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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:2178.)
© 2006 American Heart Association, Inc.

Editorials

Epidemiology Complements Immunology in the Heart

Göran K. Hansson

From the Center for Molecular Medicine and Department of Medicine at Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.

Correspondence to Göran K Hansson, CMM L8:03, Karolinska University Hospital, SE-17176 Stockholm, Sweden. E-mail Goran.Hansson@ki.se

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Epidemiology continues to play an important role in cardiovascular research. Population-based research identified serum cholesterol and blood pressure levels as risk factors for myocardial infarction and stroke. These studies were initiated after clinical and experimental studies had pointed to a role for these factors in the pathogenesis of atherosclerosis. Together, the experimental, clinical, and epidemiological studies prompted basic research into cholesterol metabolism and blood pressure regulation, which in turn made it possible to develop lipid-lowering and antihypertensive drugs. The result of these joint efforts has been a pharmacological prevention of cardiovascular disease, which saves thousands of lives every year.

See page 2345

Over the last 2 decades, inflammation has turned out to be an additional important mechanism in the pathogenesis of atherosclerosis.^1,2 Analysis of human tissue identified immune cells producing proinflammatory cytokines in plaques, experiments demonstrated significant effects of immune modulation in animal models of atherosclerosis, clinical studies of acute coronary syndromes showed early elevations of inflammatory blood markers, and epidemiological investigations revealed that elevated levels of downstream markers of inflammation, particularly CRP and interleukin (IL)-6, are associated with increased risk for myocardial infarction in healthy individuals. However, most epidemiologists have been hesitant to go beyond analysis of such downstream markers, and we therefore have insufficient population data to implicate any specific pathway within the inflammatory effector response of the immune system.

A few recent studies have explored more proximal immune mechanisms in the context of cardiovascular disease. They point to important roles for adaptive immunity in atherosclerotic heart disease . . . [Full Text of this Article]

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