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European Heart Journal Advance Access originally published online on November 4, 2005
European Heart Journal 2006 27(1):13-14; doi:10.1093/eurheartj/ehi638
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© The European Society of Cardiology 2005. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Eating, vascular biology, and atherosclerosis: a lot to chew on

Robert A. Vogel*

Division of Cardiology, Department of Medicine, University of Maryland School of Medicine, 22 South Greene Street, Room S3B06, Baltimore, MD 21201, USA

* Corresponding author. Tel: +1 410 328 8795; fax: +1 410 328 8080. E-mail address: rvogel@heart.umaryland.edu

This editorial refers to ‘Diet and inflammation: a link to metabolic and cardiovascular diseases’{dagger} by K. Esposito et al., on page 15

The first 10% of the full text of this article appears below.

Coronary risk factors, such as hypercholesterolaemia and hypertension, are primary causes of atherosclerosis, at least partly due to their adverse impact on vascular biology. Impaired vascular biological states, such as endothelial dysfunction and inflammation, however may be independently atherogenic. Three examples that suggest that vascular indexes need to be considered independent of risk factors are anti-inflammatory effects of statins, hormone replacement therapy (HRT), and post-prandial endothelial dysfunction and inflammation. The REVERSAL and PROVE IT-TIMI 22 trials demonstrated that changes in LDL cholesterol and C-reactive protein independently correlated with coronary atherosclerosis progression and coronary heart events.1,2 On-treatment C-reactive protein was as predictive of subsequent coronary events as was LDL cholesterol. Prior to the recent HRT . . . [Full Text of this Article]

Dietary implications

Drug effects

Clinical use of post-prandial measurements


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Related articles in EHJ:

Diet and inflammation: a link to metabolic and cardiovascular diseases
Katherine Esposito and Dario Giugliano
EHJ 2006 27: 15-20. [Abstract] [FREE Full Text]