非心源性胸痛患者的食管动力异常及兰索拉唑治疗

目的：探讨食管运动功能检查及兰索拉唑治疗试验对非心源笥胸痛患者病因诊断的价值。方法 对６３例经临床及心血管方面检查明显为非心脏起因的发作性胸痛患者进行内镜、食管测压、２４ｈ食腔内ＰＨ监测及７天的兰索拉唑治疗试验。结果：６３例中符合胃食管反流病（ＧＥＲＤ）４４例（７０％）,非特异性食管运动障碍６例（１０％）,贲门失弛症３例（５％）,未明原因１０例,兰索拉唑治疗试验对诊断ＧＥＲＤ的敏感性为９１％, 安     

Esophageal motility disorders

Esophageal motility disorders consist of a complex array of disturbances in normal esophageal function associated with dysphagia, gastroesophageal reflux, and noncardiac chest pain. A thorough knowledge of normal esophageal anatomy and physiology is important to a full understanding of these motility derangements. Through a complicated interaction of neuromuscular and hormonal influences, the voluntary act of swallowing transforms into an automated sequence of peristaltic waves propelling food and liquids into the stomach in concert with coordinated relaxation of the sphincters. Anatomic and physiologic barriers exist within the esophagus protecting against gastroesophageal reflux and aspiration. With improvements in diagnostic tools such as barium contrast radiography, scintigraphy, pH measurements, and esophageal manometrics with provocative testing, motility disorders have become better defined and understood. Primary motility disorders consist of achalasia, diffuse esophageal spasm (DES), "nutcracker esophagus," hypertensive lower esophageal sphincter, and nonspecific esophageal motility dysfunction (NEMD). A host of secondary and miscellaneous motility disorders also affect the esophagus, including scleroderma and other connective tissue diseases, diabetes mellitus, Chagas' disease, chronic idiopathic intestinal pseudo-obstruction, and neuromuscular disorders of striated muscle. Gastroesophageal reflux disease (GERD) may also be promoted by associated motility disturbances. Treatment modalities include surgical myotomy; dilatation; and pharmacologic manipulations, including use of nitrates, calcium-channel blockers, H2-blockers, and psychotropic drugs where appropriate.     

Esophageal motility disorders with thoracic pain of unknown origin

35 patients with angina-like chest pain underwent esophageal manometry after a coronary artery disease had been ruled out by angiography. Furthermore, patients after gastric or esophageal surgery, with pathologic upper gastrointestinal endoscopy or with pathologic gastroesophageal reflux as seen on 24-hour-pH-metry were excluded from this study. 29 out of 35 patients (83%) had a normal manometric study, six patients (17%) had a motility disorder; five of these showed an unspecific dismotility pattern and were asymptomatic while the study was done; only one patient presented with esophageal spasm. Since only this latter patient was symptomatic while the study was done, a correlation between symptoms and this motility disorder seems likely. --If pathologic gastroesophageal reflux has been ruled out, esophageal manometry can establish a diagnosis in only 3% of patients with angina-like chest pain without esophageal symptoms (dysphagia, odynophagia, heartburn or regurgitation). We conclude that this complicated examination should not be done in these patients.     

Esophageal chest pain

Recurrent chest pain frequently results in significant disability and anxiety, even after cardiac disease has been excluded. A stepwise approach is recommended for the diagnosis of pulmonary conditions, musculoskeletal disorders and structural problems of the upper gastrointestinal tract that can produce chest pain. If a search for these disorders proves negative, an esophageal source of chest pain should be strongly suspected. Although gastroesophageal reflux disease is the most common and easily treated cause of esophageal chest pain, esophageal motility disorders should also be considered. Motility disorders include achalasia, diffuse esophageal spasm, nutcracker esophagus, hypertensive lower esophageal sphincter and nonspecific motility disorders.     

Esophageal manometrics in patients with angina-like chest pain.

Fifty-eight patients with angina-like chest pain had esophageal manometric testing. Forty-three had no evidence of coronary artery disease at the time of referral or at subsequent contact; 15 patients were proven to have coronary artery disease. High-amplitude contraction waves were the most frequently found manometric abnormality (15 patients). Less frequent were increased duration of contractions, achalasia, and diffuse esophageal spasm; the latter was present in only 3 patients. An approach to the interpretation of information obtained during manometry is presented. Using this approach, the esophagus was strongly implicated as the cause of the pain in 20 patients and was suspect in 18 others. Seven patients had results that exonerated the esophagus, and in the 13 remaining individuals, the esophagus was probably not the offending organ.     

Esophageal motility disorders in critically ill patients: a 24-hour manometric study

OBJECTIVE: Impaired tubular esophageal motility is involved in the pathogenesis of gastroesophageal reflux disease, which, in turn, has been shown to cause nosocomial pneumonia in critically ill patients. As multiple factors are involved, this pilot study was undertaken to evaluate whether, similarly, impaired esophageal motility may contribute to nosocomial infections by determining esophageal motility in critically ill patients undergoing mechanical ventilation and sedation in comparison to that of a healthy control group. DESIGN: Open, single-centered study. PATIENTS AND METHODS: Fifteen consecutive ventilated intensive care unit (ICU) patients with different diseases and three regimens of analgo-sedation were included: group 1: no analgo-sedation, group 2: ketamine and benzodiazepines, and group 3: fentanyl and benzodiazepines. Six healthy volunteers were studied as controls. Twenty-four hour esophageal anterograde (propulsive) and retrograde motility changes were assessed by a manometry system. RESULTS: The frequencies of contractions were 0.67 +/- 0.1/min (no analgo-sedation) 0.093 +/- 0.02 (ketamine) and 0.076 +/- 0.01 (fentanyl) (p < 0.05 as compared to controls). The amplitudes (% of maximum) were 98 % (control), 58 % (analgo-sedation), 38 % (ketamine) and 42 % (fentanyl; p < 0.05 for the comparison of fentanyl and ketamine with controls). Whereas the percentage of propulsive contractions was significantly decreased in patients (no sedation: 45 %, ketamine: 34 %; fentanyl: 35 %, p < 0.05) as compared to controls (72 %), the percentage of retrograde contractions increased: no sedation: 29 %, ketamine: 34 % and fentanyl: 37 % as compared to controls: 10 %, p < 0.05. Analysis according to the underlying diseases showed marked inhibition of motility parameters within any disease group in comparison with controls. CONCLUSIONS: Irrespective of the underlying disease, propulsive motility of the esophageal body is significantly reduced during any kind of sedation in critically ill patients. Possibly central as well peripheral drug-related effects are involved in such a depression. Twenty-four hour motility recordings appear to be a valuable and feasible method to quantify and analyze esophageal motor disorders in critically ill patients.     

Cocaine-associated chest pain

The pathophysiology of cocaine leading to myocardial ischemia is multifactorial. Given the paucity of well-designed clinical studies, treatment is directed toward the potential mechanisms involved in the development of myocardial ischemia. Fortunately, morbidity and mortality in this patient population are low, and the vast majority of patients will not suffer AMI or other cardiac complications. Long-term prognosis is excellent for those who abstain from continued cocaine use.     

Non-cardiac chest pain

Psychiatric illness is present in up to 50 per cent of new patients attending a cardiac clinic with chest pain. This article provides guidance on the positive diagnostic features of such illness.     

Cocaine-induced chest pain

Cocaine-associated chest pain is a clinical entity that crosses all socioeconomic groups and hence will be encountered by many physicians. The initial evaluation and treatment of cocaine-induced chest pain are similar to those of patients who have non-cocaine-induced chest pain, but there are several notable exceptions. This article reviews the pathophysiology, evaluation, management, and disposition decisions unique to patients presenting with cocaine-induced chest pain.     

Cocaine-associated chest pain

Current estimates establish that more than 30 million people in the United States use cocaine. Cardiovascular complaints commonly occur among patients who present to emergency departments(EDs) after cocaine use, with chest pain the most common complaint in several studies. Although myocardial ischemia and infarction account for only a small percentage of cocaine-associated chest-pain, physicians must understand the pathophysiology of cocaine and appropriate diagnostic and treatment strategies to best manage these patients and minimize adverse outcomes. This article reviews the pharmacology of cocaine, its role in the pathogenesis of chest pain with specific emphasis on inducing myocardial ischemia and infarction, and current diagnostic and management strategies for cocaine-associated chest pain encountered in the ED.