The Prevention Of Cardiovascular Disease: Have We Really Made Progress?

Thomas A. Pearson


Health Affairs. 2007;26(1):49-60. 

In This Article

Approaches To CVD Prevention: Secondary, Primary, And Primordial

Definitions of Types of Prevention

Secondary prevention. has been classically defined as the prevention of disease recurrence and death after the onset of symptomatic disease. Because the strongest predictor for death or a recurrent CVD event is having a history of CVD, patients with such a history are all considered to be at very high risk. Primary prevention traditionally has been the prevention of the onset of symptomatic disease through the treatment of risk factors for CVD, such as treating hypertension to prevent stroke. Primordial prevention describes efforts to reduce the onset of the risk factors known to predispose people to CVD. For example, lifestyle modifications to maintain ideal body weight and to limit sodium consumption are means of preventing the development of high blood pressure.

Blurring of Distinctions Between Types of Prevention

The secondary, primary, and primordial prevention distinctions are of decreasing usefulness. The advent of a variety of imaging and noninvasive testing modalities have demonstrated the ability to identify asymptomatic people with apparently established CVD.[8] Tests such as exercise electrocardiography, coronary calcium scoring using computed tomography (CT) scans, ankle-brachial blood pressure indexes, and so forth provide evidence for the asymptomatic presence of atherosclerotic disease. Whether this early identification of disease will lead to prevention of symptoms is not frequently investigated, which makes it difficult for policymakers to accept or prioritize the use of these new technologies.

Epidemiologic studies such as the Framingham Heart Study have provided support for the identification of high-risk people using risk-factor profiles.[9] In the instance of diabetes mellitus, history of a stroke, or symptomatic peripheral arterial disease, the risk is considered so high that these patients are considered to have a coronary heart disease equivalent, with a risk similar to a myocardial infarction (MI) survivor.[10] In addition, the Framingham study developed equations to estimate absolute risk, on the basis of the level and number of risk factors, to quantify individuals risks over the next ten years for death from MI or coronary disease.[11]

Using these tools, today s approach is to stratify people on the basis of risk. This may be viewed from a cost-effectiveness perspective, in which the total cost of a prevention program would be minimized by limiting costly and side effect prone treatments to people at high enough risk to prevent adequate numbers of CVD cases to balance treatment costs. Several interventions have attractive cost-effectiveness ratios of $50,000 $70,000 per year of life saved.[12] A small(but growing) number of people would be at high risk (arbitrarily defined as more than 20 percent risk per ten years), demanding aggressive risk-factor management, prophylactic medications, and treatment of symptoms of CVD.[13] A larger group would be considered to be at moderate risk (10 20 percent risk), benefiting from risk-factor management with less costly drugs and devices. Finally, low-risk people (less than 10 percent risk) would benefit from health education, modification of harmful health behavior, and a healthier environment, at little direct personal cost.

Risk-factor Paradigm in CVD Prevention

Fundamental to any prevention of CVD is the role of risk factors in the etiology of CVD and in their modification to reduce CVD risk. Risk factors may be classified into three groups (Exhibit 1): nonmodifiable, behavioral, and physiological.[14] Nonmodifiable risk factors are still useful in risk assessment. Behavioral risk factors may be direct causes of CVD but may also cause physiological risk factors. These common factors might be addressed not only in clinical settings through individual counseling, but might be better addressed at the population level through societal change and public health initiatives. Physiological risk factors are those measured in a clinical setting. As such, they might be addressed with behavioral change advice but frequently require pharmacologic interventions by a care provider.

Exhibit 1.

Need for a Combined Approach to CVD Risk Reduction

The risk-factor paradigm in Exhibit 1 identifies at least three opportunities for intervention to reduce CVD mortality: treatment of the symptomatic patient; treatment of behavioral and physiologic risk factors to reduce risk of disease onset or progression in individuals; and modification of deleterious risk behavior at the population level to prevent the onset of risk factors themselves. In reality, a balance of the three is required, with priorities set by the efficacy and cost-effectiveness of the interventions. Treatment of symptomatic disease does not inhibit the atherosclerotic disease process, which, left unimpeded, will reemerge with symptomatic disease from new lesions in other arterial beds. Treatment of risk factors has excellent efficacy and cost-effectiveness as part of the long-term therapy for CVD.[15]

Perhaps the best evidence for the merits of a balance of primordial, primary, and secondary prevention approaches is illustrated by Lee Goldman and Francis Cook, who analyzed factors explaining the reduction in U.S. mortality from coronary heart disease between 1968 and 1978.[16] They concluded that only a small part of the decline could not be explained. Population-wide changes in blood cholesterol (presumably from changes in the U.S. diet) and reductions in cigarette smoking accounted for 54 percent of the decline. Changes in health care, including treatment of hypertension, emergency coronary care, and revascularization, accounted for another 39.5 percent. This illustrates the contribution of a broad and balanced CVD prevention effort, rather than one focused on a single risk factor or stage of disease.


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