(Circulation. 2004;110:2774-2777.)
© 2004 American Heart Association, Inc.
Editorial |
From the Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis (A.T.H., A.R.F.), and the Vascular Medicine Program, Minneapolis Heart Institute, Minneapolis, Minn (A.T.H.).
Reprint requests to Alan T. Hirsch, MD, Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Suite 300, 1300 S Second St, Minneapolis, MN 55454-1015. E-mail hirsc005@umn.edu
Key Words: Editorials atherosclerosis cardiovascular diseases epidemiology risk factors
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
What factors place people at risk for developing cardiovascular disease as they grow from youth to adulthood? How do both physiological and epidemiological investigations contribute to the development of the evidence that can support or refute current hypotheses regarding the development of atherosclerosis? How can the interplay of differing study designs improve our understanding of atherosclerosis?
See p 2918
Atherosclerosis is a systemic disease that is the leading cause of death in the developed world and leads to carotid artery, coronary artery, and peripheral arterial atherosclerotic syndromes. Inasmuch as atherosclerotic diseases affect as many as 64 million adults in the United States, considerable health care resources have been deployed to provide care for those affected.1 Past research findings have contributed to considerable advances in survival for individuals who have overt heart disease, stroke, and peripheral arterial disease, yet the continued aging of the population implies that the prevalence of each atherosclerotic disorder will increase in the decades ahead. In this context, investigations that provide insights into disease mechanisms and that define how vulnerability to atherosclerosis is established are now particularly valuable.
The pathophysiology of atherosclerosis is known to be dependent on multiple hereditary and environmental factors. It is presumed that these genetic and acquired factors contribute in a complex manner to a progressive pathophysiological process that causes a normal artery to develop progressive endothelial dysfunction. Loss of normal endothelial function is hypothesized to be a fundamental step in the atherosclerotic disease process. In this conceptual model, the iterative exposure of
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