answered a questionnaire believed to detect effort angina. Ischaemic heart disease (IHD) was defined as earlier infarction on ECG at rest or a pathological effort ECG. OD was defined as a positive acid perfusion test, hernia or a clear dysmotility in combination with a lower sphincter incompetence. Twenty patients had a positive effort angina questionnaire. Among these, OD was more common (n = 13) than IHD (n = 8). Five of the 20 patients had signs of both IHD and OD. Eight patients had a negative effort angina questionnaire; OD was found in 7 and IHD in 1 of these patients. It is concluded that in cases with angina-like chest pain OD should be considered.

Out of 121 patients referred to a work test on account of chest pain, 67 with a case history typical for oesophageal dysfunction have been further investigated with an acid perfusion test during continuous ECG monitoring. Neither arrhythmias nor ST-T changes were induced by the procedure. Of the 67 patients, 6 had a "positive related" acid perfusion test, 23 a "positive unrelated" and the remainder a negative test. Five of the 14 patients with pathological effort ECG belonged to the group with a positive acid perfusion test. The acid perfusion test, as a safe routine in close connection with the effort ECG in selected patients, is a useful technique for establishing whether or not the patient's symptoms have an oesophageal component.

Among 55 consecutive coronary care unit (CCU) patients with chest pain of unknown origin at discharge from hospital, signs of oesophageal dysfunction (OD) were found in 58% and signs of ischaemic heart disease (IHD) in 35% within 2-6 months. At a three-year follow-up, signs of OD were found in 62% and signs of IHD in 28%. Forty-six patients (84%) had experienced a pain similar to that which caused the CCU admission (i.e. the CCU chest pain). OD was regarded as the cause of the CCU chest pain in seven patients (13%) and as a possible cause in another nine (16%). IHD was regarded as the cause of the CCU chest pain in 17 patients (31%), four of whom had died from acute myocardial infarction during the follow-up period. All ten patients who developed coronary events, such as myocardial infarction or progressive angina pectoris, during the follow-up period had an ischaemic ECG reaction at exercise test 2-6 months after discharge from the CCU. IHD was found to be the predominant disease in terms of severity of symptoms and prognosis and was also recorded as the most common single cause of the CCU chest pain. Since OD was common and even caused severe chest pain in some patients, oesophageal origin should be considered in the differential diagnosis of chest pain in non-infarction CCU patients.

A possible relationship between heart disease, oesophageal dysfunction (OD) and symptomatology was studied in 47 patients with valvular heart disease. They were investigated with oesophageal manometry and oesophageal acid perfusion test. OD was found in 32 percent of the patients. A local pressure increase in the middle part of the oesophagus, probably an effect of cardiac enlargement and compression of the oesophagus, was found at manometry in 38 percent. The incidence of OD and of oesophageal symptoms was the same in patients with and without oesophageal compression. We did not find any indications that valvular disease in itself provokes OD, nor that symptoms of chest pain and cough in patients with valvular heart disease are due to OD.

Sixty-four patients with a history of disabling chest pain belonging to groups III or IV classified according to the NYHA criteria were examined with oesophageal function tests, coronary angiography and bicycle ergometry and also answered a symptom questionnaire. At the exercise test, 52 had effort angina; 45 (89%) of them had a pthological coronary angiogram and 22 (42%) had signs of oesophageal dysfunction (OD). OD as the single possible etiological factor for typical effort angina therefore seemed unlikely. Chest pain was absent or atypical at the exercise test in 12 patients, 11 (92%) of whom had signs of OD. This incidence is significantly higher (p less than 0.01) than that found in the patients with effort-related chest pain. Five (42%) of the 12 patients with atypical chest pain at the exercise test had a pathological coronary angiogram, an incidence which is significantly lower (p less than 0.001) than that found in the group with effort-related chest pain. In patients with a history of disabling chest pain but with atypical chest pain in connection with the exercise test, OD was more frequent than coronary disease and therefore more likely to have caused the symptoms.