A gastroenterologists view of chest pain

Esophageal disorders are common, but have been underemphasized as causes of chest pain in patients with “chest pain and normal coronary arteries,” as well as in patients with documented coronary disease. Reasons include failure to pursue evaluation once cardiac sources have been excluded; the atypical nature, location and/or radiation of pain in many patients, leading one away from proper consideration of the esophagus as a pain source; performing tests (upper GI series, fiberoptic endoscopy, oral cholecystography) that have low sensitivity for the detection of the diseases most likely to be the cause of chest pain (gastroesophageal reflux disease, the primary esophageal motility disorders). Esophageal motility testing, esophageal acid perfusion, acid reflux testing and the use of pharmacologic agents to induce chest pain and dysmotility are of greater value. In general, these tests can be performed in less than two hours. In some instances, prolonged recording of distal esophageal pH and/or motility may help identify gastroesophageal reflux or a painful primary esophageal motility disorder as the cause of chest pain. Treatment of gastroesophageal reflux disease is effective in most patients. One must be especially aggressive in the treatment of reflux in patients with coexistent coronary disease. The aim of treatment should be to eliminate pain episodes, since in these patients, pain emanating from an acid-sensitive esophagus may be confused with angina or, in some instances, actually induce myocardial ischemia. While therapy in the painful primary esophageal motility disorders is less effective than for reflux disease, several newer treatments show promise.     

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.     

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’.     

Diagnosis of chest pain with foregut symptoms in Chinese patients

AIM： To evaluate the diagnosis of chest pain with foregut symptoms in Chinese patients.
METHODS： Esophageal manometric studies, 24-h introesophageal pH monitoring and 24-h electrocardiograms （Holter electrocardiography） were performed in 61 patients with chest pain.
RESULTS： Thirty-nine patients were diagnosed with non-specific esophageal motility disorders （29 patients with abnormal gastroesophageal reflux and eight patients with myocardial ischemia）. Five patients had diffuse spasm of the esophagus plus abnormal gastroesophageal reflux （two patients had concomitant myocardial ischemia）, and one patient was diagnosed with nutcracker esophagus.
CONCLUSION： The esophageal manometric studies, 24-h intra-esophageal pH monitoring and Holter electrocardiography are significant for the differential diagnosis of chest pain, particularly in patients with foregut symptoms. In cases of esophageal motility disorders, pathological gastroesophageal reflux may be a major cause of chest pain with non-specific esophageal motility disorders. Spasm of the esophageal smooth muscle might affect the heart-coronary smooth muscle, leading to myocardial ischemia.     

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.     

Non-cardiac chest pain: Prevalence of reflux disease and response to acid suppression in an Asian population

Background:  Gastroesophageal reflux disease is thought to be the commonest cause of 'non-cardiac chest pain'. The use of proton-pump inhibitors resulting in improvement in the chest pain symptom would support this causal association.
Objectives:  To determine the prevalence of gastroesophageal reflux disease in non-cardiac chest pain and the response of chest pain to proton-pump inhibitor therapy.
Methods:  Patients with recurrent angina-like chest pain and normal coronary angiogram were recruited. The frequency and severity of chest pain were recorded. All patients underwent esophagogastroduodenoscopy and 48-h Bravo ambulatory pH monitoring before receiving rabeprazole 20 mg bd for 2 weeks.
Results:  The prevalence of gastroesophageal reflux disease was 66.7% (18/27). The improvement in chest pain score was significantly higher in reflux compared to non-reflux patients ( P  = 0.006). The proportion of patients with complete or marked/moderate improvement in chest pain symptoms were significantly higher in patients with reflux (15/18, 83.3%) compared to those without (1/9, 11.1%) ( P  < 0.001).
Conclusion:  The prevalence of gastroesophageal reflux disease in patients with 'non-cardiac chest pain' was high. The response to treatment with proton-pump inhibitors in patients with reflux disease, but not in those without, underlined the critical role of acid reflux in a subset of patients with 'non-cardiac chest pain'.     

Noncardiac chest pain of esophageal origin in patients with and without coronary artery disease

BACKGROUND/AIMS: Non-cardiac chest pain is a frequent finding in patients admitted to emergency departments, and it has been shown that many of these patients may have an esophageal cause for their pain. However, little data are available on patients primarily referred to the cardiology unit, and especially those with coronary artery disease. The purpose of this study was to assess the role of esophageal dysfunction in chest pain patients with and without coronary artery disease. METHODOLOGY: Eighty-one patients referred from a cardiology unit for chest pain and no myocardial infarction entered the study. Sixty-one patients had no evidence of coronary artery disease, whereas 20 had coronary artery disease with chest pain at rest. After the cardiological evaluation, the patients underwent esophageal function testing by means of upper endoscopy, manometry, and 24-hour pH-monitoring. RESULTS: Overall, 10% of patients (2.5% in the coronary artery disease group) had evidence of endoscopic esophagitis, 46% of esophageal motor disorders (12% in the coronary artery disease group), and 10% abnormal pH-monitoring (1% in the coronary artery disease group). CONCLUSIONS: We report that the esophagus might be responsible for non-cardiac chest pain in patients with and without coronary artery disease. In our experience, esophageal motor disorders, and not an increased acid reflux, are the abnormalities most commonly found in these patients.     

Symptomatic gastro-oesophageal reflux, abnormal oesophageal acid exposure, and mucosal acid sensitivity are three separate, though related, aspects of gastro-oesophageal reflux disease.

The Bernstein test has been used as a test of oesophageal acid sensitivity for over 30 years but its clinical value has been challenged by the advent of ambulatory pH monitoring. Furthermore, the relation between mucosal acid sensitivity, symptomatic reflux, and abnormal oesophageal acid exposure time is unclear. This study examined the relation between these three parameters in patients referred for pH monitoring with unexplained chest pain or heartburn. Fifty consecutive patients were studied - nine with non-cardiac chest pain and 41 with a history of heartburn. Symptomatic reflux was defined as a greater than or equal to 50% temporal association between pain episodes and reflux events (pH less than 4) during pH monitoring. A positive acid perfusion test (in which the patient's usual symptoms were evoked by acid, though not saline) had a 100% sensitivity, 73% specificity, and 81% accuracy for the detection of symptomatic reflux. All 10 patients with symptomatic reflux during pH monitoring had evidence of mucosal acid sensitivity. A negative acid perfusion test made symptomatic reflux unlikely. However, symptomatic reflux or a positive acid perfusion test, or both, were found in some patients with a normal oesophageal acid exposure time during pH monitoring. Mucosal acid sensitivity, abnormal oesophageal acid exposure time, and symptomatic reflux should be regarded as separate, though related aspects of reflux disease. The Bernstein test is simple, safe, and easily performed. A positive test helps to identify an oesophageal cause of symptoms, particularly in patients in whom other aspects of 'gastro-oesophageal reflux disease' are absent, or who do not have symptoms during pH monitoring.     

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'.     

Oesophageal function in patients with angina pectoris: a comparison of patients with normal coronary angiograms and patients with coronary artery disease

Oesophageal function was assessed in 52 patients with angina pectoris whose coronary angiograms were completely normal and in 21 patients with angina pectoris who had significant coronary artery disease. During a standard oesophageal manometric study, abnormalities were found in 23 (44%) patients with normal coronary angiograms but in only 2 (10%) patients with coronary artery disease (p less than 0.01). Twenty-four (46%) patients with normal coronary angiograms were found to have gastro-oesophageal reflux disease during 24-hour oesophageal pH monitoring. Of the 52 patients with normal coronary angiograms, 19 (37%) had gastro-oesophageal reflux disease and abnormal oesophageal motility, 5 (10%) had gastro-oesophageal reflux disease alone, and 7 (13%) had oesophageal motility disorder alone. The use of provocation procedures, including intravenous edrophonium during oesophageal manometry and treadmill exercise testing during pH monitoring, enabled the oesophageal abnormality to be demonstrated simultaneously with chest pain in 25 of these 31 patients. Typical angina pectoris, coincident with abnormal oesophageal motility, was precipitated in a subgroup of patients who had been shown to have oesophageal manometric abnormalities and gastro-oesophageal reflux disease by the infusion of hydrochloric acid into the oesophagus; both the chest pain and manometric abnormality resolved following the oral administration of antacid.     

Nutcracker esophagus: GERD or an esophageal motility disorder

A retrospective study was performed to determine the frequency of acid-related esophageal dysfunction in an unselected group of patients with nutcracker esophagus (NE). Five hundred seventy-two consecutive patients who underwent esophageal manometry and pH testing at one institution were evaluated. Forty-one percent were referred for evaluation of chest pain, 39% for reflux symptoms, and 20% for dysphagia, nausea, or epigastric pain. Esophageal manometry and 24-h pH monitoring were performed using standard methods. NE was defined as amplitude of phasic contractions of ≥180 mm Hg in any manometric tracing at any level of the esophagus. Abnormal total reflux was defined as >4% of the time with the esophageal pH < 4. A positive symptom index was defined as >50% of periods with pH < 4 coinciding with symptoms of chest pain or heartburn. Esophagitis was defined as an unequivocal mucosal defect if esophagogastroduodenoscopy was performed.
Forty-five patients met criteria for NE, with acid-related abnormalities found in 77%. Forty-nine percent had abnormal acid exposure time, 16% had positive symptom indexes with normal acid exposure, and 5% had endoscopic esophagitis. An additional 7% had only an increased number of reflux episodes with normal acid exposure and symptom indexes. The prevalence of NE was significantly higher in patients referred for chest pain than for typical reflux symptoms (14.3% vs 4.5%). Seventy-four percent of the patients with NE and chest pain did not have classic reflux symptoms. Seventy-six percent of 34 evaluable subjects who had been started on acid suppression were either improved or symptom free at an average of 10.7 months of follow-up.     

12导联动态心电图ST段压低诊断冠心病的价值

目的探讨24h12导联动态心电图ST段压低诊断冠心病的临床意义。方法将163例12导联动态心电图检查有缺血性ST段压低伴或不伴典型胸痛患者分为两组（A组ST段压低伴典型胸痛者88例，B组ST段压低不伴典型胸痛或无症状者75例），并与冠状动脉造影进行对比分析。结果A组88例冠状动脉造影明显狭窄79例，其中单支病变44例，双支病变25例，3支病变10例，而B组75例冠状动脉造影明显狭窄15例。以冠状动脉造影阳性为标准，A组对冠心病的诊断阳性率为89．77％，特异性为80．00％，准确度为85．28％。而B组阳性率仅为20．00％，两组阳性率差异有非常显著性意义（χ^2=80．75，P〈0．01）。结论12导联动态心电图检查缺血性ST段压低伴有典型胸痛，诊断冠心病的价值要优于仅有ST段改变者，前者阳性率和准确度较高，具有重要的临床应用价值。     

The symptom index

The symptom index is a quantitative measure developed for assessing the relationship between gastroesophageal reflux and symptoms. Controversy exists, however, over its accuracy and the appropriate threshold for defining acid-related symptoms of heartburn and chest pain. Therefore, a retrospective review was done of 153 consecutive patients referred to our esophageal laboratory. Three groups were identified: patients with normal 24-hr pH tests and no esophagitis, patients with abnormal 24-hr pH tests and no esophagitis, and patients with abnormal 24 hr pH values and endoscopic esophagitis. If symptoms occurred during the pH study, a symptom index (number of acid related symptoms/total number of symptoms x 100%) was calculated separately for heartburn and chest pain. Heartburn and chest pain episodes were similar among the three groups. However, the mean symptom index for heartburn was significantly (P<0.001) higher in the patient groups with abnormal pH values [abnormal pH/no esophagitis: 70±7.1% (±se); abnormal pH/esophagitis: 85±4.6%] as compared to those with normal studies, ie, functional heartburn (26±10.7%). The mean symptom index for chest pain was similar for all three groups. Using receiver operating characteristic curves, a heartburn symptom index≥50% had excellent sensitivity (93%) and good specificity (71%) for acid reflux disease, especially if patients complain of multiple episoldes of heartburn. In contrast, an optimal symptom index threshold for defining acid-related chest pain episodes could not be defined.     

Prior sensitization of esophageal mucosa by acid reflux predisposes to reflux-induced chest pain

Esophageal acid exposure is believed to be a major source of unexplained chest pain; but, individual episodes of reflux in pH study are not consistently associated with chest pain. Our aim was to discover whether prior sensitization of esophageal mucosa by acid reflux predisposes to reflux-induced chest pain. Ambulatory pH studies of patients referred to our laboratory from January 1991 to November 1996 with noncardiac chest pain was reviewed. We compared the frequency of esophageal acid exposure in the 30 minutes preceding chest pain episodes with a positive symptom/reflux association (+SRA) to reflux with the frequency of acid exposure in the 30 minutes preceding those chest pain episodes that were not associated with reflux negative symptom/reflux association (-SRA). We analyzed the time esophageal pH <4, symptom index (SI) defined as percentage of chest pain episodes associated with reflux in the preceding 5 minutes, and amount of reflux in the 30 minutes preceding each chest pain episode. Of 104 patients, 52 had chest pain during their pH study, 10 had high SI (> or =50%), and 42 had low SI (<50%). Those with a high SI were significantly more likely to have an abnormal pH study (p = 0.015). Chest pain associated with reflux in proceeding 5 minutes (+SRA) was strongly associated (p < 0.002) with additional reflux episodes in the preceding 25-minute period. Chest pain related to reflux is associated with sensitization of the esophageal mucosa by prior reflux events.     

Twenty-four-hour esophageal pH monitoring: the most useful test for evaluating noncardiac chest pain

STUDY OBJECTIVE: To compare the diagnostic capabilities of traditional esophageal tests (manometry and provocative testing with acid and edrophonium) and 24-hour esophageal pH monitoring in identifying an esophageal cause of chest pain. DESIGN: A prospective study of 100 consecutive patients referred by cardiologists to the esophageal laboratory for evaluation of esophageal causes of chest pain. SETTING: Tertiary-referral university hospital. METHODS: Esophageal manometry performed with 10 wet swallows of water. Acid perfusion (0.1 N hydrochloric acid) and edrophonium (80 micrograms/kg intravenously) tests were placebo-controlled with a positive study defined as replication of typical chest pain. Esophageal pH monitoring identified (1) abnormal acid exposure times in the upright, supine, or combined position, and (2) correlation between symptoms and acid reflux, i.e., symptom index. The esophagus was identified as "probably" contributing to chest pain only if the acid or edrophonium test was positive or if there was a positive correlation between symptoms and acid reflux during pH monitoring. RESULTS: Esophageal manometry was abnormal in 32 patients (32%), but patients were asymptomatic during the study. The acid perfusion test was positive in 18 of 95 patients (19%), and the edrophonium test was positive in 15 of 78 patients (19%). Abnormal acid exposure times were found in 48 patients (48%). Of the 83 patients with spontaneous chest pain during 24-hour pH testing, 37 patients (46%) had abnormal reflux parameters and 50 patients (60%) had a positive symptom index (mean positive score 56%, range 6% to 100%). CONCLUSIONS: Acid reflux is a common and potentially treatable cause of noncardiac chest pain. Traditional esophageal tests usually miss this diagnosis. Twenty-four-hour esophageal pH monitoring with symptom correlation is the single best test for evaluating patients with noncardiac chest pain.     

Severity of silent myocardial ischemia on ambulatory electrocardiographic monitoring in patients with stable angina pectoris: relation to prognostic determinants during exercise stress testing and coronary angiography

The relation of silent ischemia in patients with stable angina to known predictors of severity of coronary disease on exercise stress testing and coronary angiography is poorly defined. This issue was therefore examined with use of Holter electrocardiographic (ECG) recordings, treadmill exercise tests and angiographic indexes in 102 patients (not taking antianginal therapy) and the results were compared with Holter and treadmill findings in 42 volunteers. A total of 159 ischemic episodes (90% silent) were identified during 2,503 h on Holter recording in 97 patients (mean duration per episode 22.7 +/- 147 min; range 1 to 234). Holter recordings had a 92% specificity and an 80% positive predictive value, but a sensitivity of only 37% and a negative predictive value of 27% for coronary disease. Sixty-three patients (Group I) had no ischemia on Holter recording, 22 (Group II) had a cumulative duration of 1 to 60 min/24 h and in 12 (Group III) ischemia exceeded 60 min/24 h. There was no significant correlation between cumulative ischemia duration on Holter recording and exercise duration or time to ST segment depression on treadmill exercise. In general, the greater the number of coronary vessels involved and the higher the proximal coronary artery stenosis score, the greater the likelihood of ischemia and the longer the cumulative ischemia duration on Holter recording. Irrespective of the severity of coronary disease, in about 25% of Holter recordings in each angiographic category there were no ischemic episodes.(ABSTRACT TRUNCATED AT 250 WORDS)     

Potential relationship between gastroesophageal reflux disease and atrial arrhythmias

A potential reduction in symptoms related to atrial fibrillation after treatment of gastroesophageal reflux disease symptoms with proton pump inhibitor therapy has been previously described. However, illustration of this relationship by combined 24-hour pH and ambulatory Holter monitoring has not been performed. We report 3 patients with symptoms of both palpitations and reflux who underwent simultaneous Holter and 24-hour ambulatory pH monitoring off of antireflux therapy. All of the patients reported a reduction in arrhythmia symptoms on proton pump inhibitor therapy. The findings from this preliminary series suggest a potential relationship between gastroesophageal reflux disease and atrial arrhythmias that might improve with antireflux therapy. Patients with documentation of both atrial arrhythmias and reflux should have a trial of aggressive acid suppressive therapy To further confirm this relationship, larger prospective studies are needed to assess whether maximal acid suppression improves arrhythmias.     

The esophagus as a possible cause of chest pain in patients with and without angina pectoris

In a series of 18 patients with angina pectoris, in whom treatment over at least 3 years with nitroderivatives and Ca-antagonists had become partially ineffective on chest pain, and in 18 patients with angina-like non-cardiac chest pain, the following examinations were carried out: upper gut x-ray and endoscopy, acid perfusion test, esophageal manometry, 24-hour esophageal pH monitoring associated with Holter recording. The presence or absence of coronary insufficiency was established by means of scintigraphic and ECG tests, Holter monitoring and coronary arteriography. In both groups the majority of patients had abnormal esophageal function, but in patients with angina pectoris treated for a long period of time the motility changes were prevalently reflux-related. With respect to the origin of chest pain, the esophagus was found to be the likely cause in 4 patients with angina pectoris, and the probable cause in another 10 of the same group; it was the likely cause in 7 patients without angina pectoris, and the probable cause in another 7 of the same group. As nitroderivatives and Ca-antagonists decrease the LES tone and the amplitude of esophageal pressure waves, long-term treatment with these drugs may be taken into account in the genesis of gastro-esophageal reflux and related changes, including esophageal pain.     

How do we define non-cardiac chest pain?

Abstract:   Noncardiac chest pain (NCCP) is a heterogeneous disorder associated with substantial health-care costs and resource utilization. NCCP is defined by recurrent episodes of substernal chest pain in patients lacking a cardiac cause after a comprehensive evaluation. The magnitude of the problem is quite high because of fear of serious or life-threatening heart diseases. Patients with chest pain who present for the first time to ambulatory care or to the emergency room, only 11% to 39% are ultimately diagnosed with coronary artery disease. The likely causes of NCCP are numerous and often overlap. Diagnosing NCCP is difficult because NCCP remains a diagnosis of exclusion that encompasses heterogeneous patient populations. First, cardiac ischemic must be excluded and coronary angiography remains the gold standard. Once cardiac causes have been ruled out, a diagnosis of NCCP is made. Mostly, the source for NCCP originates in essence from the esophagus. Gastroesophageal reflux disease (GERD) is the most common esophageal diseases present in patients with NCCP. An initial empiric trail of high-dose acid suppression is the most cost-effective measure in the management of these patients. When a diagnostic workup is chosen, it centers on upper gastrointestinal endoscopy, 24-hr esophageal pH monitoring and esophageal manometry.     

Diagnostic and prognostic value of Holter-detected ST-segment deviation in unselected patients with chest pain referred for coronary angiography: a long-term follow-up analysis

OBJECTIVE: To evaluate the diagnostic and prognostic significance of ST-segment deviation detected by ambulatory Holter monitoring in unselected chest pain patients referred for coronary angiography. METHODS: Two hundred seventy-seven patients (71% were men) who underwent coronary angiography for evaluation of chest pain were studied with 24-h ambulatory Holter monitoring within 72 h of angiography. A lumen diameter reduction of > or = 50% was considered coronary artery disease. The ST-segment deviation was defined as > or = 1-mm deviation from the baseline lasting > or = 1 min separated by a minimum of 1 min. The patients were followed up for 65 +/- 21 months (mean +/- SD) for occurrences of death, myocardial infarction, hospitalization for unstable angina, and need for revascularization. RESULTS: Of the 277 patients, 223 (80%) had coronary artery disease. The prevalence of coronary artery disease was not significantly different in patients with (43 of 48 patients; 90%) and without (180 of 229 patients; 79%) Holter-detected ST-segment deviation. The diagnostic accuracy of Holter-detected ST-segment deviation in predicting the presence of coronary artery disease was poor (33%), with a sensitivity of 19% and a specificity of 91%. The presence of Holter-detected ST-segment deviation was not predictive of future cardiac events or death. CONCLUSION: The ST-segment changes detected on ambulatory Holter monitoring are of limited value in identifying coronary artery disease and predicting the future adverse cardiac events or death in unselected patients with chest pain.