Left ventricular function and oesophageal function in patients with angina pectoris and normal coronary angiograms

Left ventricular function and oesophageal function (including oesophageal manometry and pH monitoring) were investigated and a psychiatric assessment carried out in 63 patients with angina pectoris and normal coronary angiograms. Twenty two (35%) patients had regional abnormalities of left ventricular wall motion (group A). Thirty six (57%) patients had an oesophageal abnormality (group B); 19 patients had gastro-oesophageal reflux and abnormal oesophageal motility, five had gastro-oesophageal reflux alone, and 12 had abnormal oesophageal motility alone. Only four had regional abnormalities of the left ventricular wall and abnormal oesophageal function. In nine (14%) patients left ventricular and oesophageal function were normal (group C). Psychiatric morbidity was significantly less common in group A than in groups B and C and was similar in group B and group C. A definite abnormality of left ventricular function, oesophageal function, or psychiatric morbidity is present in a high proportion of patients with angina pectoris and normal coronary angiograms and in some instances this may lead to specific treatment. If quantitative assessment of left ventricular function is normal, oesophageal investigations should be performed. Endoscopy of the upper gastrointestinal tract may demonstrate oesophageal disease, but, if findings are normal, oesophageal manometry and ambulatory oesophageal pH monitoring (including during treadmill exercise testing) should be carried out.     

Left ventricular function and oesophageal function in patients with angina pectoris and normal coronary angiograms.

Left ventricular function and oesophageal function (including oesophageal manometry and pH monitoring) were investigated and a psychiatric assessment carried out in 63 patients with angina pectoris and normal coronary angiograms. Twenty two (35%) patients had regional abnormalities of left ventricular wall motion (group A). Thirty six (57%) patients had an oesophageal abnormality (group B); 19 patients had gastro-oesophageal reflux and abnormal oesophageal motility, five had gastro-oesophageal reflux alone, and 12 had abnormal oesophageal motility alone. Only four had regional abnormalities of the left ventricular wall and abnormal oesophageal function. In nine (14%) patients left ventricular and oesophageal function were normal (group C). Psychiatric morbidity was significantly less common in group A than in groups B and C and was similar in group B and group C. A definite abnormality of left ventricular function, oesophageal function, or psychiatric morbidity is present in a high proportion of patients with angina pectoris and normal coronary angiograms and in some instances this may lead to specific treatment. If quantitative assessment of left ventricular function is normal, oesophageal investigations should be performed. Endoscopy of the upper gastrointestinal tract may demonstrate oesophageal disease, but, if findings are normal, oesophageal manometry and ambulatory oesophageal pH monitoring (including during treadmill exercise testing) should be carried out.     

A prospective study of oesophageal function in patients with normal coronary angiograms and controls with angina

Aims—To compare the incidence of oesophagealabnormalities and their correlation with chest pain in patients withnormal coronary angiograms, and in controls with angina.
Patients—Sixty one patients with normal coronaryangiograms (NCA group) referred to a single cardiac centre betweenMarch 1990 and April 1991; 25 matched controls with confirmed coronary artery disease (CAD group).
Setting—Cardiac referral centre and oesophagealfunction testing laboratory.
Main outcome measures—Oesophageal manometry,provocation tests, and 24 hour ambulatory pH monitoring.
Results—Simultaneous contractions were morecommon (6.7% versus 0.8%, p<0.01), and the duration of peristalticcontractions was longer (2.9 versus 2.4 seconds, p<0.01) in the NCAgroup than in the CAD group. There were no group differences in theamplitude of peristaltic contractions, and none had nutcrackeroesophagus. Ten (16%) patients with NCA and no patients with CAD haddiffuse spasm (p=0.03). Twenty one (34%) patients with NCA, and five(20%) patients with CAD had abnormal gastro-oesophageal reflux(p>0.05). There was no significant difference between the groups inthe number of patients whose pain was temporally related to pH events. Particular chest pain characteristics, or the presence of additional oesophageal symptoms, were not predictive of an oesophageal abnormality.
Conclusion—Oesophageal function testscommonly implicate the oesophagus as a source of pain in patients withnormal coronary angiograms. With the exception of simultaneouscontractions during manometry however, the incidence of abnormalitiesand in particular the correlation of pH events with chest pain are ascommon in patients with normal coronary angiograms as in controlswith angina. The oesophagus may often be an unrecognised source of painin both groups of patients.

Keywords:oesophageal function; coronary artery disease; chest pain

     

Investigation and management of non-cardiac chest pain

Recurring substernal chest pain is an important clinical problem, causing anxiety for patients and their physicians because of the fear of possible cardiac disease. The differential diagnosis includes coronary artery disease, oesophageal disorders such as acid reflux disease and motility disturbances, musculoskeletal problems, psychological disorders including panic attacks, and a new 'fly in the ointment'--microvascular angina. History alone usually cannot distinguish cardiac from non-cardiac chest pain. After exclusion of significant coronary artery disease, attention must be turned to oesophageal disorders, which may be seen in as many as 50% of these patients. Oesophageal motility disorders, particularly the nutcracker oesophagus, are common, but the relationship between pain and abnormal contraction pressures is not well established. Provocative tests such as edrophonium (Tensilon) and balloon distension help to identify the oesophagus as the source of chest pain but do not direct therapy. Recent studies with ambulatory oesophageal monitoring suggest that gastro-oesophageal reflux may be a more common cause of chest pain than motility disorders. This is an important finding as acid reflux is a treatable problem, while therapies for motility disorders may only worsen reflux disease. The recent observation that oesophageal disorders are frequently associated and interact with psychological disorders such as anxiety, depression, somatization and panic attacks complicates the evaluation and understanding of chest pain. How these various abnormalities may be linked is an unresolved issue. Increased central nervous system stimulation and altered visceral and/or central pain sensitivity could be the common factors. It is hoped that further research into these areas will lead to new understandings of and possible solutions to the complex problem of non-cardiac chest pain.     

Gastroesophageal reflux in patients with angiographically normal coronary arteries: an uncommon cause of exertional chest pain.

OBJECTIVES--To investigate the association between exertional chest pain and gastroesophageal reflux in patients with normal coronary angiograms and in controls by measuring oesophageal pH during treadmill exercise tests and to compare the results with routine ambulatory monitoring. DESIGN--Case control study. SETTING--Tertiary referral cardiac unit. PATIENTS--50 consecutive patients with chest pain and completely normal coronary angiograms and 16 controls with coronary artery stenoses. MAIN OUTCOME MEASURES--Episodes of acid reflux and chest pain during treadmill exercise; a symptom index expressing the percentage of episodes of pain related to acid reflux during ambulatory monitoring. RESULTS--Four (8%) patients and two (12%) controls had reflux during treadmill exercise (NS). 32 (64%) and 16 (100%) reported chest pain, but only three (6%) and two (12%) had coincident reflux (NS). Reflux was as frequent before, during, and after treadmill exercise (five (8%) v six (9%) v two (3%)) in the 66 subjects; (NS). 19 (38%) patients and three (19%) controls had abnormal reflux on ambulatory monitoring (NS). Eight (16%) and three (19%) had a symptom index > 50%, but six and two of these reported pain without coincident reflux during treadmill exercise. CONCLUSION--There are many potential causes of chest pain in patients with angiographically normal coronary arteries. Although gastroesophageal reflux is commonly implicated and many patients have a high incidence of spontaneous reflux during ambulatory monitoring, it rarely occurs during exertion and the association with chest pain is poor.     

Oesophageal motility disorders

Oesophageal motility disorders comprise various abnormal manometric patterns which usually present with dysphagia or chest pain. Some, such as achalasia, are diseases with a well defined pathology, characteristic manometric features, and good response to treatments directed at the pathophysiological abnormalities. Other disorders, such as diffuse oesophageal spasm and hypercontracting oesophagus, have no well defined pathology and could represent a range of motility changes associated with subtle neuropathic changes, gastro-oesophageal reflux, and anxiety states. Although manometric patterns have been defined for these disorders, the relation with symptoms is poorly defined and the response to medical or surgical therapy unpredictable. Hypocontracting oesophagus is generally caused by weak musculature commonly associated with gastro-oesophageal reflux disease. Secondary oesophageal motility disorders can be caused by collagen vascular diseases, diabetes, Chagas' disease, amyloidosis, alcoholism, myxo-oedema, multiple sclerosis, idiopathic pseudo-obstruction, or the ageing process.     

Chest pain as a predictor of coronary artery disease in patients with obstructive aortic valve disease

To clarify the association between chest pain and significant coronary artery disease in patients who have aortic valve disease, 76 consecutive candidates for aortic valve replacement were evaluated prospectively with use of a historical questionnaire and coronary arteriography. Of the 76 patients, 19 (25 percent) had no chest pain, 21 (28 percent) had chest pain that was not-typical of angina pectoris and 36 (47 percent) had chest pain typical of angina pectoris. In 18 of 19 patients the absence of chest pain correlated with the absence of coronary artery disease. The single patient without chest pain who had coronary artery disease had evidence of an inferior myocardial infarction in the electrocardiogram. Thus, absence of chest pain and the absence of electrocardiographic evidence of infarction predicted the absence of coronary disease in all cases.

The presence of chest pain did not predict the presence of coronary artery disease, but the more typical the pain of angina pectoris the more likely were patients to have significant coronary artery disease. Of the 21 patients with atypical chest pain, 6 (29 percent) had coronary artery disease, but of the 36 patients with typical angina pectoris 23 (64 percent) had significant coronary artery disease. In addition, when patients with chest pain not typical of angina pectoris also had coronary artery disease, the diseased vessels usually supplied smaller areas of the left ventricle than when the pain was typical of angina pectoris. In 21 of 23 patients (91 percent) with typical angina pectoris and significant coronary artery disease, lesions were present in the left coronary artery. There was no systolic pressure gradient across the aortic valve that excluded the presence of coronary artery disease, although all patients with a calculated aortic valve area of less than 0.4 cm² were free of coronary artery disease. Patients with severe left ventricular dysfunction were more likely to have normal coronary arteries.     

Acute noncardiac chest pain in a coronary care unit. Evaluation by 24-hour pressure and pH recording of the esophagus.

Twenty-four-hour recording of esophageal pressure and pH was performed successfully in 41 patients admitted to the coronary care unit of a general hospital who had an episode of acute, prolonged retrosternal chest pain and who were initially suspected of suffering from coronary artery disease (severe angina pectoris, myocardial infarction), but in whom the pain was subsequently shown not to be of cardiac origin. The recordings were analyzed with fully automated techniques. A pain episode was considered to be related to abnormal esophageal motility when contraction amplitudes or durations in the pain episode exceeded the patient's upper limit of normal (97.5th percentile) or when the proportion of abnormal propagated contractions (simultaneous, nontransmitted) in the pain episode was significantly increased (chi 2 test). Thirty patients (73%) had one or more pain episodes (in total 63 pain episodes) during the 24-hour recording. Forty-three percent of the pain episodes was related to abnormal motility and 30% to reflux, and 27% was not related to esophageal function disturbance. Using the criterium that the symptom index had to be greater than or equal to 75%, it was found that the pain was related to reflux in 13 patients (43%) and to motor abnormalities in 10 patients (33%). It is concluded that in the majority of patients acutely admitted with noncardiac chest pain, esophageal motor abnormalities and reflux can be shown to be the likely cause of the symptoms.     

Musculo-skeletal pathology in patients with angina pectoris and normal coronary angiograms

PURPOSE: To evaluate the role of the musculo-skeletal apparatus in patients with angina pectoris despite normal coronary angiograms. DESIGN: A survey of patients and controls investigated by blinded observers. SETTING: A tertiary cardiologic referral centre. SUBJECTS: Thirty women and 18 men (mean age 52.9 years) with chest pain of an average duration of 3 years and 11 months were investigated. All had normal resting electrocardiograms. No patients showed evidence of left ventricular hypertrophy or valvular heart disease on echocardiography and all had a normal coronary angiogram. All had left ventricular ejection fraction > 50%, and none had signs of coronary vasospasm. Eighteen healthy persons (10 women and eight men, mean age 51.2 years) served as controls. MAIN OUTCOME MEASURES: The group frequency of chest wall complaints, spinal radiograph and physical examination findings; pressure pain thresholds. RESULTS: The patients had significantly more complaints of pain from the neck, chest, and thoracic spine, and sensations and pain radiating to the arms than the controls. The patients had more degenerative findings on radiograph than the controls, mainly at levels C4-C7. Physical examination showed that abnormal findings were significantly more frequent in patients than in the control group in the anterior and posterior chest wall, in the spine at levels Th1-Th6 and in the muscles of the neck and shoulder girdle. There were no statistically significant differences in pain thresholds or in neurological examination. CONCLUSION: The musculo-skeletal abnormalities observed in the patients could include reflex mechanisms. Whether the abnormal findings are mainly responsible for the angina pectoris symptoms or merely epiphenomena warrants further study.     

Ambulatory 24 hour intraoesophageal pH and pressure recordings v provocation tests in the diagnosis of chest pain of oesophageal origin.

Fifty patients with non-cardiac chest pain underwent 24 hour intraoesophageal pH and pressure recording and provocation tests to determine the relative value of both techniques in establishing the oesophageal origin of the chest pain. Twenty six patients (52%) had at least one positive provocation test: the acid perfusion test was positive related in 18 patients (36%), the edrophonium test in 16 patients (32%), the vasopressin test in five patients (10%), and the balloon distension test (performed in only 20 patients) in one (5%). The 24 hour pH and pressure recording correlated spontaneous chest pain attacks with abnormal motility or gastro-oesophageal reflux in 19 patients (38%). Fourteen of these patients also had at least one positive provocation test. Therefore, 24 hour pH and pressure recordings are only slightly better than a set of provocation tests in identifying the oesophagus as the cause of chest pain (10% diagnostic gain). In the case of oesophageal chest pain, however, 24 hour recording appeared to be the only way to identify the nature of the underlying oesophageal abnormality that caused the spontaneous pain attacks--for example, gastro-oesophageal reflux, motility disorders, or irritability of the oesophagus.     

Angina pectoris with normal coronary angiograms

Of patients with angina pectoris who undergo cardiac catheterization, angiographically normal-appearing coronary arteries are found in a significant minority. Multiple etiologies have been proposed to explain chest pain in this setting, including psychiatric illness, esophageal motility disorders or acid reflux, and limited coronary flow response to stress. A fundamental abnormality in this patient population may be abnormal visceral pain perception. Evidence for and against various etiologies as well as a management strategy for the patient with chest pain are presented in this article, both with respect to the decision for performing cardiac catheterization and the management after demonstration of angiographically normal coronary arteries.     

High prevalence of gastroesophageal reflux in patients with clinical unstable angina and known coronary artery disease

OBJECTIVES: Esophageal disease may mimic acute anginal pain. However, the prevalence of gastroesophageal reflux in the acute setting of patients with clinically unstable angina (UA) pectoris is not known. The aim of this study was to determine the co-existence of coronary artery disease (CAD) and gastroesophageal reflux in UA, and to study the feasibility of esophageal investigation in the chest pain unit. DESIGN: 22 patients with clinical UA and confirmed CAD were monitored by continuous vector cardiography and pH-measurement during 24 h of observation. Symptoms of chest pain and episodes of ischemia and reflux were recorded. RESULTS: 11 patients (50%) showed abnormal gastroesophageal reflux and another three (14%) had an increased number of reflux episodes. pH-measurements and esophageal manometry were well tolerated. Few chest pain episodes were recorded during the study period, and no association between chest pain, reflux, and ischemia could be shown. CONCLUSION: Esophageal reflux is common in patients with UA and established CAD. As reflux-related chest pain may imitate angina pectoris, it is clinically important that gastroesophageal examination in patients with UA seems to be feasible and well tolerated in the 'acute setting'.     

Esophageal motility in cases of chest pain with normal coronarography

The aim of this study was to assess the incidence of oesophageal abnormalities and to determine their nature in patients with retrosternal chest pain and normal coronary angiography with a negative coronary spasm provocation test. Oesophageal manometry was carried out in all cases with or without a spasm provocation (usually alkalosis) test. Forty consecutive patients were studied: 19 men (47.7 +/- 10.0 years) and 21 women (54.7 +/- 7.5 years). A history of gastro-intestinal disorder was obtained in 57 p. 100 of cases (hiatal hernia and/or gastro-oesophageal reflux, biliary lithiasis and/or cholecystectomy, gastritis). Seventeen patients had broad based powerful oesophageal contractions which are an established cause of pain; they were recorded under basal conditions in 5 cases and after a provocation test in 12 cases. Two patients had a megaoesophagus without giant waves. Thirteen patients had manometric signs of reflux (malposition and hypotonia of the lower oesophageal sphincter) of whom 7 had giant waves on provocation. In addition, three patients experienced pain during gastro-oesophageal reflux (1 case) or hypotonia of the lower oesophageal sphincter (2 cases). In all, a very probable oesophageal origin of the chest pain was demonstrated in 22 patients (55 p. 100 of cases).     

Abnormal gastro-oesophageal reflux in Chinese with atypical chest pain

Although atypical chest pain has been well described in the Western population, its frequency in Chinese is unknown. Over a period of 42 months, we studied 521 Chinese patients with chest pain and identified 108 patients (20.7%) whose pain was not related to cardiac causes, as determined by exercise ECG or cardiac catheterization. Using 24 h ambulatory pH monitoring and baseline oesophageal manometry, 28.7, 19.4 and 5.6% of these patients were found to have abnormal reflux parameters, abnormal manometric findings or both, respectively. There were significantly more patients complaining of chest pain during the study in the gastro-oesophageal reflux disease (GERD) group than in the non-GERD group (16/31 vs 20/77; P< 0.001). The lower oesophageal sphincter pressure was lower in those with abnormal reflex parameters than in those with normal reflux parameters (12.7±5.4 vs 17.8±5.8 mmHg; P< 0.05). There was no significant difference in symptoms, such as heartburn (54.8 vs 42.9%), regurgitation (38.7 vs 35.1%) and dysphagia (19.4 vs 24.7%), among the two groups. Non-specific changes were the most frequent baseline motility pattern. In conclusion, atypical chest pain and gastro-oesophageal reflux disease are not uncommon in Chinese and this deserves special emphasis as the continuation of anti-anginal drugs may aggravate their condition.     

Follow-up study of morbidity in patients with angina pectoris and normal coronary angiograms and the value of investigation for esophageal dysfunction

A postal questionnaire was used to assess the symptoms, use of medical facilities, and employment status of patients with angina pectoris and normal coronary angiograms following cardiac catheterization. In a retrospective study of 187 patients, 66 had left ventricular dysfunction demonstrated by abnormal regional wall motion and 121 had normal left ventricular function. At follow-up twelve to forty-six months following catheterization, 89% with left ventricular dysfunction and 82% with normal ventricular function had continued to experience chest pain. There was no significant change in the admission rate to hospital because of chest pain or the proportion of patients who were working, after catheterization as compared with before, in either group. Some patients with left ventricular regional wall motion abnormalities appeared to have progressive left ventricular dysfunction. In a prospective study of 63 patients, detailed investigation of esophageal function was performed. Twenty-two patients had left ventricular wall motion abnormalities. The majority of the 41 patients with normal left ventricular wall motion had esophageal abnormalities that were treated appropriately. At follow-up six to twenty-four months following catheterization significantly fewer patients with normal left ventricular function continued to experience chest pain compared with those with left ventricular dysfunction. Following catheterization the hospital admission rate fell significantly and the proportion of patients working increased significantly in the group with normal left ventricular function. The hospital admission rate and employment status of patients with left ventricular dysfunction did not change significantly following angiography. These findings suggest, therefore, that investigation for and treatment of esophageal dysfunction should be performed in patients with angina pectoris, normal coronary angiograms, and normal left ventricular function.     

Prevalence of coronary disease in patients with aortic stenosis]

We analyzed a consecutive series of 188 patients, older than 44 years, with significant aortic stenosis, who underwent coronary arteriography (73 women and 115 men). There were 38 patients (20.2%) with coronary artery disease ( or = 50% reduction in the luminal diameter). Sixty-eight patients had typical angina pectoris, 52 atypical angina, and 68 did not have chest pain. We found to have coronary disease in 29.4%, 23.1% and 8.8% respectively. Sensitivity of typical angina to detect coronary disease was 52.6%, with an specificity of 68%, and a negative predictive value of 85%. Inclusion of atypical angina improved the sensitivity to 84.2%, and the negative predictive value to 91.2%, but lessened the specificity to 41.4%. Six patients among the 38 with coronary disease (15.7%), did not have chest pain, and 3 of them were younger than 60 years. We conclude that absence of angina is not enough to exclude coronary artery disease in patients 50 years old with aortic stenosis being considered for aortic valve replacement.     

High prevalence of gastroesophageal reflux in patients with clinical unstable angina and known coronary artery disease

Objectives: Esophageal disease may mimic acute anginal pain. However, the prevalence of gastroesophageal reflux in the acute setting of patients with clinically unstable angina (UA) pectoris is not known. The aim of this study was to determine the co‐existence of coronary artery disease (CAD) and gastroesophageal reflux in UA, and to study the feasibility of esophageal investigation in the chest pain unit. Design: 22 patients with clinical UA and confirmed CAD were monitored by continuous vector cardiography and pH‐measurement during 24?h of observation. Symptoms of chest pain and episodes of ischemia and reflux were recorded. Results: 11 patients (50%) showed abnormal gastroesophageal reflux and another three (14%) had an increased number of reflux episodes. pH‐measurements and esophageal manometry were well tolerated. Few chest pain episodes were recorded during the study period, and no association between chest pain, reflux, and ischemia could be shown. Conclusion: Esophageal reflux is common in patients with UA and established CAD. As reflux‐related chest pain may imitate angina pectoris, it is clinically important that gastroesophageal examination in patients with UA seems to be feasible and well tolerated in the ‘acute setting’.     

Prediction of coronary artery disease by left ventricular regional wall motion abnormalities in patients with stenosis of the aortic valve

To identify predictive factors for coronary artery disease in patients with stenosis of the aortic valve the clinical histories, haemodynamic measurements, biplane contrast left ventriculograms, and coronary angiograms of 83 consecutively catheterised patients with valvar aortic stenosis were examined retrospectively. The mean (SD) age was 66.4 (9.1) years and 78% were men. Fifty five patients had significant coronary artery disease (greater than or equal to 50% diameter narrowing). Forty five (82%) of 55 patients with and 23 (82%) of 28 patients without coronary disease had angina. Heart failure occurred in a third of the patients; these patients were on average older, were more likely to be female, and had lower ejection fractions and cardiac outputs than patients in whom failure did not occur. Calculated valve area, transvalvar gradient, and left ventricular end diastolic pressure did not discriminate between patients with and without coronary disease. Syncope was less common than angina and heart failure and was associated with significantly lower valve areas and higher gradients than those found in patients without syncope. Left ventricular regional wall motion abnormalities were equally common in the groups with and without angina and predicted coronary artery disease with 94% accuracy. The absence of regional wall motion abnormality was an insensitive marker of normal coronary arteries as 45% of such patients had coronary disease. Five of the 83 patients had significant coronary disease without angina or regional wall motion abnormality. In patients with aortic stenosis angina did not predict the presence of coronary artery disease; therefore, it is advisable to have the results of coronary angiography before aortic valve replacement in a population such as this. Two of the patients with heart failure and severe aortic stenosis had regional wall motion abnormality with normal coronary arteries. Thus in some patients left ventricular failure produced by increased afterload may itself be a cause of left ventricular regional wall motion abnormality.     

Prediction of coronary artery disease by left ventricular regional wall motion abnormalities in patients with stenosis of the aortic valve.

To identify predictive factors for coronary artery disease in patients with stenosis of the aortic valve the clinical histories, haemodynamic measurements, biplane contrast left ventriculograms, and coronary angiograms of 83 consecutively catheterised patients with valvar aortic stenosis were examined retrospectively. The mean (SD) age was 66.4 (9.1) years and 78% were men. Fifty five patients had significant coronary artery disease (greater than or equal to 50% diameter narrowing). Forty five (82%) of 55 patients with and 23 (82%) of 28 patients without coronary disease had angina. Heart failure occurred in a third of the patients; these patients were on average older, were more likely to be female, and had lower ejection fractions and cardiac outputs than patients in whom failure did not occur. Calculated valve area, transvalvar gradient, and left ventricular end diastolic pressure did not discriminate between patients with and without coronary disease. Syncope was less common than angina and heart failure and was associated with significantly lower valve areas and higher gradients than those found in patients without syncope. Left ventricular regional wall motion abnormalities were equally common in the groups with and without angina and predicted coronary artery disease with 94% accuracy. The absence of regional wall motion abnormality was an insensitive marker of normal coronary arteries as 45% of such patients had coronary disease. Five of the 83 patients had significant coronary disease without angina or regional wall motion abnormality. In patients with aortic stenosis angina did not predict the presence of coronary artery disease; therefore, it is advisable to have the results of coronary angiography before aortic valve replacement in a population such as this. Two of the patients with heart failure and severe aortic stenosis had regional wall motion abnormality with normal coronary arteries. Thus in some patients left ventricular failure produced by increased afterload may itself be a cause of left ventricular regional wall motion abnormality.     

Pain perception and brain evoked potentials in patients with angina despite normal coronary angiograms.

OBJECTIVE: To evaluate the role of nociception in patients with angina despite normal coronary angiograms and to investigate whether any abnormality is confined to visceral or somatosensory perception. METHODS: Perception, pain threshold, and brain evoked potentials to nociceptive electrical stimuli of the oesophageal mucosa and the sternal skin were investigated in 10 patients who had angina but normal coronary angiograms, no other signs of cardiac disease, and normal upper endoscopy. Controls were 10 healthy volunteers. The peaks of the evoked potential signal were designated N for negative deflections and P for positive. Numbers were given to the peaks in order of appearance after the stimulus. The peak to peak amplitudes (P1/N1, N1/P2) were measured in microV. RESULTS: (1) Angina pectoris was provoked in seven patients following continuous oesophageal stimulation. (2) Distant projection of pain occurred after continuous electrical stimulation of the oesophagus in four patients and in no controls. (3) Patients had higher oesophageal pain thresholds (median 16.3 mA v 7.3 mA, P = 0.02) to repeated stimuli than controls, whereas the values did not differ with respect to the skin. There were no intergroup differences in thresholds to single stimuli. (4) Patients had substantially reduced brain evoked potential amplitudes after both single oesophageal (P1/N1, median values: 7.2 microV, controls: 29.0 microV; N1/P2: 16.5 microV, controls: 66.0 microV; P < 0.001 for both) and skin (N1/P2: 13.5 microV; controls: 76.0 microV; P < 0.001) stimuli despite the similar pain thresholds. CONCLUSION: Central nervous system responses to visceral and somatosensory nociceptive input are altered in patients who have angina despite normal coronary angiograms.