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© 1989 Oxford University Press

research-article

Blood Pressure, Cigarette Smoking and Heart Attack in the WHO Co-operative Trial of Clofibrate

KENNETH G GREEN*, AUSTIN HEADY** and MICHAEL F OLIVER{dagger}

*Ex-ICI Pharmaceuticals PLC Alderley Park, Macclesfield, UK.
**Department of Clinical Epidemiology and General Practice, Royal Free Hospital School of Medicine London, UK.
{dagger}Cardiovascular Research Unit, University of Edinburgh Scotland, UK.

Green K G (c/o Heady, Department of Clinical Epidemiology and General Practice, Royal Free Hospital School of Medicine, London, NW3 2PF, UK), Heady J A and Oliver M F. Blood pressure, cigarette smoking and heart attack in the WHO co-operative trial of clofibrate. International Journal of Epidemiology 1989, 18: 355–360.

In the WHO sponsored trial of clofibrate and its follow-up, about 15000 men were observed for a mean period of 13.2 years. As expected, incidence of heart attacks (HA) was directly related to serum cholesterol, blood pressure (BP) and cigarette smoking. The previously reported lower incidence of HA in men receiving clofibrate compared with controls was most noticeable in hypertensive heavy smokers (P<0.01).

BP was slightly lower in smokers than non-smokers (P<0.01). The difference in BP was greater in the trial visit before HA. Smokers also had higher plasma fibrinogen levels (P<0.05). The combination of reduced diastolic BP, and therefore myocardial perfusion pressure, with an increased thrombogenic tendency, might explain the high incidence of HA in smokers.

Clofibrate apparently reduced fibrinogen levels, which might account for its specially good effect in preventing HA in smokers. However, the ill effects of smoking are still evident at a lower level in the men taking clofibrate and the drug is no substitute for giving up the habit.

Clofibrate is not recommended for widespread use, except in subjects with marked lipid and/or blood fibrinogen abnormalities after dietary measures have been tried.

Received 1 November 1988


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