http://atvb.ahajournals.org/content/36/2/e1.extract?etoc
+ Author Affiliations
- Correspondence to Claudia Calcagno, MD, PhD, Translational and Molecular Imaging Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029. E-mail claudia.calcagno@mssm.edu
Atherosclerosis is a systemic disease
of the arterial vessel wall. Although the mortality due to
cardiovascular events is
decreasing, the prevalence of atherosclerosis
and its comorbidities, and the consequent heath care costs are expected
to rise
sharply in the near future.1
Because the precise cause and pathogenesis of this complex, multifactorial disease are still not fully understood, the clinical
assessment of cardiovascular risk has been traditionally based on population risk factors (RFs).2
However, this approach still largely fails to capture the individual’s
cardiovascular risk: most cardiovascular events occur
in patients with 1 or few traditional RFs,
whereas individuals classified as high risk may never experience
clinical events.3
The past 10 years have seen a
significant paradigm shift in our understanding of the mechanisms of
atherogenesis. From being
considered the mere result of passive lipid
accumulation in the vessel wall, atherosclerosis is now classified as an
active
inflammatory condition.4,5 The presence of abundant, active inflammatory cells is a known hallmark of high risk, vulnerable atherosclerotic plaques.4,5 Many studies have identified several systemic proinflammatory conditions (such as lupus,6 rheumatoid arthritis,7–9 and primary cardiovascular events themselves10)
as emerging, independent RFs for atherosclerosis. New evidence suggests
that atherosclerosis arises from the complex influence
of genetic, environmental, and behavioral
variables on systemic and local inflammation through a complex network
of molecules,
cells, and organs.
Thanks to the recent technological advancements of high-throughput ‘-omics’, a plethora of the genes, proteins, and cells
…
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