Peptic ulcer disease

Peptic ulcer disease usually occurs in the stomach and proximal duodenum. The predominant causes in the United States are infection with Helicobacter pylori and use of nonsteroidal anti-inflammatory drugs. Symptoms of peptic ulcer disease include epigastric discomfort (specifically, pain relieved by food intake or antacids and pain that causes awakening at night or that occurs between meals), loss of appetite, and weight loss. Older patients and patients with alarm symptoms indicating a complication or malignancy should have prompt endoscopy. Patients taking nonsteroidal anti-inflammatory drugs should discontinue their use. For younger patients with no alarm symptoms, a test-and-treat strategy based on the results of H. pylori testing is recommended. If H. pylori infection is diagnosed, the infection should be eradicated and antisecretory therapy (preferably with a proton pump inhibitor) given for four weeks. Patients with persistent symptoms should be referred for endoscopy. Surgery is indicated if complications develop or if the ulcer is unresponsive to medications. Bleeding is the most common indication for surgery. Administration of proton pump inhibitors and endoscopic therapy control most bleeds. Perforation and gastric outlet obstruction are rare but serious complications. Peritonitis is a surgical emergency requiring patient resuscitation; laparotomy and peritoneal toilet; omental patch placement; and, in selected patients, surgery for ulcer control.     

Update on Helicobacter pylori treatment

One half of the world's population has Helicobacter pylori infection, with an estimated prevalence of 30 percent in North America. Although it is unclear whether eradication of H. pylori improves symptoms in patients with nonulcer dyspepsia, there is strong evidence that eradication of this bacteria improves healing and reduces the risk of recurrence or rebleeding in patients with duodenal or gastric ulcer. A "test-and-treat" strategy is recommended for most patients with undifferentiated dyspepsia. With this approach, patients undergo a noninvasive test for H. pylori infection and, if positive, are treated with eradication therapy. This strategy reduces the need for antisecretory medications as well as the number of endoscopies. The urea breath test or stool antigen test is recommended. Until recently, the recommended duration of therapy for H. pylori eradication was 10 to 14 days. Shorter courses of treatment (i.e., one to five days) have demonstrated eradication rates of 89 to 95 percent with the potential for greater patient compliance. A one-day treatment course consists of bismuth subsalicylate, amoxicillin, and metronidazole, all given four times with a one-time dose of lansoprazole. In children with documented H. pylori infection, however, all regimens should continue to be prescribed for seven to 14 days until short-course treatment is studied and its effectiveness has been established in this population.     

Evaluation and management of nonulcer dyspepsia

When no organic cause for dyspepsia is found, the condition generally is considered to be functional, or idiopathic. Nonulcer dyspepsia can cause a variety of symptoms, including abdominal pain, bloating, nausea, and vomiting. Many patients with nonulcer dyspepsia have multiple somatic complaints, as well as symptoms of anxiety and depression. Extensive diagnostic testing is not recommended, except in patients with serious risk factors such as dysphagia, protracted vomiting, anorexia, melena, anemia, or a palpable mass. In these patients, endoscopy should be considered to exclude gastroesophageal reflux disease, peptic or duodenal ulcer, and gastric cancer. In patients without risk factors, consideration should be given to empiric therapy with a prokinetic agent (e.g., metoclopramide), an acid suppressant (histamine-H2 receptor antagonist), or an antimicrobial agent with activity against Helicobacter pylori. Treatment of patients with H. pylori infection and nonulcer dyspepsia (rather than peptic ulcer) is controversial and should be undertaken only when the pathogen has been identified. Psychotropic agents should be used in patients with comorbid anxiety or depression. Treatment of nonulcer dyspepsia can be challenging because of the need to balance medical management strategies with treatments for psychologic or functional disease.     

Management of Helicobacter pylori infection

Helicobacter pylori is the cause of most peptic ulcer disease and a primary risk factor for gastric cancer. Eradication of the organism results in ulcer healing and reduces the risk of ulcer recurrence and complications. Testing and treatment have no clear value in patients with documented nonulcer dyspepsia; however, a test-and-treat strategy is recommended but for patients with undifferentiated dyspepsia who have not undergone endoscopy. In the office setting, initial serology testing is practical and affordable, with endoscopy reserved for use in patients with alarm symptoms for ulcer complications or cancer, or those who do not respond to treatment. Treatment involves 10- to 14-day multidrug regimens including antibiotics and acid suppressants, combined with education about avoidance of other ulcer-causing factors and the need for close follow-up. Follow-up testing (i.e., urea breath or stool antigen test) is recommended for patients who do not respond to therapy or those with a history of ulcer complications or cancer.     

Gastroscopic real-time 13C-urea breath test

BACKGROUND AND STUDY AIMS: Biopsy-based Helicobacter urease testing (HUT) may constitute a hazard in patients with bleeding disorders, those receiving anticoagulant therapy, and those with communicable diseases. In addition, definitive test results may not immediately be available. The aim of this study was to investigate the feasibility of breath testing for H. pylori during gastroscopy (gastroscopic breath testing, GBT) in comparison with the standard HUT in a prospective, randomized, and controlled study. PATIENTS AND METHODS: A total of 119 patients were randomly allocated to undergo H. pylori testing with either HUT (n = 61) or GBT (n = 58) with 75 mg of 13C-labeled urea by endoscopic instillation. Breath samples were continuously analyzed using molecular correlation spectroscopy, displaying real-time results. The procedure time and time until definitive test results were obtained (mean plus or minus standard deviation) were recorded. RESULTS: H. pylori was detected in 10 of 49 patients (20.4 %) with HUT and in 16 of 53 (30.2 %) with GBT. Contraindications to biopsy prevented HUT in 12 of 61 patients. GBT results could not be obtained in one of the 58 patients due to respiratory disease and in four for technical reasons. Slightly less time was required to carry out HUT than GBT (121 +/- 30 s vs. 164 +/- 36 s; P < 0.001). Definitive test results were available within 14.0 +/- 2.2 min using GBT in comparison with 19.6 +/- 9.1 h for HUT ( P < 0.001). GBT prolonged the time spent by the patient in the endoscopy room by only 5.6 min in comparison with HUT (45.1 +/- 8.5 min vs. 39.5 +/- 10.3 min; P < 0.01). CONCLUSIONS: GBT provides immediate, definitive results and allows H. pylori testing in patients in whom biopsies are contraindicated, with only minimal prolongation of the procedure time.     

Evaluation of urinary rapid test for Helicobacter pylori in general practice

There is increasing interest in noninvasive tests for the diagnosis of Helicobacter pylori (H. pylori) infection. One such test, a urine-based rapid test kit (RAPIRUN H. pylori Antibody, Otsuka Pharmaceutical Co., Ltd.) for detection of antibody to H. pylori, has been developed and is considered ideal. In addition to its noninvasiveness and safe handling-due to use of urine as a sample-the assay procedure used for the urinary rapid test is very simple. Only 10-20 minutes are required to complete an assay, and no instruments are needed. The aim of this study was to examine the clinical usefulness of this urine-based rapid test. A total of 189 patients, including 76 patients with gastroduodenal disease, were recruited. A pair of random single-void urine and serum samples was collected from each of the 189 patients, and antibody to H. pylori in the urine and serum samples was measured using the urine-based rapid test kit and three commercially available serum-based ELISA kits. For the patients with gastroduodenal disease, invasive diagnostic methods using endoscopic biopsy specimens such as culture, histology, and rapid urease test were also performed. The sensitivity, specificity, and accuracy of the urinary rapid test were evaluated on the basis of the three serum ELISA results or the invasive diagnostic results. In addition, various urinalyses were performed, and the effects of substances existing in urine on the urinary rapid test results were examined. Of the 189 patients, the urinary rapid test was positive for 110 (58.2%), negative for 78 (41.3%), and invalid for only one patient (0.5%). Based on the three serum-based ELISA results, the sensitivity, specificity, and accuracy of the urinary rapid test were 93.7, 88.9, and 92.2%, respectively. On the basis of the biopsy-based test results, the sensitivity of the urinary rapid test was 100% and its accuracy (95.2%) was equivalent or superior to that of each serum-based ELISA. In addition, no significant differences were observed between groups positive and negative on urinary rapid testing in any urinalysis parameter examined. The novel urinary rapid test kit evaluated in this study enables simple, rapid, and accurate diagnosis of H. pylori infection, and is an ideal test method for point-of-care testing.     

Helicobacter pylori: aggressor or innocent bystander?

Helicobacter pylori seeks gastric mucosa, whether found in the stomach, duodenum, or Barrett's esophagus. Definitive diagnosis can be secured by appropriate stains of mucosal biopsies and culture, but the rapid urease test, breath isotope studies, and serologic testing are also useful. The frequency of colonization increases with advancing age, but infection occurs earlier in underdeveloped countries. Although the reservoir is uncertain, water or food transmission seems likely. There is sufficient evidence to assign an etiologic role to the bacteria in the causation of type B antral gastritis. H. pylori is found in areas of gastric metaplasia within the duodenum and is associated with duodenitis. Although acute infection leads to hypochlorhydria, chronic colonization has little effect on acid secretion. Studies have thus far failed to establish a convincing relationship between H. pylori and nonulcer dyspepsia, although the bacteria may play a role in selected patients. H. pylori is found in association with most idiopathic gastric and duodenal ulcers, but it is unclear as to whether the bacteria plays a causative or permissive role. The organism has a predilection for intercellular spaces and the mucous layer, thus affording relative isolation from luminally active antibiotics. Monotherapy with bismuth preparations transiently eliminates the bacteria, but recolonization is rapid, probably due to regrowth of sequestered organisms. A combination of metronidazole, bismuth, and tetracycline (or amoxicillin) affords the best eradication rate, but the potential side effects of this program should be considered. The present therapy of duodenal ulcer disease is effective and without significant risk. Treatment of H. pylori should be reserved for those patients who relapse on adequate maintenance therapy. If a safe and effective antibiotic becomes available, more frequent testing and earlier treatment intervention may become more attractive. H. pylori is probably an "innocent bystander" for most patients, but the bacteria may sufficiently impair the defenses of the antral and duodenal mucosa to facilitate the development and relapse of ulcer disease in subsets of patients.     

Laboratory tests for the evaluation of Helicobacter pylori infections.

Helicobacter pylori is a highly motile bacterium with multiple unipolar flagella, and it produces the urease enzyme. The flagella and urease are the virulence factors of H. pylori. H. pylori often establishes a chronic infection in the stomach that may lead to gastric and duodenal ulcers, gastric cancers, gastric lymphomas, and other gastrointestinal diseases. There are several different invasive and noninvasive clinical laboratory tests for H. pylori. Laboratory testing is not indicated in asymptomatic patients and should be considered only if treatment of H. pylori infection is planned. Invasive tests for H. pylori, such as tissue histology, culture, and rapid urease tests, are used if an endoscopy is performed on the patient. The noninvasive tests for H. pylori, such as enzyme antibody and urea breath tests, are recommended in patients whose symptoms do not warrant endoscopy. The urea breath test is very useful and is recommended to evaluate effectiveness in the eradication and treatment of H. pylori infections. Nucleic acid tests can complement other diagnostic procedures, and are useful in evaluating fixed biopsy tissue, environmental samples, gastric juices, oral secretions, and stool samples.     

Resistance problems in gastrointestinal infections

A variety of world-wide resistance problems in bacterial gastrointestinal pathogens have emerged within the last decade. Particularly, antibiotics used to treat salmonella, campylobacter and Helicobacter pylori have lost their efficacy in a high proportion of isolates. Of major clinical significance is the resistance of H. pylori to metronidazole and clarithromycin, of Campylobacter spp. to fluoroquinolones and macrolides and of Salmonella spp. to fluoroquinolones and third generation cephalosporins. Of special concern is the spread of multiresistant isolates. Fortunately, in Clostridium difficile the resistance rate against metronidazole or vancomycin appears to be still low. Numerous investigations provided convincing evidence that the major source of emergence and dissemination of bacterial resistance is the use of antibiotics in food animals. This applies in particular to multiresistant strains of salmonella and campylobacter. A restricted use of antibiotics in the livestock is clearly warranted to control the unlimited development of resistance. The following recommendations should be considered in the care of infections with H. pylori, Campylobacter and Salmonella: 1) Treatment of H. pylori should be restricted to ulcer disease and gastric lymphoma. Eradication is not indicated in asymptomatic patients or patients with gastrointestinal pathologies that are not related to H. pylori. 2) Anti-H. pylori antibiotics should include metronidazole, clarithromycin, amoxicillin or tetracycline in combination of two of them. They should be used in short terms and in the recommended dosages together with proton pump inhibitors. If ulcers relapse after the first eradication, the resistance pattern should be determined. 3) In Campylobacter enterocolitis, antibiotics should be reserved for more severe cases. Resistance testing to exclude quinolone resistance is encouraged if antibiotics are considered. 4) In Salmonella gastroenteritis antibiotics do not significantly improve the course of infection. Their use should thus be restricted to patients which are at risk for disseminated disease including infants, elderly and immunosuppressed persons. 5) Since multiresistant Salmonella are common, resistance testing is highly recommended.     

Possible absence of Helicobacter pylori in the early stages of duodenal ulceration

BACKGROUND: Helicobacter pylori is thought to be a cause of duodenal ulceration, but there is some evidence that it is found less often in early than in later disease. AIM: To assess the presence of H. pylori in patients undergoing endoscopy for dyspepsia, with respect to their duration of symptoms. DESIGN: Retrospective case note review. METHODS: Patients were categorized as having a history greater or less than 6 months, and as H. pylori-positive or -negative, using biopsy rapid urease, culture and PCR tests. RESULTS: Thirty-two duodenal ulcer patients with a history >6 months were all H. pylori-positive according to the PCR test; the five with a shorter history were H. pylori-negative. No patient H. pylori-negative by PCR was positive by the other tests. DISCUSSION: H. pylori was (at least) less commonly present before 6 months. It is possible that H. pylori, although nearly always present after 6 months, is not present at the onset of the disease. Confirmation of this finding would imply that infection with the organism is not the cause of duodenal ulceration, but a factor producing recurrence and chronicity.     

抗原抗体联合诊断幽门螺旋杆菌在社区的临床应用价值

目的：研究基于免疫胶体金技术建立的 Hp抗原抗体联合诊断法在社区医院早期诊断 Hp感染的实用性是否优于其他方法。方法对2014年8月至2015年12月期间分别从北京、武汉、广州及深圳四地收集符合纳入标准的208例患者同步完成快速尿素酶（RUT）、微生物学培养、13C-尿素呼气、血清 Hp-IgG、粪便 HpSA（SAT）、病理组织切片染色检查,并比较上述检查项目Hp检出率的差异。结果 Hp感染阳性患者占总受检样本53．85％,Hp-IgG联合SAT诊断 Hp的敏感性和特异性分别为90．18％和97．92％;相较于其他非侵入检测法,Hp-IgG与SAT联合能显著提高对 Hp诊断的准确性和诊断效率。结论血清IgG联合SAT检测法可作为基层医院诊断 Hp的首选方法,该法适用于广大不发达地区或城市社区医院用于 Hp感染的早期诊断。     

HP根除影响胃食管反流病患者预后的临床及病理分析

目的:探讨根除幽门螺杆菌(Helicobacter pylori, HP)对胃食管反流病(gastro esophageal reflux disease, GERD)疗效及预后的影响。方法:98例GERD患者,均为HP阳性,试验前均行胃镜检查评估食管炎程度及胃粘膜组织病理学改变,然后所有患者随机分为2组:HP根除组49例,接受HP清除三联疗法;对照组49例,仅服用奥美拉唑(20 mg,每日2次)。1周后所有患者开始连续8周的奥美拉唑(20 mg/d)初始治疗阶段,8周后症状缓解及糜烂性食管炎愈合患者开始奥美拉唑10 mgd的维持治疗阶段,直至试验第12个月。初始治疗后症状未完全缓解或内镜下食管炎未完全愈合、维持阶段症状或内镜下食管炎复发为失效病例。试验结束时所有患者均行胃镜复查及14 C呼气试验。结果:试验前共有33 例患者(33.7%)内镜检查发现糜烂性食管炎;试验结束后HP根除组47例患者HP转阴(95.9%),HP阳性组3 例转阴(6.1%),两组HP根除率差异显著(P<0.01);HP根除组16例失效,HP阳性组有7例失效,两者相比差异显著(P<0.05);然而,HP阳性组患者胃体萎缩及胃体肠化较HP根除组明显增多。结论:HP根除可降低质子泵抑制剂(PPI)治疗GERD的疗效,同时HP根除对患者胃体萎缩及胃体肠化有预防作用。     

Update on the evaluation and management of functional dyspepsia

Dyspepsia affects up to 40 percent of adults each year and is often diagnosed as functional (nonulcer) dyspepsia. The defining symptoms are postprandial fullness, early satiation, or epigastric pain or burning in the absence of causative structural disease. These symptoms may coexist with symptoms of functional gastrointestinal disorders, such as gastroesophageal reflux and irritable bowel syndrome, as well as anxiety and depression. The history and physical examination can help identify other possible causes of the symptoms. Warning signs of serious disease, such as cancer, are unintended weight loss, progressive dysphagia, persistent vomiting, evidence of gastrointestinal bleeding, and a family history of cancer. In these cases, more extensive laboratory investigation, imaging, and endoscopy should be considered as clinically indicated. During the initial evaluation, a test-and-treat strategy to identify and eradicate Helicobacter pylori infection is more effective than empiric treatment and more cost-effective than initial endoscopy. Eradication of H. pylori helps one out of 15 patients with functional dyspepsia diagnosed by endoscopy, but may not be cost-effective. Treatment options that may be beneficial for functional dyspepsia include histamine H2 blockers, proton pump inhibitors, and prokinetic agents. Although psychotropic medications and psychological interventions have no proven benefit in patients with functional dyspepsia, they are appropriate for treating common psychiatric comorbidities.     

Reflux disease and Barrett's esophagus

Gastroesophageal reflux disease (GERD) is a common clinical problem. New information suggests that infection with Helicobacter pylori may protect patients from developing GERD and its complications. Endoscopy may be used by clinicians to tailor GERD therapy, but an empirical trial of a proton-pump inhibitor may be an alternative diagnostic approach. Studies continue to show that laparoscopic antireflux surgery is a cost-effective treatment option for patients requiring maintenance therapy with proton-pump inhibitors. However, the minimally invasive nature of the operation should not alter the indications for antireflux surgery, especially for patients with atypical symptoms. It remains unclear why some patients with GERD develop Barrett's esophagus, whereas others do not. Recent guidelines suggest that patients with long-standing GERD symptoms, especially white men over 50 years of age, should undergo endoscopy at least once to screen for Barrett's esophagus. Debate concerning short-segment Barrett's esophagus continues. Intestinal metaplasia at a normal-appearing gastroesophageal junction may be associated with intestinal metaplasia of the stomach and infection with H. pylori, whereas short tongues of intestinal metaplasia in the esophagus are associated with GERD. Cancer surveillance is indicated in short-segment Barrett's esophagus, as dysplasia may develop in these patients. Barrett's esophagus is the only known risk factor for the development of esophageal adenocarcinoma, but the incidence of adenocarcinoma may be lower than previously reported. New clinical guidelines for endoscopic surveillance suggest that the surveillance interval should be lengthened to every two years in patients without dysplasia. Newer treatment options, such as thermal ablation and photodynamic therapy, continue to show promise, but are not yet ready for routine clinical use.     

Pretreatment endoscopy--pro & contra: endoscopy is needed before treatment in all patients with gastroesophageal reflux disease

Most current endoscopic guidelines do not recommend the use of routine esophagoscopy in the evaluation of patients with typical symptoms of gastroesophageal reflux disease (GERD), unless alarm features are present. In patients with known reflux esophagitis, esophagoscopy is considered to have no role either in the further management or follow-up. Screening of reflux patients for Barrett's esophagus is not considered to be cost-effective. On the basis of a critical review of the available literature, and of some recent papers in particular, we disagree with these suggestions. We would argue, on the contrary, that a negative esophagoscopy can provide the GERD patient with reassurance, and that esophagoscopy allows targeted therapy to be offered if it is positive for esophagitis. When Barrett's esophagus is diagnosed, it usually leads to a surveillance program being initiated. The potential benefits of endoscopy for the patient's quality of life are probably underestimated when financial issues alone are taken into account. Even if it is true that a large percentage of GERD patients do not have endoscopic abnormalities (those with nonerosive reflux disease), surrogate tests such as the proton-pump inhibitor test or symptom questionnaires do not provide a more accurate diagnosis. We would therefore suggest that, at least in the specialist setting, all patients with suspected GERD should undergo accurate symptom analysis as well as endoscopic evaluation before treatment is started.     

Helicobacter pylori susceptibility testing by disc diffusion

The bacterium Helicobacter pylori is found in c. 40% of the population and is responsible for the development of duodenal disease. Triple treatment with a proton-pump inhibitor or bismuth salt plus two antibiotics is now commonplace in all patients diagnosed. As antibiotic resistance reduces treatment efficacy, it is time to consider routine susceptibility testing to guide individual patient treatment and surveillance of antibiotic resistance. There are no published nationally agreed standards for disc diffusion testing of H. pylori. After reviewing the literature, we recommend the following method for disc diffusion tests. A suspension of cultures < or = 4 days old equivalent to McFarland Standard no. 4 (10(8) cfu/mL) should be used on Mueller-Hinton or Columbia agar base with 5-10% blood, using a metronidazole disc strength of 5 Ig and a clarithromycin disc strength of 2 microg. Anaerobic pre-incubation of plates is unnecessary. A H. pylori control susceptible to metronidazole (e.g. NCTC 12822) should be used. Zone sizes with the Mueller-Hinton agar base for metronidazole testing are <16 mm resistant, 16-21 mm intermediate and >21 mm susceptible. We suggest that isolates in the intermediate zone should be re-tested by Etest. Zone sizes with the Columbia agar base for metronidazole testing are <10 mm resistant and > or = 10 mm susceptible. Co-infection with two strains, which may be a mixture of isolates susceptible and resistant to metronidazole leading to conflicting susceptibility results, occurs in 5-10% of patients. Zone sizes with Mueller-Hinton agar and Columbia blood agar for clarithromycin testing are resistant no zone and susceptible any zone.     

粪便抗原检测对幽门螺杆菌感染的诊断价值

目的：研究幽门螺杆菌粪便抗原（HpSA）检测诊断幽门螺杆菌（HP）感染的临床应用价值。方法：采用ELISA法检测98例因上消化道症状接受胃镜检查病人的HpSA,同时进行细菌培养,快速尿素酶试验和^14C－尿素呼气试验检查。将后三项检查中二项阳性或细菌培养一项阳性作为诊断HP感染的金标准。结果：金标准诊断HP感染,阳性54例,阴性44例。金标准阳性的54例中,HpSA检测阳性为51例,阴性为3例;金标准阴性的44例中,HpSA检测阴性为42例,阳性为2例。HpSA检测诊断HP感染的敏感度94．4％（51／54）,特异度95．5％（42／44）,准确度94．9％（93／98）,阳性预测值96．2％（51／53）,阴性预测值93．3％（42／45）。结论：HpSA检测有较高的敏感性和特异性,是一种简便可靠,非侵入性的诊断HP感染的方法,易于临床推广。     

Update on exercise stress testing

Exercise stress testing is an important diagnostic tool for the evaluation of suspected or known cardiac disease. In 2002, the American College of Cardiology (ACC) and the American Heart Association (AHA) revised their guidelines for exercise testing. Ten categories from the ACC/ AHA 1997 guidelines were modified: ST heart rate adjustment, unstable angina, older patients, acute coronary syndromes, chest pain centers, acute myocardial infarction, asymptomatic patients, valvular heart disease, rhythm disturbances, and hypertension. Adjustment of the ST heart rate can identify myocardial ischemia in asymptomatic patients with elevated cardiac risk. Intermediate- and low-risk patients with unstable angina, acute coronary syndromes, or chest pain should undergo exercise stress testing when clinically stable. Provided they are stable, patients who have had acute myocardial infarction can undergo a submaximal exercise test before discharge or a symptom-limited exercise stress test any time after two to three weeks have elapsed. In asymptomatic patients with cardiac risk factors, the exercise stress test may provide valuable prognostic information. Aortic regurgitation is the only valvular heart disorder in which there is significant evidence that exercise stress testing is useful in management decisions. The stress test also can be used in older patients to identify the presence of coronary artery disease. However, because of other comorbidities, a pharmacologic stress test may be necessary. Exercise stress testing can help physicians successfully evaluate arrhythmia in patients with syncope. The exercise stress test also can help identify patients at risk of developing hypertension if they show an abnormal hypertensive response to exercise.     

Evaluation of the patient with angina pectoris

All patients with chronic stable angina presumed to be due to coronary artery disease should undergo exercise stress testing early in evaluation for evidence of high-risk coronary disease. If the exercise stress test shows early positive findings, patients should undergo cardiac catheterization to exclude left main coronary vessel disease and three-vessel disease with concomitant left ventricular dysfunction. Patients with unstable angina who are subsequently stabilized on medical therapy should undergo a limited exercise stress test before discharge from the hospital to identify those at high risk. An ambulatory ECG is also helpful in evaluating for evidence of silent ischemia in these patients.