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Editorial |
From the Québec Heart Institute, Laval Hospital Research Center, Québec, Canada
Correspondence to Jean-Pierre Després, PhD, FAHA, Québec Heart Institute, Laval Hospital Research Center, Pavilion Marguerite-DYouville, 4th Floor, 2725, Chemin Sainte-Foy, Sainte-Foy QC, Canada G1V 4G5. Email Jean-Pierre.Despres@crhl.ulaval.ca
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Although epidemiological and clinical studies conducted over the last 40 years have identified variables which became well accepted "classical" coronary heart disease (CHD) risk factors (such as increased cholesterol and low-density lipoprotein (LDL) cholesterol levels, diabetes, hypertension, smoking, etc.),1,2 it was also obvious that these parameters had limited ability to discriminate for CHD events.3 Therefore, which additional lifestyle or biological variables could help identify, at reasonable costs in clinical practice, individuals at increased risk of CHD remains a question of considerable importance.4
See pages 1868 and 1874
In this regard, we have moved in lipidology beyond the following simple sequence of events (hyperlipidemia, atherosclerosis, CHD) as it is now recognized that acute coronary syndromes are the consequence of a complex interplay between the presence of known or unknown risk factors and atherosclerosis.5 For instance, factors modulating the balance between fibrinolysis and thrombosis are also involved,6 and considerable evidence has been published over the last decade to support the notion that CHD also has an inflammatory component.7
Largely driven by the pioneering work of Ridker and colleagues,810 results of epidemiological studies, of primary and secondary prevention studies as well as of trials conducted in patients with acute coronary syndromes, have revealed that the plasma concentration of a relatively simple marker of inflammation, C-reactive protein (CRP), could predict the risk of a first or a recurrent coronary event, beyond the contribution of classical risk factors.11 Whether CRP, an acute phase protein, plays a direct role in the etiology of CHD or whether
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