(Circulation. 1999;100:e100.)
© 1999 American Heart Association, Inc.
Circulation Electronic Pages |
New Risk Factors in Primary Prevention
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Introduction |
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 Top Introduction |
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At the great cardiology conferences, preventionists tend to gather in small rooms like early Christians in the Roman Empire, lamenting their failure to spread the word. Among the obstacles discussed in Barcelona at the XXIst Congress of the European Society of Cardiology were the continuing malign influences of the tobacco and food industries, the social class and educational inequalities of heart disease (the poor still die young), the dearth of relevant training at medical schools, and the power games in which specialists claim "ownership" of an activity that should be multidisciplinary. In Europe, a political obstacle is the fact that the European Union’s public health program from 1993 through 2000 barely mentioned coronary heart disease—although, as in the United States, this remains by far the most common cause of death—and the European Commission offers scant funding for prevention projects at the European level.
In the United States, low funding may have a different origin. From 1985 to 1995, allocations to the National Heart, Lung, and Blood Institute rose by only 4.5% (the total budget of the National Institutes of Health rose by 31.3%), and the proportion of funds allocated to heart disease by the Institute actually decreased. Charles Hennekens, Professor of Epidemiology and Public Health, University of Miami, Florida, speculated in Barcelona that cardiology may be the victim of its own success—that the remarkable reduction of cardiovascular mortality during the past few decades may have led to a perception that the disease is already beaten.
Prof Hennekens delivered the European Society of Cardiology Lecture on Population Sciences. Cardiovascular disease, he declared, is not beaten. Indeed, from 1992 to 1993 in the United States, the age-adjusted mortality rate from cardiovascular diseases increased from 181.3 to 182.7 per 100 000 persons. Cardiovascular disease remains the leading cause of death in men older than 45 and in women older than 60. An alarming observation is that American high school seniors exercise less than their parents did; moreover, 1 in 5 of these students smokes cigarettes and 1 in 3 is overweight. Worldwide, the 3 decades leading to 2020 will see cardiovascular disease moving from fifth to first place as a cause of premature death and disability–partly because of decreases in malnutrition and infectious disease (more people reach adult life), but also because of steep rises in cigarette smoking. So, asked Prof Hennekens, can science offer anything new in primary or secondary prevention?
One preventive factor receiving much attention is low to moderate alcohol consumption, which seems to reduce myocardial infarction by one-third to one-half. Heavy alcohol consumption, however, is second only to cigarettes as a cause of premature death in most developed countries, and the complexity of alcohol’s metabolic, physiologic, and psychologic effects will likely preclude overall policy recommendations. In an individual, the power of alcohol to prevent myocardial infarction and occlusive stroke must be weighed against small increases in hemorrhagic stroke, clear increases in blood pressure at higher doses, and small increases in breast cancer.
Other promising hypotheses for primary prevention include the effects of low-dose aspirin, antioxidant vitamins, and estrogen replacement therapy. The evidence on low-dose aspirin is by far the strongest, but an overall policy recommendation would again be premature: although the risk of myocardial infarction is lowered, insufficient data exist to indicate whether strokes and deaths are increased or reduced.
About half of all patients experiencing coronary events have no established risk factors, and potential new markers under investigation include homocystine (primarily atherogenic), fibrinogen (thrombotic), C-reactive protein (inflammatory), and certain genotypes (ACE, for example). Genetics, smoking, and diet all affect homocystine levels, and additional folate might decrease the risk of myocardial infarction by reducing homocystine. This hypothesis, and the possible benefit of reducing fibrinogen, is now being investigated in randomized trials. Infections, smoking, diabetes, and periodontal disease all increase proinflammatory cytokines, whereas aspirin, non-steroidal anti-inflammatory drugs, and corticosteroids decrease them. These cytokines raise C-reactive proteins, increase coagulation, and cause an unfavorable lipid profile that includes low high-density lipoprotein cholesterol and high triglycerides. An intriguing observation is that the effect of aspirin on the risk of myocardial infarction seems greatest in those with the highest C-reactive protein levels. These complex interrelations and their possible clinical relevance are now being evaluated in basic and clinical epidemiologic studies as well as in randomized trials.
Will the assessment of these new markers add to our ability to say who is at risk of cardiovascular disease? Probably the answer is yes, and some of these markers will become routinely measured. However, in Prof Hennekens’ view, the benefits of their modification, if any, are likely to be small in relation to the large reductions of risk that can already be achieved through lifestyle changes. A problem in the United States, he declared, is that most people prefer the prescription of pills to the proscription of harmful lifestyles. For example, stopping cigarette smoking will cut cardiovascular risk by half, beginning within a matter of months, and maintenance of an active lifestyle and ideal body weight decreases risk of coronary disease by 35% to 55%. In the United States, the continuing epidemic of obesity is a major and avoidable cause of premature death.
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