Using inflammatory biomarkers to guide lipid therapy
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Corresponding author Brendan M. Everett, MD, MPH Center for Cardiovascular Disease Prevention, Brigham and Women’s Hospital, 900 Commonwealth Avenue East, Boston, MA 02215, USA. E-mail: [email protected] Current Cardiovascular Risk Reports 2008, 2:29–34 Current Medicine Group LLC ISSN 1932-9520 Copyright © 2008 by Current Medicine Group LLC
Inflammation plays a fundamental role in the pathophysiology of atherothrombotic cardiovascular disease, and lipid-lowering agents appear to have clinically relevant anti-inflammatory properties. In addition to lowering low-density lipoprotein (LDL) cholesterol, statins improve endothelial function, are clinically effective in a time frame that often precedes LDL reduction, and lower inflammatory markers such as C-reactive protein (CRP) in a largely LDL-independent manner for individual patients. Data from the CARE, AFCAPS/TexCAPS, PROVE IT–TIMI 22, REVERSAL, and A to Z trials suggest that statins provide greater clinical benefit in those who achieve LDL and CRP reductions than in those who achieve LDL reduction alone. We discuss evidence underlying potential anti-inflammatory properties of several lipid-lowering therapies, their impact on measures of endothelial function and vascular inflammation and on subsequent risk reduction, and the use of inflammatory biomarkers as an adjunct to LDL in the monitoring of lipid-lowering therapy.
Introduction Inflammation plays a central role in the development of atherothrombosis [1•]. Although cardiovascular disease has long been understood as a consequence of lipid disorders, the basic steps of atheroma formation are driven by vascular inflammation, including endothelial injury, leukocyte recruitment, extracellular matrix deposition and plaque formation, subsequent plaque rupture, and arterial thrombosis. As scientists and clinicians have come to understand this process in more detail, a number of serum markers of key steps in this inflammatory process have emerged, including adhesion molecules (intercellular adhesion molecule-1 [ICAM-1], vascular cell adhesion
molecule-1 [VCAM-1], E selectin, P selectin), chemokines (tumor necrosis factor-B, soluble CD40 ligand, interleukin-6 [IL-6], monocyte chemoattractant protein-1 [MCP-1]), matrix metalloproteinases, hemostatic factors (thromboxane A 2), and integrated measures of systemic vascular inflammation such as C-reactive protein (CRP) and lipoprotein-associated phospholipase A 2 (Lp-PLA 2). Evidence suggests that practicing physicians may want to use some of these markers to help monitor therapy for lipid disorders. This article reviews the evidence that current therapies for dyslipidemia possess clinically relevant anti-inflammatory properties, describes evidence supporting the use of inflammatory markers in guiding the use of these medications, and outlines some directions for research efforts.
Treatment of Hyperlipidemia The ability to effectively treat hyperlipidemia with medication has been instrumental in reducing death from cardiovascular disease. Bile acid binding resins [2] and sur
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