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SUMMARY Data from two community studies on men from South Wales and the west of England suggest that the effects of smoking on the haemostatic system remain for many years after giving up. Long term correlations between several variables, including plasma fibrinogen and white cell count, and the length of time after giving up were seen in ex-smokers. Dose response relations were apparent in current smokers in terms of the white cell count and two haematological variables, the packed and mean cell volumes. These long term correlations probably reflect the toxicity of other agents in tobacco smoke besides nicotine and carbon monoxide, which act only in the short term. Identification of these agents may further our understanding of the mechanism by which cigarette smoking is associated with atherosclerotic disease.Evidence is accumulating that haemostatic factors have a pathogenetic role in ischaemic heart disease' 2 and stroke.3 Smoking habit is known to affect substantially several haemostatic factors4 I and is also a major risk factor for ischaemic heart disease.6 7 This paper examines the activity of several haemostatic factors in non-smokers, smokers, and ex-smokers in two community studies on men from South Wales and the west of England. Material and methods STUDY POPULATIONSAll men aged between 45 and 59 years resident in the town of Caerphilly and five outlying villages (total population 41000) were included in the study. Subjects were selected principally from electoral registers and a private census carried out by letter and houseto-house survey. Age and sex registers and practice records were also used as an additional check on the eligible population. Twenty one general practitioners served the area covered by the survey working in seven independent surgeries. Accepted for publication 13 March 1987 In Bristol computerised age and sex registers of patients were available for all 16 general practitioners who worked from two health centres serving Speedwell, a largely residential district of east Bristol (total population 32 000). All male subjects aged 45 to 59 years of age on September 1 1979 were selected and invited by letter from their general practitioner to participate in the survey. SURVEY METHODSIn Caerphilly a total of 2818 men were included and invited to attend one of seven local clinics for a medical examination. A total of 2512 (89%) subjects were examined. A questionnaire was filled in by all subjects for details of medical history, occupation, and smoking habit, and other data.In the Bristol population 2550 men were included in the study, and 2348 (92%) subjects were seen at the Speedwell clinic. Questionnaires used in this survey were identical in essential respects with those used in Caerphilly. LABORATORY METHODSAll subjects were seen at a morning haematology clinic, and a venous blood sample was obtained with 909 on 11 May 2018 by guest. Protected by copyright.

The Caerphilly Collaborative Heart Disease Study is based on a large cohort of men who were ages 49 to 64 years at the time of the study. We report the results for platelet aggregation measured in whole blood from a subsample of 308 men. The index of sensitivity used was the minimum concentration of adenosine diphosphate that produced a defined degree of impedance change in the Chronolog 560 aggregometer. There was a marked association between aggregation and prevalent ischemic heart disease (IHD). The odds ratios and 95% confidence intervals (Cl) for prevalent IHD in men with the most sensitive platelets compared with those with the least sensitive platelets were 3.6 (95% Cl: 1.1 to 12.2) for angina; 7.3 (95% Cl: 2.0 to 24.3) for previous myocardial infarction (Ml); and 2.7 (95% Cl: 1.0 to 7.6) for electrocardiogram evidence of ischemia. The confidence limits for these odds ratios are large because of the small sample size, but the estimates of odds ratio are relatively large compared to similar relationships between the traditional risk factors of serum cholesterol, blood pressure, smoking, and prevalent IHD (1.5 to 2.5). A number of factors that might confound the relationships between platelets and IHD were examined, but the associations remained statistically significant when these were taken into account. (Arteriosclerosis 10:1032-1036, November/December 1990) E vidence is accumulating that platelets play a key role in ischemic heart disease (IHD). Case-control studies demonstrate positive relationships between increased platelet aggregation and IHD 12 but of course suffer from the inferential dilemma of whether differences in platelet aggregation preceded the IHD event or were caused by it.Platelet aggregability is usually assessed by turbidimetric methods with the use of platelet-rich plasma (PRP) prepared by centrifugation and diluted to a standard platelet concentration. These preparatory procedures are likely to modify the subsequent behavior of the platelets, and in addition to this, red blood cells and other components of whole blood that may affect platelet behavior are removed and are not involved in the test. A more realistic procedure for public health screening would seem to be the testing of platelets in whole blood. In this article, we report the association between aggregation measured in whole blood by an impedance method and IHD in a population sample of older men. MethodsIn the Caerphilly Heart Disease Study, 3 a major emphasis is put on tests of hemostasis, including the measurement of platelet aggregation to adenosine diphosFrom the MRC Epidemiology Unit, Cardiff, South Wales, UK, and INSERM, Unite 63, Bron, France.Stephen Rogers is now at the Institute of Medical Research, Tari, Papua New Guinea.Address for correspondence: Dr. P.C. Elwood, MRC Epidemiology Unit, 4 Richmond Road, Cardiff CF2 3AS, South Wales, UK.Received January 18, 1990; revision accepted May 1, 1990. phate (ADP) in PRP. Toward the end of the second phase of examinations of the men in this cohort, resources became a...

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A randomized controlled trial has been set up to examine the effect of diet on the secondary prevention of myocardial infarction, involving 2033 men. The trial has a factorial design, subjects being randomized independently to receive advice or no advice regarding three dietary factors: 1. a reduction in total fat and an increase in polyunsaturated fat intake; 2. an increase in fatty fish intake; 3. an increase in cereal fibre intake. Nearly half the men under 70 years of age who survived myocardial infarction during the recruitment period entered the trial, the commonest reason for exclusion being that the subject was already eating (or intended to eat) a diet which included one or more of the regimens being investigated. Detailed dietary questionnaires were completed by each subject after 6 months in the trial. The results suggest that compliance with the advice is reasonably good. The differences between the diets of the groups given and not given advice on fish and fibre were substantial; the difference attributable to advice on fat has been somewhat less than anticipated, partly because of failure to comply with advice and partly because of spontaneous changes in the diets of control subjects.