The Caerphilly Collaborative Heart Disease Study is based on a large cohort of men (2,398) aged 49-66 years at the time of study. Platelet aggregation induced by collagen, thrombin, and ADP was measured in fasting blood samples and was related to prevalent angina, past myocardial infarction, and electrocardiographic evidence of ischemic heart disease. A number of subjects had taken aspirin, other nonsteroidal anti-inflammatory drugs, or other drugs affecting platelet aggregation 7 days before blood sample collection; after the exclusion of these subjects, data were available for 1,811 men. No relations were demonstrated with angina, but significant relations were shown between past myocardial infarctions and electrocardiographic evidence of ischemia and ADP-induced aggregation (both primary and secondary) and between electrocardiographic evidence of ischemia and thrombin-induced aggregation. The strongest relation indicated more than a twofold increase in the odds of a past myocardial infarction in subjects of the highest fifth of ADP-induced primary platelet aggregation compared with the lowest fifth. No significant relations were detected with collagen-induced aggregation. Accounting for a number of possible confounding factors had a relatively small impact on the relations between platelet aggregation and ischemic heart disease. Other evidence, including the well-established effect of aspirin on reducing the incidence of ischemic heart disease, indicates that the relations we describe are unlikely to be simply an effect of IHD on platelets.

Objective-To examine the associations between air temperature and risk factors for ischaemic heart disease. Method-Data on risk factors are available from up to 2036 men in the Caerphilly Prospective Heart Disease Study. Daily temperatures were obtained from the Meteorological Office. Relations between these were examined by regression. Results-The coldest month of the year has a mean temperature that is 16°C lower than that in the warmest month. A fall in temperature of this magnitude is associated with higher blood pressures (by 3-5 mm Hg) and a lower concentration of high density lipoprotein cholesterol (by 0-08 mmolRl). The most important effects however, seem to be on the haemostatic system. Fibrinogen is 0*34 gil higher in the coldest month than in the warmest (p < 0.001) and a, macroglobulin, a protein that inhibits fibrinolysis, is also raised. Platelet count is increased by 30%!. of a standard deviation and the sensitivity of platelets in whole blood to adenosine diphosphate is increased by cold. Conclusions-These effects on haemostasis, together with the effect on blood pressure, could explain a large part of the increase in ischaemic heart disease in the winter but are unlikely to explain much of the difference in mortality within different areas of England and Wales. (Br Heart3J 1993;70:520-523) Deaths from ischaemic heart disease and admissions to hospital for both myocardial infarction and pulmonary embolus are considerably higher in winter than the summer.l1 The meteorological factor of greatest importance seems to be temperature.25 West and Lowe have further suggested that the between town variation in the mortality of ischaemic heart disease in England and Wales may be a consequence of differences in environmental temperatures.6 The extent to which the seasonal rise in ischaemic heart disease and related mortality is truly cardiovascular is uncertain. Some have suggested that the effect of temperature is on respiratory disease and the apparent excess in cardiovascular deaths in winter is simply due to miscoding of the cause of death.7 Bainton et al showed that the proportionate increase in deaths was similar in both young and old patients, leading them to conclude that the effect of temperature on the cardiovascular system is direct.8 On the other hand, Mackenbach et al, who examined the seasonal pattern of deaths in The Netherlands over nine years, suggest that there is both an instantaneous effect of winter on the cardiovascular system, and a delayed effect mediated by respiratory infections.9In this report we examine the associations between ambient air temperature and a range of risk factors for ischaemic heart disease, including blood pressure, lipids, platelets, and other factors related to thrombosis. Patients and methodsThe Caerphilly study is fully described elsewhere.'10 1 It is based on a large cohort of men in South Wales. Each man was first seen at an afternoon or evening clinic at which blood pressure was recorded on a random zero muddler sphygmomanometer. Men were ...

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...

Summary.A platelet test that is predictive of myocardial infarction (MI) and/or stroke would enable the targeting of anti-platelet drugs towards high-risk patients. The predictive power of several platelet tests for MI and for stroke was examined in 2000 older men in the Caerphilly Cohort Study of Heart Disease, Stroke and Cognitive Decline. The tests were: aggregation to adenosine diphosphate (ADP) in platelet-rich plasma (PRP); aggregation to ADP in whole blood measured using an impedance method and a test of platelet aggregation induced in whole blood by high-shear flow. Around 200 MIs and 100 ischaemic strokes occurred during a 10-year follow-up. Neither primary nor secondary aggregation in PRP was predictive of MI. However, the fifth of men in whom the primary response to ADP was least, showed the highest risk of a subsequent stroke [relative odds (RO) 1´64; 95% confidence interval (CI) 1´12±2´43]. Aggregation in whole blood was not predictive of MI but, again, the fifth of men with the least platelet response showed the highest stroke incidence (RO 1´79; 95% CI 1´06±3´00). Retention of platelets in the high-shear test was not predictive of either event.