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B2 Editorial
Figure 2 Assessment and management of global cardiometabolic risk. This illustration emphasizes the notion that in addition to assessing and managing
‘traditional’ risk factors, targeting excess visceral adiposity/ectopic fat could lower the risk of CVD through its effects on several determinants of
cardiometabolic risk.
practice would lead to different therapeutic manage- inflammation (e.g. C-reactive protein), insulin resistance
ment is a question frequently raised.13 To address this (insulin), an atherogenic dyslipidaemia (apolipoprotein B
issue, additional prospective data with hard CVD end and LDL particle size), and possibly select cytokines
points and a comprehensive set of morphometric and derived from adipose tissue (e.g. adiponectin and
metabolic markers are needed to sort the key predictors interleukin-6) may be useful in risk assessment but their
of risk beyond what is currently assessed by physicians. added value in global risk assessment, is frequently
At present, there is evidence14–17 that markers of debated due to the lack of adequate data. Furthermore,
Editorial B3
there are no data available on whether visceral adiposity Cardiometabolic Risk which is supported by an unrestricted
and ectopic fat predict CVD beyond or independently grant from Sanofi-Aventis awarded to Université Laval.
from classical CVD risk factors. Studies are underway to
address these issues. Conflict of interest: none declared.
An additional limitation that has not been adequately
addressed with our current approach to diagnose the
metabolic syndrome is that it is an all or none diagnosis
(present vs. absent) rather than containing graded com-
ponents assessing severity. In addition, because of this References
dichotomized classification, a diagnosis of the metabolic
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the diabetes epidemic. Nature 2001;414:782–787.
efficacy of therapy.18 Thus, the metabolic syndrome, at
2. Després JP. Is visceral obesity the cause of the metabolic syndrome?
least as assessed in clinical practice under current guide- Ann Med 2006;38:52–63.
lines cannot be considered as a target of therapy. 3. Després JP, Lemieux I. Abdominal obesity and metabolic syndrome.
In this supplement issue, the importance of visceral adi- Nature 2006;444:881–887.
posity as the most common component of the metabolic 4. Reaven GM. Banting lecture 1988. Role of insulin resistance in human
disease. Diabetes 1988;37:1595–1607.
syndrome is emphasized. However, although visceral adi-
5. Ferrannini E, Buzzigoli G, Bonadonna R, Giorico MA, Oleggini M,
posity increases relative CVD risk and risk of the develop- Graziadei L, Pedrinelli R, Brandi L, Bevilacqua S. Insulin resistance
ment of diabetes through its cluster of abnormalities, it is