Coronary heart disease is the leading cause of death for both men and women in the United States. One of the most characteristic and troubling features of coronary disease is the sudden and unexpected onset of symptoms in clinically stable patients and sometimes in even previously healthy individuals.

The development of symptoms is associated with an increased risk of sudden death, acute myocardial infarction, and other life-threatening complications. The development of symptoms suggestive of coronary disease therefore mandates prompt and accurate diagnosis and treatment.

The cardinal symptom of coronary artery disease (CAD) is angina, which classically presents as a squeezing or strangulating deep chest discomfort that may radiate to the arm or jaw. Angina that is brought on by exercise stress and is relieved promptly after cessation of exertion is termed "typical angina." Stable angina is a pattern of symptoms that has been unchanged for 6 or more weeks. Unstable angina is a pattern of symptoms that is new in onset, changing in severity or frequency, occurring at rest, or lasting longer than 20 minutes.

The evaluation of suspected coronary disease is complicated by the fact that chest discomfort has many causes, and bona fide coronary disease may present in an atypical fashion. Thus, a population of patients with symptoms suggestive of coronary disease includes some patients with acute, life-threatening medical problems, some patients with other medical problems mimicking CAD, and even some "worried well" in need only of reassurance.

The evaluation and treatment of this highly heterogeneous population is the difficult task for clinicians in emergency departments (ED) and in office practice. The key goal of these clinicians must be to identify the patient's short-term risk. The high-risk patient may develop life-threatening complications and require hospitalization and immediate therapy. The low-risk patient may need further evaluation, but in a less urgent and less costly setting. Because identification of patient risk is central to all further patient management in unstable angina, this evidence report focuses on clinical and laboratory markers of patient risk, such as results of diagnostic tests (troponin values, stress testing, echocardiography, and nuclear scintigraphy).

Because chest pain units attempt to "risk stratify" (group patients according to their degree of risk) based on readily available data, an assessment of the efficacy of chest pain units is significant to this report. Our in-depth review focused on information that would be readily available to all providers caring for patients with suspected unstable angina. Information in this report applies to adult men and women.

Private health plans and government health insurance programs in the United States base their coverage decisions on evidence criteria, rather than explicit cost-effectiveness criteria. As health spending continues to grow rapidly, however, approaches to coverage policy that ignore costs fail to meet the needs of consumers, employers, health plans, and federal and state governments. I describe the role of evidence-based criteria in formal coverage decision making and contrast the ways that these criteria differ from cost-effectiveness criteria. Finally, I discuss options for incorporating considerations of cost-effectiveness into coverage policy and other aspects of benefit design.

To assess the benefits of intervention programs against Helicobacter pylori infection, we estimated the baseline curves of its incidence and prevalence. We developed a mathematical (compartmental) model of the intrinsic dynamics of H. pylori, which represents the natural history of infection and disease progression. Our model divided the population according to age, infection status, and clinical state. Case-patients were followed from birth to death. A proportion of the population acquired H. pylori infection and became ill with gastritis, duodenal ulcer, chronic atrophic gastritis, or gastric cancer. We simulated the change in transmissibility consistent with the incidence of gastric cancer and duodenal ulcer over time, as well as current H. pylori prevalence. In the United States, transmissibility of H. pylori has decreased to values so low that, should this trend continue, the organism will disappear from the population without targeted intervention; this process, however, will take more than a century.

BACKGROUND: Cigarette smoking is a major risk factor for several chronic oxidative diseases that can be ameliorated by antioxidants.

OBJECTIVES: This study identified the typical dietary intakes and the major food group contributors of the antioxidants beta-carotene, vitamin C, and vitamin E by smoking status.

DESIGN: The 1994-1996 Continuing Survey of Food Intakes by Individuals (CSFII) provided the current sample (n = 6749), who were categorized as non- (n = 3231), former (n = 1684), and current (n = 1834) smokers. In the CSFII, individuals' food intakes were estimated with two 24-h dietary recalls. Data were analyzed by using a chi-square test with a simultaneous Fisher's z test, analysis of variance with Scheffe's test, multivariate analysis of covariance, and analysis of covariance with Bonferroni adjustment for multiple comparisons.

RESULTS: The sample consisted of 3707 men and 3042 women. Current smokers tended to be younger with less education and lower incomes than nonsmokers and former smokers. The average body mass index (in kg/m(2)) of current smokers was 25.8, the lowest of the 3 groups. Current smokers had the lowest dietary antioxidant intake. Fatty foods such as luncheon meats, condiments and salad dressings, and ground beef contributed more to the antioxidant intakes of current smokers than to those of the other 2 groups, whereas fruit and vegetables contributed less. Current smokers consumed the fewest numbers of servings of all nutrient-bearing groups in the food guide pyramid, except the meat group.

CONCLUSION: Future interventions should target the clustering of cigarette smoking and other unhealthy lifestyle habits, eg, an imprudent diet.

Context: Helicobacter pylori commonly infects humans; however, its mode of transmission remains unknown.

Objective: To determine how humans-the primary host for H pylori-shed the organism into the environment.

Design: Controlled clinical experimental study conducted from February through December 1998.

Setting: Clinical research unit of a hospital in northern California.

Patients: Sixteen asymptomatic H pylori-infected and 10 uninfected adults.

Intervention: A cathartic (sodium phosphate) and an emetic (ipecac) were given to all infected subjects and an emetic was given to 1 uninfected subject.

Main Outcome Measure: Confirmed H pylori isolates cultured from stool, air, or saliva before and after catharsis and emesis and from vomitus during emesis. Isolates were fingerprinted using repetitive extragenic palindromic (REP) polymerase chain reaction and species identity was confirmed by sequencing the 16s ribosomal RNA gene.

Results: All vomitus samples from infected subjects grew H pylori, often in high quantities. Air sampled during vomiting grew H pylori from 6 (37.5%) of the 16 subjects. Saliva before and after emesis grew low quantities of H pylori in 3 (18.8%) and 9 (56.3%) subjects, respectively. No normal stools and only 22 (21.8%) of 101 induced stools grew the organism, although 7 (50.0%) of 14 subjects had at least 1 positive culture (2 stool culture samples were contaminated by fungus and were not included). Fingerprints of isolates within subjects were identical to one another but differed among subjects. No samples from uninfected subjects yielded H pylori.

Conclusions: Helicobacter pylori can be cultivated uniformly from vomitus and, occasionally, from saliva and cathartic stools. The organism is potentially transmissible during episodes of gastrointestinal tract illness, particularly with vomiting.