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Risk factor burden in midlife: is it water under the bridge?
  1. Douglas Darden1,
  2. Jarett D Berry2,3
  1. 1Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA
  2. 2Division of Cardiology, University of Texas Southwestern Medical Center, Dallas, Texas, USA
  3. 3Department of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, Texas, USA
  1. Correspondence to Dr Jarett D Berry, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-9047, USA; jarett.berry{at}

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The contribution of traditional cardiovascular disease (CVD) risk factors such as smoking, hypercholesterolaemia, hypertension and diabetes to long-term cardiovascular risk is well established.1 For decades, it has been observed that a single measurement of one of these risk factors is associated with a graded, dose-dependent increase in CVD risk across the lifespan. It has also been observed that a single measurement of these risk factors in early life is also associated with long-term cardiovascular risk.2 How can it be that a single measurement of a risk factor at the age of 20 can translate into a consistent increase in risk despite all of the potential downstream changes in risk factors, including treatment?

Atherosclerosis is a lifelong disease. The early data from Vietnam War casualties demonstrated that atherosclerosis is apparent in young adulthood.3 And these early forms of atherosclerosis are not random; in the Bogalusa Heart Study, atherosclerosis at the time of autopsy was strongly associated with the presence of traditional risk factors prior to traumatic death in young adults.4 More recent data from the Coronary Artery Risk Development In Young Adults study demonstrate that the cumulative exposure to dyslipidemia prior to age 35 years is associated with an increased risk for coronary artery calcium in middle age, even after accounting for subsequent changes in lipid levels.5 Thus, atherosclerosis is a cumulative …

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  • Contributors DD has contributed in a way to share authorship. JDB had full access to all data in the study and had final responsibility for the decision to submit for publication. Both authors have read and agreed to the manuscript as written.

  • Funding JDB receives funding from the Dedman Family Scholar in Clinical Care endowment at University of Texas Southwestern Medical Center and 14SFRN20740000 from the American Heart Association prevention network. He has also received speaking fees from Merck.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.

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