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’.     

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.     

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.     

Ambulatory esophageal manometry,pH-metry,and holter ECG monitoring in patients with atypical chest pain

Standard Holter electrocardiographic (ECG) monitoring was combined with ambulatory esophageal manometry and pH-metry in 25 patients with atypical chest pain in order to determine whether an association could be found between spontaneous pain episodes and ischemic ECG changes or esophageal dysfunction. Results of ambulatory testing were compared to those obtained with standard esophaeal manometry and provocative testing. Twenty-two of the 25 patients experienced a total of 88 pain episodes during ambulatory testing. Although 15 of the 22 patients (68%) experiencing pain during testing had at least one pain episode that corelated temporally with gastroesophageal reflux, esophageal dysmotility or ischemic ECG changes, 65% of all pain episodes were unrelated to abnormal esophageal events or ECG changes. Seventeen percent of pain episodes were associated with gastroesophageal reflux, 15% with esophageal dysmotility,and 2% with a combined acid reflux and esophageal dysmotility event. Only one pain episode was associated with ischemic ECG changes. Twelve of the 15 patients with chest pain episodes associated with reflux or esophageal dysmotility had othe identical pain episodes in which there was no correlation. Reproduction of a patient's pain during standard manometry with provocative testing did not predict a strong correlation between the patient's spontaneous pain episodes and esophageal dysfunction during ambulatory recordings. In summary, patients with atypical chest pain have relatively few spontaneous pain episodes that correlate with gastroesophageal reflux, esophageal dysmotility, or ischemic ECG changes. It appears that different stimuli can trigger identical episodes of chest pain, which suggests that many of these patients may have dysfunction of their visceral pain sensory mechanisms.     

The contribution of gastroesophageal reflux to chest pain in patients with coronary artery disease.

OBJECTIVE: To describe the effectiveness of investigating and treating the cause of refractory chest pain in patients with coronary artery disease who are receiving optimal antianginal therapy. DESIGN: Cohort study. SETTING: Tertiary referral center. PATIENTS: Between January 1988 and December 1989, 34 patients were identified as having angiographically proven coronary artery disease and atypical chest pain symptoms despite their having received aggressive medical or surgical antianginal therapy, or both. INTERVENTION: Patients with confirmed acid-related symptoms were treated with high-dose histamine-2 (H2) blockers or omeprazole for 8 weeks in an open-label study. MEASUREMENTS: Esophageal manometry and simultaneous 24-hour pH and Holter studies; global improvement in or disappearance of chest pain. RESULTS: Of the 34 patients, 30 (88%) experienced their identical chest pain symptoms during the study. A total of 164 pain episodes was recorded: 38 (23.2%) correlated with acid reflux; 6 (3.7%) were related to cardiac ischemia; and the remaining 120 (73.2%) had no identifiable cause. Of these 30 patients, 20 (67%) had some of their episodes of chest pain (range, 14% to 100%) secondary to acid reflux. After 8 weeks of vigorous acid suppression, 13 of these 20 patients had marked improvement or resolution of chest pain. Four other patients had ischemia-related episodes of chest pain that responded to more aggressive antianginal therapy. No episodes of acid reflux were clearly followed by ischemic chest pain. One patient had both acid- and ischemic-related episodes of chest pain that were indistinguishable. Overall, 24 of 34 (71%) patients had a definite cause of chest pain identified by combined pH and Holter monitoring. CONCLUSIONS: Gastroesophageal reflux disease is a common, treatable cause of chest pain in patients with coronary artery disease who have atypical symptoms and remain symptomatic despite aggressive antianginal therapy. Combined Holter and 24-hour esophageal pH studies are complementary investigations for elucidating the cause of chest pain in these patients.     

Visceral chest pain in unstable angina pectoris and effects of transcutaneous electrical nerve stimulation (TENS)

A substantial proportion of patients with chest pain referred to hospital, show signs of coronary artery disease. Anginal pain could be conceptualized as a warning signal for coronary artery disease and impending death. But, for many reasons this theory is partly disputed. Firstly, not all ischemic episodes are accompanied by anginal pain (silent ischemia). Secondly, chest pain indistinguishable from true angina pectoris may be the result of other abnormalities of thoracic viscera. Nevertheless acute severe cardiac ischemia often gives rise to anginal chest pain. Unstable angina pectoris is carrying a higher risk for future events in spite of intensive medical treatment. A special problem are patients awaiting coronary intervention because of severe ischemia and maximum medical treatment, who experience ischemic pain. New treatment regimens are needed for these patients. This review discusses the symptom of visceral pain from the heart, angina pectoris, its relation to ischemia and unstable angina pectoris. It also addresses the role of afferent nerve stimulation (transcutaneous electrical nerve stimulation, TENS) in the treatment of severe angina pectoris as well as recent findings of TENS applicability in unstable angina.     

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.     

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.     

Esophageal Disorders in Patients with Chest Pain and Mitral Valve Prolapse

The origin of chest discomfort in patients with mitral valve prolapse is controversial. We performed esophageal manometry in 18 patients with mitral valve prolapse, chest pain, and no significant coronary artery disease at cardiac catheterization. Fourteen of the 18 had esophageal disorders: five had diffuse esophageal spasm and two had hypertensive lower esophageal sphincter-motility disorders associated with chest pain syndromes; five mitral valve prolapse patients had hypotensive lower esophageal sphincters, a finding that increases the probability of symptomatic gastroesophageal reflux; and two had nonspecific motor abnormalities. Esophageal disorders may provide an explanation for chest discomfort experienced by certain patients with mitral valve prolapse.     

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.     

Chest Pain at Rest in Patients with Coronary Artery Disease (Myocardial Ischemia, Esophageal Dysfunction, or Panic Disorder?)

Severe nonexertional (resting) chest pain may bedue to myocardial ischemia, esophageal dysfunction,psychiatric disorder, or any combination thereof andfrequently poses a difficult diagnostic challenge. Our aim was to investigate causes of chest painin patients with coronary artery disease. Forty-fivepatients with angiographically proven obstructivecoronary lesions and recurrent chest pain at rest were studied; 18 had refractory pain despite cardiactherapy (problem group), and 27 had documentedmyocardial ischemia (control group). Esophagealmanometry, edrophonium provocation, 24-hr pH studies,and psychiatric interview were performed in all patients. Theclinical evolution and the outcome of specific treatmentduring follow-up was used to establish the etiology ofchest pain. Esophageal dysfunction was identified in all problem patients and in 52% of controls,and the esophagus was incriminated as the source of painin 8 (44%) and 5 (18.5%), respectively. After a meanfollow-up of 49 months (range 24-76 months), the cause of chest pain in the problem groupwas identified as panic disorder in 9 patients (50%),gastroesophageal reflux in 6 (33%), esophagealdysmotility in 2 (11%), and gallstone disease in 1 (6%). Of the control patients, 18 (67%) had ischemicpain alone, while 9 had concurrent causes: panicdisorder in 5 (19%) and esophageal dysfunction in 4(15%). Esophageal dysfunction and psychiatricdisturbances are common in patients with coronary arterydisease presenting with resting chest pain, and maycontribute to patients' symptoms.     

Esophageal Aperistalsis and Gastroesophageal Reflux Disorder: Return of Peristalsis after H2-Blocker Therapy

Objectives: Distal esophageal aperistalsis has rarely been reported among patients with gastroesophageal reflux disorder. The purpose of this study, therefore, was to address the frequency with which disorders of peristalsis in general-and distal esophageal aperistalsis in particular-occur in adults with gastroesophageal reflux disorder. Patients and Methods: We studied 314 patients who were referred to our gastrointestinal motility laboratory. On the basis of the endoscopic data, they were divided into three groups: group I, symptomatic patients without endoscopic esophagitis; group II, patients with mild endoscopic esophagitis; and group III. patients with erosive esophagitis. An age-matched group of patients with chest pain unrelated to reflux served as the control. Results: Some form of peristaltic dysfunction was recorded in 56% of the patients with gastroesophageal reflux disorder, significantly more than in the control group ( p < 0.01). A significant correlation existed between the esophageal motor dysfunction scores and the severity of reflux disease. Distal esophageal aperistalsis was present in 3.1% of the reflux groups. There was a correlation between severity of reflux disease and the prevalence of aperistalsis. Aperistalsis occurred in none of the patients in group I, in 3.6% of group II, and in 12.5% of group III ( p < 0.0001). Seven of the patients with aperistalsis who has been treated with H2-blockers were reexamined 4 months later. Return of peristalsis was seen in three of them. Conclusion: Esophageal aperistalsis can be seen in a minority of patients with severe gastroesophageal reflux disorder and is probably a reversible condition.     

Transient ST-segment depression as a marker of myocardial ischemia during daily life

Patients with angina and coronary artery disease (CAD) have many episodes of transient ST-segment depression during ordinary daily life, and these are often asymptomatic. To investigate this signal as a marker of myocardial ischemia, 30 patients with chronic stable angina and CAD underwent positron tomography, recording the regional myocardial uptake of rubidium-82, pain and ST-segment changes before, during and after 59 technically satisfactory exercise tests, 35 cold pressor tests and 22 episodes of unprovoked ST depression. Exercise resulted in 53 episodes of ST depression with angina and in 5 episodes without pain. After cold pressor tests, there were 3 episodes of ST depression and pain and 12 of painless ST depression. Only 9 episodes of unprovoked ST depression were accompanied by pain. Tomography showed independent evidence of ischemia in 63 (97%) of the total 65 episodes of ST depression with angina and in all 30 episodes of painless ST depression. In each patient perfusion defects occurred in the same myocardial segment during painful and painless ST depression and responses were significantly different from those in 16 normal subjects studied in the same way. These findings support the use of transient ST depression in continuous monitoring to assess the activity of CAD, but only in patients with typical angina pectoris, ST depression during exercise and proved CAD. They strengthen the evidence derived from ambulatory monitoring for a wider picture of the disease than is generally appreciated, with more frequent episodes of silent myocardial ischemia than of angina pectoris.     

Effect of Helicobacter pylori infection on the gastroesophageal reflux in patients with atypical chest pain

The role of Helicobacter pylori (Hp) infection in the course of gastroesophageal reflux disease (GERD) is still controversial. The aim of this study was to compare the results of endoscopic, histologic and pH-metric examinations of esophagus in patients diagnosed because of atypical chest pain, infected and not-infected by Hp. In 172 patients diagnosed because of atypical chest pain were made: interview, physical examination, gastroduodenoscopy with esophageal and gastric mucosa biopsy as well as esophageal pH-metry. Hp infection was diagnosed on the basis of positive urease test or/and histologic examination. In 49 (28%) subjects pathological gastroesophageal acid reflux was diagnosed (above 4.5% of monitoring time with pH < 4). Percentage of Hp infected patients among subjects with pathological (69%) and not-pathological (74%) gastroesophageal acid reflux did not differ significantly. Hp infected patients, in comparison to Hp-negative, had similar esophageal mucosa endoscopic appearance and greater intensity of histologic changes in esophageal mucosa. Studied patients group did not differ in respect of esophageal pH-metry parameters values, besides of greater number of esophageal alkalization (pH > 7) episodes in Hp-negative subjects. CONCLUSIONS: 1) Hp infection was diagnosed in 72% of patients with atypical chest pain. 28% had pathological gastroesophageal acid reflux. 2) Gastroesophageal acid reflux was not related to Hp infection. 3) Greater intensity of histologic changes in esophageal mucosa of Hp-positive patients with accompanying lack of differences in endoscopic estimation and similar endanger on gastric acid in pH-metry suggests protective role of esophageal alkalization against esophageal mucosa injury or higher intensity of regenerative inflammatory processes in Hp-positive patients.     

Angina-like esophageal pain: differentiation from cardiac pain by history

Consecutive patients coming as an emergency with chest pain due to myocardial ischemia or esophageal disease were interviewed on admission to the hospital, before they had been fully investigated. Classical features of angina pectoris were equally common in both groups and "crescendo angina" was often found in patients with esophageal disease. Features that helped to distinguish esophageal from cardiac pain were: an atypical response to exercise, pain that continued as a background ache, retrosternal pain without lateral radiation, pain that disturbed sleep, and the presence of certain esophageal symptoms. A positive diagnosis will be made more often in cases of suspected but unsubstantiated coronary disease by clinicians who are aware that esophageal pain and angina may be indistinguishable.     

Esophageal contribution to chest pain in patients with coronary artery disease

We conducted a prospective study to determine the role of the esophagus in causing chest pain in patients with established CAD on optimum therapy. Thirty-two men with documented CAD who complained of frequent and usually daily retrosternal chest pain were evaluated. Following a standard esophageal manometry and acid perfusion test, simultaneous two-channel ambulatory Holter monitor and esophageal pH record tests were performed for 24 hours. Fifty-three episodes of chest pain were documented in 20 patients; 11 patients were free of pain. Of the 20 patients who complained of chest pains, 17 (85 percent) demonstrated at least one episode of PPR, defined as a drop in distal esophageal pH to less than 4 within ten minutes before or after the onset chest pain. Episodes of asymptomatic GER were common. The correlation of PPR with chest pain was 70 percent (37/53 episodes) and of ischemic ECG changes with chest pain 13 percent (7/53); in the remaining, there was no correlation with either. Two patients demonstrated simultaneous PPR and ischemic ECG changes. Seventeen esophageal motility abnormalities were observed in 14 patients (45 percent). It is our conclusion that esophageal disorders contribute to chest pain in patients with documented CAD. In this group, GER plays a greater role than in those with normal coronary arteries. In addition, esophageal motility disorders are common in these patients. Esophageal testing can be undertaken safely in these patients.     

Provocation of transient lower esophageal sphincter relaxations by meals in patients with symptomatic gastroesophageal reflux

The effect of a meal on the rate of transient lower esophageal sphinter (LES) relaxations and patterns of gastroesophageal reflux was investigated in 49 patients referred for evaluation of gastroesophageal reflux. Esophageal motility and pH were recorded concurrently before and after a standard meal. In the patients with symptomatic reflux, the meal induced a four-to sevenfold increase in the gastroesophageal reflux through two mechanisms: a four-to fivefold increase in the rate of transient LES relaxations and an increase in the proportion of transient LES relaxations accompanied by reflux from 47% to 68^. Overall the rate of reflux episodes that occurred by mechanisms other than transient LES relaxation did not increase significantly. An exception to these findings were those in six patients with chronically absent basal LES pressure in whom transient LES relaxations could not be scored. In these patients, reflux increased postprandially through mechanisms other than transient LES relaxation. These findings confirm the pivotal importance of transient LES relaxations in the pathogenesis of gastroesophageal reflux.     

计算机断层摄影术冠状动脉造影诊断冠心病和评价冠状动脉病变的价值

目的:研究计算机断层摄影术冠状动脉(冠脉)造影(CTCA)在急性胸痛患者中诊断冠心病和评价冠脉病变程度的价值.方法:回顾性入选133例临床诊断为不稳定性心绞痛的急性胸痛患者,分别接受64排CTCA和冠脉造影检查.以定量冠脉造影(QCA)为诊断标准,评价CTCA诊断冠心病和冠脉病变程度的准确性.结果:CTCA诊断冠心病的敏感性93.4%,阳性预测值94.2%.Pearson相关分析示:CTCA和冠脉造影评价的冠脉直径狭窄程度显著相关(P<0.001).Logistic回归分析示,钙化程度是CTCA诊断冠心病敏感性的独立影响因素(RR=2.37,95%CI:1.35-4.18,P=0.003).ROC曲线分析显示,钙化积分对预测冠脉三支血管存在≥50%或≥75%狭窄有预测作用,P均<0.05.结论:CTCA在急性胸痛患者中对冠心病的筛查和冠脉病变程度的评价有较高价值.     

Continuous electrocardiographic recording in Prinzmetal's variant angina pectoris. A report of four cases

Four patients with Prinzmetal's variant angina pectoris were subjected to continuous electrocardiographic recording. In three of them several episodes of ST segment elevation unaccompanied by pain were recorded. In one patient, identical electrocardiographic alterations were observed both in presence or in absence of pain, while in the others a good correlation was evident between pain and severity of the electrocardiographic abnormalities. In two patients transmural myocardial infarction complicated the course of the angina. In contrast to the classical findings, in these patients the attacks of chest pain did not cease after the infarction, but became more frequent and severe. The electrocardiographic alterations of the anginal episodes occurred in the same myocardial areas involved by the infarction, so that a reversible superposition of electrocardiographic signs of acute ischaemia on those of recent necrosis was observed.Continuous electrocardiographic recording provided the best means of investigation of these patients with the variant form of angina pectoris.