Chest pain at rest in patients with coronary artery disease. Myocardial ischemia, esophageal dysfunction, or panic disorder?

Severe nonexertional (resting) chest pain may be due to myocardial ischemia, esophageal dysfunction, psychiatric disorder, or any combination thereof and frequently poses a difficult diagnostic challenge. Our aim was to investigate causes of chest pain in patients with coronary artery disease. Forty-five patients with angiographically proven obstructive coronary lesions and recurrent chest pain at rest were studied; 18 had refractory pain despite cardiac therapy (problem group), and 27 had documented myocardial ischemia (control group). Esophageal manometry, edrophonium provocation, 24-hr pH studies, and psychiatric interview were performed in all patients. The clinical evolution and the outcome of specific treatment during follow-up was used to establish the etiology of chest pain. Esophageal dysfunction was identified in all problem patients and in 52% of controls, and the esophagus was incriminated as the source of pain in 8 (44%) and 5 (18.5%), respectively. After a mean follow-up of 49 months (range 24-76 months), the cause of chest pain in the problem group was identified as panic disorder in 9 patients (50%), gastroesophageal reflux in 6 (33%), esophageal dysmotility in 2 (11%), and gallstone disease in 1 (6%). Of the control patients, 18 (67%) had ischemic pain alone, while 9 had concurrent causes: panic disorder in 5 (19%) and esophageal dysfunction in 4 (15%). Esophageal dysfunction and psychiatric disturbances are common in patients with coronary artery disease presenting with resting chest pain, and may contribute to patients' symptoms.     

Utilization of reducing power in light-limited cultures of Chromatium vinosum DSM 185

BACKGROUND: The onset of acute myocardial infarction and sudden cardiac death has a circadian variation, with the peak occurrence between 6 AM and 12 noon. OBJECTIVES: To determine if a circadian variation exists for transient myocardial ischemia in patients admitted to the coronary care unit with unstable coronary syndromes. METHODS: The sample was selected from patients enrolled in a prospective clinical trial who had had ST-segment monitoring for at least 24 hours and had had at least one episode of transient ischemia. The 24-hour day was divided into 6-hour periods, and comparisons were made between the 4 periods. RESULTS: In 99 patients, 61 with acute myocardial infarction and 38 with unstable angina, a total of 264 (mean +/- SD, 3 +/- 2) ischemic events occurred. Patients were more likely to have ischemic events between 6 AM and noon than at other times. A greater proportion of patients complained of chest pain between 6 AM and noon than during the other 3 periods. However, more than half the patients never complained of chest pain during ischemia between 6 AM and noon. CONCLUSION: Transient ischemia occurs throughout the 24-hour day; however, ischemia occurs more often between 6 AM and noon. An important nursing intervention for detecting ischemia is continuous electrocardiographic monitoring of the ST segment, even during routine nursing care activities, which are often at a peak during the vulnerable morning hours.     

Comparison of coronary endothelial dynamics with electrocardiographic and left ventricular contractile responses to stress in the absence of coronary artery disease

Coronary artery endothelial dysfunction has been proposed as a cause of myocardial ischemia and symptoms in patients with angina-like chest pain despite normal coronary angiograms, especially those with ischemic-appearing ST-segment depression during exercise (syndrome X). We measured coronary vasomotor responses to acetylcholine (3 to 300 microg/min) in 42 patients (27 women and 15 men) with effort chest pain and normal coronary angiograms who also had normal electrocardiograms and echocardiograms at rest. All patients underwent treadmill exercise testing and measurement of systolic wall thickening responses to dobutamine (40 microg/kg/min) during transesophageal echocardiography. There were no differences in the acetylcholine-stimulated epicardial coronary diameter (+5+/-13% vs +1+/-13%, p=0.386) and flow (+179+/-90% vs +169+/-96%, p=0.756), or in the systolic wall thickening responses (+134+/-65% vs +118+/-57%, p=0.445) from baseline values in the 12 syndrome X patients compared with the 30 patients with negative exercise test results. In patients in the lowest quartile of coronary flow responses to acetylcholine, dobutamine increased systolic wall thickening by 121+/-73%; 3 had ischemic-appearing ST-segment depression during this stress. This contractile response to dobutamine was no different than the increase in systolic wall thickening (129+/-48%, p=0.777) in patients in the highest quartile of coronary flow responses, 3 of whom also had ischemic-appearing ST-segment depression during this stress. Thus, coronary endothelial dysfunction in the absence of coronary artery disease does not account for ischemic-appearing ST-segment depression in patients with chest pain despite normal coronary angiograms. Further, coronary endothelial dysfunction is not associated with myocardial contractile responses to stress consistent with myocardial ischemia.     

Identification and characterization of cerebral cortical response to esophageal mucosal acid exposure and distention

BACKGROUND & AIMS: Esophageal acid exposure is a common occurrence in healthy individuals and patients with esophagitis. Clinically, perception of this exposure ranges from no perception to severe heartburn and chest pain. Cerebral cortical response to esophageal mucosal contact to acid has not been systematically studied. The aim of this study was to elucidate cerebral cortical response to esophageal acid exposure in normal individuals by functional magnetic resonance imaging (FMRI). METHODS: We studied 10 normal healthy volunteers. Cortical FMRI response to 10 minutes of intraesophageal perfusion of 0.1N HCl (1 mL/min) was determined, and the results were compared with those of saline infusion and balloon distention. RESULTS: Acid perfusion did not induce heartburn or chest pain but increased FMRI signal intensity by 6.7% +/- 2.0% over the preperfusion values. No increase was detected for saline infusion. FMRI signal intensity to balloon distention was similar to that of acid perfusion. Activation latency, activation to peak, and the deactivation periods for response to acid perfusion were significantly longer than those of balloon distention (P < 0.05). CONCLUSIONS: Contact of esophageal mucosa with acid, before inducing heartburn, evokes a cerebral cortical response detectable by FMRI. Temporal characteristics of this response are significantly different from those induced by esophageal balloon distention.     

Intraesophageal balloon distension test in Chagas' disease patients with noncardiac chest pain

Patients with Chagas' disease often have chest pain as a prominent symptom. The objective of this study was to compare the results of intraesophageal balloon distension in chagasic and nonchagasic patients with chest pain not caused by coronary obstruction. We studied 40 patients with chest pain and angiographically normal coronary arteries, 25 with a positive serologic test for Chagas' disease (Chagas group, 16 women, mean age 53+/-10 years), and 15 with a negative serologic test (control group, 11 women, mean age 46+/-10 years). All patients had radiologic and endoscopic examinations of esophagus, stomach, and duodenum, esophageal manometry with the acid infusion test in the distal esophagus, and intraesophageal balloon distension. None of them had esophageal dilation or any signs of cardiovascular disease. A 25-mm-long latex balloon located 10 cm above the lower esophageal sphincter was inflated and deflated over a period of 10 sec at 1-ml increments of air until the subjects reported chest pain or to a maximum volume of 20 mi. The test caused chest pain in 14 subjects in the control group (93%) and in 12 in the Chagas' disease group (48%, P < 0.05). The mean volume of air that caused chest pain was 10+/-3 ml in the control group and 15+/-4 ml in the Chagas' disease group (mean+/-SD, P < 0.05). The maximum intraesophageal pressure during the examination was higher in Chagas' disease patients with chest pain during balloon distension (60 +/- 21 mm Hg) than in patients who did not have chest pain (37 +/-18 mm Hg, P < 0.05) and did not differ from the control group (48+/-16 mm Hg, P > 0.05). With the other examinations there was no difference between groups or between patients with or without chest pain during the balloon distension test. Although esophagitis was observed in 47% of patients in the control group and in 40% of the Chagas' disease group, the acid infusion test was positive in 27% of patients in the control group and in 4% of patients in the Chagas' disease group. We conclude that, as compared to a group of patients with similar chest pain, chagasic patients are less sensitive to esophageal distension. Thus, it is unlikely that their chest pain is related to esophageal mechanisms.     

Esophageal dysmotility elicited by acid perfusion in children with esophagitis

OBJECTIVE: To determine the importance of acid reflux-induced dysmotility in the genesis of noncardiac chest pain in children. METHOD: We performed esophageal manometries during intraesophageal perfusion with 0.9% NaCl or 0.1 N HCl in 19 children (age, 14.5 +/- 0.5 yr) with gastroesophageal reflux, biopsy-proven esophagitis, and complaints of at least one episode of chest pain per day. RESULTS: Baseline esophageal motilities were normal in all patients. Eight of 19 children (42%) complained of chest pain during intraesophageal acid perfusion. In three of these eight patients, complaints of chest pain during acid perfusion were temporally associated with "conversion" of previously normal motility patterns to manometric tracings, indicating esophageal dysmotility. Compared with findings during saline perfusion, esophageal acid exposure in these three children resulted in significant increases in both the duration (13.6 +/- 4.0 vs 3.2 +/- 0.2 s, p < 0.05) and amplitude (105.2 +/- 7.8 vs 61.2 +/- 2.1 mm Hg, p < 0.05) of esophageal contractions during wet swallows. Symptoms of chest pain resolved in all patients after therapy with H2-receptor antagonists. CONCLUSIONS: These data represent the first demonstration of acid-induced esophageal dysmotility in children with chest pain and suggest that reflux-induced motor abnormalities contribute to the onset and/or exacerbation of chest pain in pediatric patients with gastroesophageal reflux and esophagitis.     

Typical and atypical presentations of gastroesophageal reflux disease. The role of esophageal testing in diagnosis and management

Gastroesophageal reflux disease (GERD) is a common disease with many typical and atypical forms of presentation. In the classic presentations of GERD with heartburn and regurgitation, esophageal testing, except for endoscopy, is only required for poorly responding patients or prior to surgical therapy. The atypical presentations of GERD, including chest pain, asthma, and ear, nose, and throat complaints, frequently are not associated with heartburn or regurgitation. Esophageal testing, particularly 24-hour pH monitoring is key to making the diagnosis and ensuring adequate acid suppression.     

Effect of pneumatic dilation on gastroesophageal reflux in achalasia

The aims of this study were to assess the effect of pneumatic dilation on gastroesophageal reflux in achalasia, differentiate esophageal acid due to lactate from acid due to gastroesophageal reflux, and determine if chest pain and heartburn are reliable indicators of gastroesophageal reflux. Eight untreated achalasia patients underwent pre- and postdilation esophageal fluid/food residue lactate and pH analysis, esophageal manometry, 24-hr pH monitoring, and symptom assessment. All patients had a successful clinical outcome and a decrease in lower esophageal sphincter pressure from 29.1 +/- 12.7 to 14.7 +/- 3.8 mm Hg (mean +/- SD; P = 0.04). Abnormal acid exposure was present in two patients before and two patients after dilation. Postdilation acid exposure was mild. Lactate was detected before dilation in all patients. A lactate concentration >2 mmol/liter was associated with acidic residue and one abnormal 24-hr pH profile. There was no correlation between an abnormal 24-hr pH test and age, lower esophageal sphincter pressure, or duration of symptoms prior to treatment. Chest pain and heartburn were unrelated to drops in pH. Gastroesophageal reflux is rare in untreated achalasia and esophageal acidity may result from ingestion of acidic foods or production of lactate. Mild gastroesophageal reflux occurs after dilation but is of no clinical significance. Chest pain and heartburn are not indicators of acid reflux in achalasia.     

Diurnal variation of adrenocortical activity in chronic fatigue syndrome

The nutcracker esophagus, a primary motor disorder, is frequently associated with noncardiac chest pain. However, there are no data on whether its diagnosis, as in other esophageal motility disorders, is delayed. Since the disorder is frequently heralded by alarming symptoms such as chest pain and dysphagia, diagnosis should be made as soon as possible. In this study we assessed the diagnostic delay, if any, in patients with the nutcracker esophagus. Moreover, we were interested in whether the abnormalities described in the distal esophagus could also involve the entire viscus. Fifty-four subjects (age range 23-78 yr) with the nutcracker esophagus were assessed for clinical and manometric variables as an overall group and after dividing them into subgroups according to their symptoms. The manometric variables were compared with those obtained in 61 controls (age range 21-67 yr). Overall, a diagnosis of nutcracker esophagus was made after an average period of 36 +/- 6 months, and surprisingly, this was not different in the various subgroups complaining of either chest pain, dysphagia, or both. Analysis of manometric variables showed that the mean amplitude of contractions was significantly higher in the patients' group at all esophageal body levels, even in the proximal portions. Again, there were no significant differences among the subgroups of nutcracker esophagus with respect to the symptoms. Notwithstanding the presence of alarming symptoms, such as chest pain and dysphagia, the nutcracker esophagus is diagnosed on average after 3 years from the onset of symptoms. Manometric assessment seems to confirm that this entity may indeed represent a primary esophageal motor disorder. The major dysfunction is due to an abnormal increase of contraction amplitude of the entire esophageal body.     

Is Barrett's esophagus characterized by more pronounced acid reflux than severe esophagitis?

OBJECTIVE: Barrett's esophagus is related to gastroesophageal reflux disease (GERD). However, only a small fraction of patients with GERD develop Barrett's esophagus. We evaluated whether gastroesophageal acid reflux is more pronounced in Barrett's patients than in patients with moderate or severe endoscopic esophagitis. METHODS: Retrospective evaluation of results of esophageal manometry and 24 hour ambulatory pH monitoring performed between 1990 and 1996 at the Leiden University Medical Center in those patients who also underwent endoscopy < or = 3 months before pH-metry. Included were 51 patients with Barrett's esophagus, 30 patients with severe esophagitis, 45 patients with moderate esophagitis, and 24 healthy control subjects. RESULTS: Patients with Barrett's esophagus had significantly increased acid reflux time (p < 0.01-0.05) compared to patients with moderate, but not compared to patients with severe esophagitis. Distal esophageal body motility and LES pressure were significantly (p < 0.01-0.05) reduced in patients with Barrett's esophagus compared to patients with moderate esophagitis but not compared to those with severe esophagitis. CONCLUSION: Although acid reflux is increased in patients with Barrett's esophagus and esophageal motility is impaired, other factors apart from acid exposure and motility contribute to the development of Barrett's esophagus.     

Oesophageal sensitivity to acid in patients with non-cardiac chest pain: is the oesophagus hypersensitive?

During the past decade, gastro-oesophageal reflux disease has been shown to be the most common identifiable cause of non-cardiac chest pain of oesophageal origin. The development of combined pH-pressures recording systems has also contributed to a better understanding of the underlying mechanisms of pain perception. Beside typical gastro-oesophageal reflux disease, many patients with non-cardiac chest pain appear to have an hypersensitivity to acid or mechanical stimuli, or both. Despite new insights into the pathophysiology of gastro-oesophageal reflux disease, therapy is limited to the suppression of noxious stimuli by antisecretory drugs or surgery. New therapeutic approaches using drugs affecting visceral perception, and well-controlled placebo trials are urgently needed.     

Multiple attachment mechanisms of corneal epithelial cells to a polymer--cells can attach in the absence of exogenous adhesion proteins through a mechanism that requires microtubules

STUDY OBJECTIVE: To determine whether emergency patients with acute chest pain and low suspicion of acute myocardial infarction (AMI) can be managed cost-effectively and safely in a dedicated chest pain center (CPC) that incorporates mandatory stress testing. METHODS: We assembled a prospective observational case series of consecutive adult patients transferred from the emergency department to a nine-bed, 23-hour CPC in a 564-bed community hospital from January 13 through May 31, 1994. In our institution, all emergency patients with acute nontraumatic chest pain of unclear origin, suggestive of myocardial ischemia but with a low probability of AMI, are transferred to the CPC for further evaluation. All patients in whom AMI is ruled out undergo individually appropriate cardiac diagnostic testing in accordance with CPC clinical guidelines. Patients with end-stage coronary artery disease transferred to the CPC for a "rule-out" protocol only did not undergo further diagnostic testing. Admitted and discharged patients were followed through chart review and telephone survey, respectively. RESULTS: Of the 502 patients transferred to the CPC, 477 (95%) completed follow-up at 14 days. Four hundred ten (86%) were discharged home. Those discharged after diagnostic evaluation yielded negative findings had 100% survival and zero diagnosis of AMI at 5-month follow-up. Overall mortality and incidence of AMI on long-term follow-up for all patients transferred to the CPC were .4% and .2%, respectively. Sixty-seven patients (13%) were admitted from the CPC, of whom 44 (66%) had a final diagnosis of ischemic heart disease (IHD) or AMI. Twenty-four patients with IHD (55%; 6% of stress-tested group) were identified only on further stress testing. Of these patients, seven underwent percutaneous transluminal coronary angioplasty or coronary artery bypass grafting during hospitalization. All were discharged home without major morbidity. Four hundred twenty-four patients (84%) underwent stress testing. The cost of mandatory stress testing to identify one patient with IHD after AMI was ruled out was $3,125. An average cost-per-case savings of 62% was achieved for each patient transferred to the CPC who would have been hospitalized before the inception of the CPC. CONCLUSION: Mandatory stress testing is a safe, cost-effective, and valuable diagnostic and prognostic tool in CPC patients.     

Design and synthesis of small semi-mimetic peptides with immunomodulatory activity based on myelin basic protein (MBP)

Bile reflux has been implicated in the pathogenesis and malignant degeneration of Barrett's esophagus, but clinical studies in patients with adenocarcinoma arising in Barrett's esophagus are lacking. Ambulatory esophageal measurement of acid and bile reflux was performed with the previously validated fiberoptic bilirubin monitoring system (Bilitec) combined with a pH probe in 20 asymptomatic volunteers, 19 patients with gastroesophageal reflux disease (GERD) but no mucosal injury, 45 patients with GERD and erosive esophagitis, 33 patients with GERD and Barrett's esophagus, and 14 patients with early adenocarcinoma arising in Barrett's esophagus. Repeat studies were done in 15 patients under medical acid suppression and 16 patients after laparoscopic Nissen fundoplication. The mean esophageal bile exposure time showed an exponential increase from GERD patients without esophagitis to those with erosive esophagitis and benign Barrett's esophagus and was highest in patients with early carcinoma in Barrett's esophagus (P <0.01). Pathologic esophageal bile exposure was documented in 18 (54.5%) of 33 patients with benign Barrett's esophagus and 11 (78.6%) of 14 patients with early adenocarcinoma in Barrett's esophagus. Nissen fundoplication but not medical acid suppression resulted in complete suppression of bile reflux. Bile reflux into the esophagus is particularly prevalent in patients with Barrett's esophagus and early cancer. Bile reflux into the esophagus can be completely suppressed by Nissen fundoplication but not medical acid suppression alone.     

Heartburn requiring frequent antacid use may indicate significant illness

BACKGROUND: Many otherwise healthy individuals with episodic heartburn self-medicate with over-the-counter antacids. We evaluated clinical characteristics of subjects who had never been medically diagnosed as having any upper gastrointestinal tract disorder and who used antacids for symptomatic relief of heartburn. SUBJECTS AND METHODS: Subjects with at least 3 months of frequent heartburn relieved by antacids, and with heartburn on at least 4 of 7 days during the week prior to study entry, had their medical history and gastrointestinal pathological characteristics recorded. Tests included esophagogastroduodenoscopy, esophageal motility and sensitivity studies, and 24-hour pH monitoring. RESULTS: Of 178 subjects screened, 13 were excluded on the basis of other gastrointestinal diseases at baseline, including diffuse esophageal spasm, peptic ulcer disease, dysplastic columnar metaplasia of the esophagus (Barrett's esophagus), and adenocarcinoma. Ten subjects were ineligible because of insufficient baseline heartburn. The remaining 155 eligible subjects had heartburn for an average of 11 years. Forty-seven percent had daily symptoms and 70% described heartburn severity as moderate, even though on endoscopy most (53%) had normal-appearing esophageal mucosa (grade 0 or 1). Esophageal acid sensitivity was present in 86% of subjects. Mean lower esophageal sphincter pressures and esophageal contractile amplitudes were at the lower limits of normal and total esophageal acid contact time was slightly increased. CONCLUSIONS: Chronic heartburn can reflect a wide range of diagnostic findings, including important underlying pathological features, and may warrant a full medical examination to detect such abnormal conditions and to permit selection of appropriate therapy.     

pH-metric analysis after successful antireflux surgery: comparison of 24-hour pH profiles in patients undergoing floppy fundoplication or Roux-en-Y duodenal diversion

Fundoplication is the most widely used antireflux method, whereas Roux-en-Y duodenal diversion (partial gastrectomy, vagotomy, and Roux-en-Y reconstruction) has been used in fewer patients with more complicated gastroesophageal reflux disease. Abnormal esophageal pH values are normalized after successful fundoplication. However, very little is known about possible changes in the pH profile after successful Roux-en-Y duodenal diversion. A total of 37 patients with severe gastroesophageal reflux disease were treated by fundoplication (n=22) or Roux-en-Y duodenal diversion (n=15). Postoperatively all patients in both groups were symptom free and healing of esophagitis was verified endoscopically. After fundoplication, the 24-hour esophageal acid exposure decreased significantly (P=0.03) and the pH profile normalized (pH<4 in 5.8%+/-2.4% of the recorded time). However, the decrease in esophageal acid exposure was not significant (P=0.77) after successful Roux-en-Y reconstruction and the pH profile remained abnormal (pH<4 in 15.1%+/-4.3%). It was concluded that 24-hour esophageal pH monitoring is a reliable means of assessing the results of fundoplication, but the current test criteria should be reexamined in evaluating the results of Roux-en-Y duodenal diversion. Healing of esophagitis after Roux-en-Y duodenal diversion despite abnormal acid reflux, as shown by 24-hour pH measurements, suggests that duodenal contents also have a role in the pathogenesis of esophagitis in an acid milieu.     

Severe dysphagia, dysmotility, and unusual saccular dilation (diverticulum) of the esophagus following excision of an asymptomatic congenital cyst

Iatrogenic dysmotility syndromes, particularly achalasia-like conditions, occasionally complicate esophageal and paraesophageal surgery. We describe a patient who developed a very unusual (and as far as we know unreported) syndrome characterized by severe dysphagia, esophageal dysmotility (segmental simultaneous contractions of the distal esophagus), and very large saccular outpouching (diverticulum) involving the right wall of the distal half of the esophagus as a consequence of excision of an asymptomatic congenital cyst. The cyst had been discovered as an incidental finding on a preemployment chest x-ray. Our patient's dysphagia did not improve with nonsurgical treatments that are usually successful for idiopathic and iatrogenic achalasia.     

Spread of vancomycin-resistant enterococci: differences between the United States and Europe

We investigate whether symptoms of pressure, tightness, and/or pain in the chest, neck, and/or throat after administration of the 5HT1B/1D agonist avitriptan were associated with objective impairment of the myocardial function on 12-lead electrocardiogram (ECG), continuous ECG (Holter) monitoring, and echocardiography. Migraine sufferers who in two-thirds of all attacks treated with sumatriptan had experienced chest/throat/neck symptoms were chosen for study. Baseline measures included vital signs, a 12-lead ECG and an echocardiogram. Patients (n = 51) who had no clinically significant abnormality at baseline received a high dose (150 mg) of avitriptan orally outside of a migraine attack. If pressure, tightness, and/or pain in the chest, neck, and/or throat occurred, an ECG was obtained, and a repeat echocardiogram was done while the symptoms were present in order to monitor for impairment of myocardial function. If symptoms of these types did not occur within 60 min after administration of the study drug, a second echocardiogram was obtained. Forty-five patients (88%) reported at least one adverse event and 23 (45%) experienced pressure, tightness, and/or pain in the chest, neck, and/or throat after administration of avitriptan. No clinically significant myocardial abnormalities were observed in any patients, even in those who had experienced the targeted symptoms. No other serious adverse event occurred. We concluded that the typical 5HT1B/1D agonist-induced chest/throat/neck symptoms are most unlikely to be of cardiovascular origin.     

Olfactory stimuli provoke diffuse esophageal spasm: reversal by ipratropium bromide

Diffuse esophageal spasm (DES) is a motor disorder of the esophageal smooth muscle characterized by multiple spontaneous contractions and by swallow-induced contractions that are of simultaneous onset, large amplitude, long duration, and repetitive occurrence. Although the pathogenesis of DES is unknown, provocative studies with cholinergic stimulation, esophageal balloon distention, or acid instillation have suggested involvement of both sensory and motor mechanisms. This report describes a patient with DES who would predictably become symptomatic with dysphagia and chest pain upon inhalation of perfume or other strong odors. Using esophageal scintigraphy to quantitate and analyze esophageal transit in this patient, we report for the first time that olfactory stimulation triggers episodes of DES and that such phenomena are mediated through the vagus nerve, because they can be ameliorated by the administration of ipratropium bromide. These observations suggest a new (sensory) pathway for the induction of DES and raise the intriguing possibility that inhaled anticholinergics may have a therapeutic role in the management of spastic esophageal motility disorders.     

Laparoscopic Toupet fundoplication for gastroesophageal reflux disease with poor esophageal body motility

Impaired esophageal body motility is a complication of chronic gastroesophageal reflux disease (GERD). In patients with this disease, a 360-degree fundoplication may result in severe postoperative dysphagia. Forty-six patients with GERD who had a weak lower esophageal sphincter pressure and a positive acid reflux score associated with impaired esophageal body peristalsis in the distal esophagus (amplitude <30 mm Hg and >10% simultaneous or interrupted waves) were selected to undergo laparoscopic Toupet fundoplication. They were compared with 16 similar patients with poor esophageal body function who underwent Nissen fundoplication. The patients who underwent Toupet fundoplication had less dysphagia than those who had the Nissen procedure (9% vs.44%; P=0.0041). Twenty-four-hour ambulatory pH monitoring and esophageal manometry were repeated in 31 Toupet patients 6 months after surgery. Percentage of time of esophageal exposure to pH <4.0, DeMeester reflux score, lower esophageal pressure, intra-abdominal length, vector volume, and distal esophageal amplitude all improved significantly after surgery. Ninety-one percent of patients were free of reflux symptoms. The laparoscopic Toupet fundoplication provides an effective antireflux barrier according to manometric, pH, and symptom criteria. It avoids potential postoperative dysphagia in patients with weak esophageal peristalsis and results in improved esophageal body function 6 months after surgery.     

Coronary arteriovenous malformations in a patient with hereditary hemorrhagic telangiectasia--a case report

Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu) disease is characterized by cutaneous, mucosal, and visceral vascular anomalies. Two patients were previously described with coronary artery aneurysms (ectasia) associated with this disease. This report describes a patient with Osler-Weber-Rendu disease in whom multiple coronary arteriovenous malformations were identified during coronary angiography. The patient presented with anginal chest pain resulting from severe anemia. Upper gastrointestinal endoscopy revealed multiple angiodysplastic lesions throughout the esophagus and stomach.