Chapter

Coronary heart disease: epidemiology and prevention

Harry Hemingway and Michael Marmot

in Oxford Textbook of Medicine

Fifth edition

Published on behalf of Oxford University Press

Published in print May 2010 | ISBN: 9780199204854
Published online November 2011 | e-ISBN: 9780199570973 | DOI: http://dx.doi.org/10.1093/med/9780199204854.003.161302_update_001

Series: Oxford Textbooks

Coronary heart disease: epidemiology and prevention

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Unlike many medical conditions that are common, disable, and kill, cardiovascular disease (CVD)—already the most common cause of death in the world, and expected to account for a growing proportion of all deaths—is almost entirely preventable.

Socioeconomic factors and habits of society, including (1) a diet high in saturated fat, (2) sedentary living, and (3) smoking, are important underlying determinants of the population rate of coronary disease. Myocardial infarction (MI) mortality rates vary widely between countries (e.g. more than 10-fold higher in Russia than Japan) and change rapidly over time within countries (e.g. 50% decline in 20 years in western Europe; increases in Russia in the 1990s). Coronary heart disease (CHD) is the most common cause of death in women, and while there is a male excess in MI incidence, women are less protected from angina pectoris.

There are strong, unconfounded relationships between several risk factors and CHD mortality and nonfatal myocardial infarction. Those with the strongest effect are (1) age, (2) country, and (3) presence of symptomatic or preclinical disease. Based on recent individual patient data meta-analysis, systolic blood pressure and cholesterol have a log-linear relation with CHD mortality, with no evidence of lower threshold at every age up to the ninth decade of life. A lower blood pressure is associated with a lower risk, whatever the starting level. The implications of this are profound: shifting the distribution of such a risk factor in the whole population by an apparently small amount has a major effect on population rates of disease, e.g. a 5-mmHg reduction in the population mean systolic blood pressure (e.g. achieved through reductions in dietary salt) is predicted to decrease event rates by 20%.

Observations in cohort studies that specific dietary components—including antioxidant vitamins (A, C, and E), B vitamins, folate, and ω – 3 fats (from fish)—may reduce the rate of coronary events have not been supported by the available randomized trial evidence. Likewise, hormone replacement therapy appeared protective in observational studies, but the Women’s Health Initiative and other trials showed that it was not.

Nine simple risk factors together may account for 90% of the population attributable risk of myocardial infarction across 52 countries in the Interheart study. Yet, despite this apparent triumph of explanation, meta-analyses of peripheral blood markers of inflammatory, haemostatic, and other processes support medium to strong associations for a number of novel factors, independent of established risk factors. The causal significance, or the contribution to prediction, of these ‘biomarkers’ awaits clarification.

Genetic factors—meta-analyses support a small effect of more than 10 common polymorphisms in the aetiology of CHD, although how they interrelate with other genes, or with the environmental factors is not known. Even an apparently ‘simple’ (one gene, dominant inheritance, and complete penetrance) disorder, familial hypercholesterolaemia, probably has complex interactions with the environment in determining the distal phenotype of premature coronary death.

While simple risk factors combine to predict CHD events in individuals, most events occur among people who are not at high risk. For this reason, treatment of high-risk individuals is a palliative action in public health terms.

A major challenge for CHD epidemiology in the future is to understand the macroeconomic and societal forces which influence population rates in the context of the molecular and genetic mechanisms through which they operate.

Chapter.  11740 words.  Illustrated.

Subjects: Cardiovascular Medicine

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