The WHO MONICA Project, although designed to study longitudinal trends within populations, provides the opportunity for relating rates of validated CHD deaths to nonfatal myocardial infarction across populations. There are major differences between populations in nonfatal as well as fatal coronary event rates. They refute suggestions that high CHD mortality rates are associated with high case-fatality rates or a relative excess of sudden deaths. The high proportion of CHD deaths for which no diagnostic information is available is a cause for concern.
Questionnaire and biochemical measures of smoking were studied in 211 hospital outpatients. Eleven different tests of smoke intake were compared for their ability to categorize smokers and nonsmokers correctly. The concentration of cotinine, whether measured in plasma. saliva. or urine, was the best indicator of smoking. with sensitivity of 96-97 per cent and specificity of 99-100 per cent. Thiocyanate provided the poorest discrimination. Carbon monoxide measured as blood carboxyhaemoglobin or in expired air Introdluction Self-reports of smoking status may not always be reliable, particularly in situations where smokers feel under strong pressure to give up smoking but have not been able to achieve this.'-3 A number of biochemical markers have been used to validate claims of nonsmoking, including measures based on thiocyanate,4-7 nicotine,8 cotinine,9-" and carbon monoxide.4 6"" These measures differ widely in availability, cost, and ease of administration. Measures based on nicotine have the advantage of being specific to tobacco but require expensive laboratory instrumentation. Levels of thiocyanate and carbon monoxide are easier to determine but may be raised through exposures unrelated to smoking, such as traffic emissions and diet. Few studies have attempted to compare the various biochemical tests." We report here a study in which all the markers of smoking currently in widespread use are compared for their ability to categorize smokers and nonsmokers correctly. Methods SubjectsThe subjects for the study were 215 outpatients at St.Mary's Hospital, London. On arrival for their clinic appointment, they were asked to fill in a self-completion questionnaire giving details of smoking habits and to provide samples of blood, expired air, saliva, and urine. There was no prior warning of the survey, but consent for the biochemical tests was obtained before completion of the questionnaire. gave sensitivity and specificity of about 90 per cent. Sensitivities of the tests were little affected by the presence among the claimed nonsmokers of a group of 21 "deceivers" who concealed their smoking. It is concluded that cotinine is the measure of choice, but for most clinical applications carbon monoxide provides an acceptable degree of discrimination and is considerably cheaper and simpler to apply. (Am J Public Health 1987; 77:1435-1438 cigarette smokers at some time and 90 (43 per cent) said that they were current smokers of cigarettes, pipes, or cigars. Reported mean cigarette consumption in the cigarette smokers was 13.2 cigarettes per day, and 97 per cent reported having smoked on the test day. with a mean time since last cigarette of 1.5 hours.The concentration of nicotine and cotinine in plasma, saliva, and urine was determined by gas chromatography.'3"14 Carboxyhaemoglobin concentrations were measured with an IL282 CO-Oximeter and carbon monoxide in expired air after breath-holding with a portable CO analyzer incorporating an ethanol filter.'5 Thiocyanate was measured by an automated modification of the A...
miological studies have reported positive associations between the risk of coronary heart disease (CHD) and plasma fibrinogen levels. Fibrinogen is the major coagulation protein in blood by mass, the precursor of fibrin, and an important determinant of blood viscosity and platelet aggregation. [38][39][40][41] Because fibrinogen levels can be reduced considerably by lifestyle interventions that also affect levels of established risk factors (such as regular exercise, smoking cessation, and moderate alcohol consumption), there is interest in the possibility that measurement (or modification) of fibrinogen may help in disease prediction or prevention. [38][39][40]42 A meta-analysis of published data from 18 such studies, involving about 4000 CHD cases, indicated a relative risk of 1.8 (95% confidence interval [CI], 1.6-2.0) per 1-g/L increase in plasma fibrinogen level. 43 However, such analyses are not able to provide detailed assessments of the nature of any independent association of fibrinogen level with CHD or with other vascular and nonvascular outcomes. [43][44][45] This meta-analysis differs from previous analyses in several ways that should increase its reliability and scientific value. First, it is large and comprehensive: the data comprise 6944 first nonfatal myocardial infarction (MI) or stroke events and 13 210 deaths (cause-*The Authors/Writing Committee, Authors/Members, and Other Members of the Fibrinogen Studies Collaboration are listed at the end of this article.
This document was developed by a consensus conference initiated by Kristian Thygesen, MD, and Joseph S. Alpert, MD, after formal approval by Lars Rydén, MD, President of the European Society of Cardiology (ESC), and Arthur Garson, MD, President of the American College of Cardiology (ACC). All of the participants were selected for their expertise in the field they represented, with approximately one-half of the participants selected from each organization. Participants were instructed to review the scientific evidence in their area of expertise and to attend the consensus conference with prepared remarks. The first draft of the document was prepared during the consensus conference itself. Sources of funding appear in Appendix A. The recommendations made in this document represent the attitudes and opinions of the participants at the time of the conference, and these recommendations were revised subsequently. The conclusions reached will undoubtedly need to be revised as new scientific evidence becomes available. This document has been reviewed by members of the ESC Committee for Scientific and Clinical Initiatives and by members of the Board of the ESC who approved the document on April 15, 2000.*
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