"Risky business": ten years is not a lifetime.

To address these deficiencies in the prediction of risk, several investigators have included other markers of risk such as biomarkers related to inflammation, genotypes, or imaging tests with traditional risk factors to improve CHD risk prediction. These analyses have resulted in the creation of novel risk-prediction schemes such as the Reynolds risk score, which added family history and high-sensitivity C-reactive protein (hs-CRP) to blood pressure, smoking, total and high-density lipoprotein cholesterol, and hemoglobin A1C to predict risk.2 However, whether algorithms have used biomarkers such as hs-CRP, imaging tests such as coronary calcium score or carotid intima-media thickness, or novel genotypes such as the single-nucleotide polymorphism on chromosome 9p21, the improvements in risk prediction have been modest. Other investigators have suggested that anybody who is not at very low risk should get an imaging test to further stratify risk.3 On the other hand, there have been efforts to identify the “lifetime risk” of CHD for individuals in various age groups. The concept of lifetime risk was highlighted in the National Cholesterol Education Program Adult Treatment Panel (ATP) III guidelines4 and is an important one, especially for individuals who are young to middle-aged. Traditional risk factors become manifest more often in the 4th and 5th decades of life when the estimated lifespan based on national averages is at least another 4 to 5 decades. Hence, estimating a 10-year risk may give individuals a false sense of security that they have a low risk for CHD, when in reality, this may not be true when their entire lifetime is considered. In the current issue of Circulation, Berry et al5 further demonstrate the importance of the concept of lifetime risk by observing that among individuals 50 years of age who have low risk by the Framingham Risk Score, equal numbers of individuals have a low lifetime risk and a high lifetime risk. Furthermore, they show that those with a low short-term (10-year) and a high lifetime risk have a greater burden and progression of subclinical atherosclerosis measured by imaging tests (carotid intima-media thickness and coronary calcium score) than those with low short-term and lifetime risks. To test their hypothesis, they used 2 population-based studies, the Coronary Artery Risk Development in Young Adults (CARDIA) study and the Multi-Ethnic Study of Atherosclerosis (MESA). Although this analysis provides important proof that not everybody with low risk is similar, certain limitations must be mentioned. The authors have already pointed out that they used the Framingham Risk Score in ethnicities in which it has not been well validated. Furthermore, it is unclear what therapy, if any, these individuals had over the course of the follow-up. Finally, it is unclear whether the individuals with low short-term and low lifetime risk remained the same throughout the course of the study or how many of them progressed to a higher lifetime risk on subsequent examinations. There clearly are limitations with the concept of lifetime risk as well. If one has a single elevated risk factor, one could have a high lifetime risk. For example, a 40-year-old man with a blood pressure of 118/78 mm Hg who is a nonsmoker and has a total cholesterol of 178 mg/dL has a lifetime CHD risk of 5%, whereas the same man with a total cholesterol of 201 mg/dL has a lifetime CHD risk of 46%. Clearly, as clinicians, we see such fluctuations in measurements of total cholesterol. Furthermore, given that the presence of any 1 elevated risk factor can confer a high lifetime risk, do we treat everybody with a high lifetime risk more aggressively? Primary prevention statin trials, such as the AngloScandinavian Cardiac Outcomes Trial (ASCOT),6 have already shown that treatment with statins in an individual with hypertension, a traditional risk factor, decreases the risk of CHD events, which supports the concept that perhaps treating individuals with a high lifetime risk would be of value. Added to this are the results from another recent primary prevention trial, Justification for the Use of statins in Primary prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER),7 which showed the efficacy of statins in individuals with low-density lipoprotein cholesterol (LDL-C) 130 mg/dL but with hs-CRP levels 2 mg/L. The economic burden of The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association. From the Section of Atherosclerosis and Vascular Medicine, Department of Medicine, Baylor College of Medicine and Center for Cardiovascular Disease Prevention, Methodist DeBakey Heart and Vascular Center, Houston, Tex. Correspondence to Christie M. Ballantyne, MD, Baylor College of Medicine, 6565 Fannin, M.S. A-601, Houston, TX 77030. E-mail [email protected] (Circulation. 2009;119:362-364.) © 2009 American Heart Association, Inc.