In this presentation Dr. Ridker discusses new findings from the Val-MARC (Valsartan – Managing BP Agressively and Evaluating Reductions in hsCRP) trial that were presented at the 21st Annual Scientific Meeting of the American Society of Hypertension, in New York.

Inflammation plays a major role in atherothrombosis, and based on findings from experimental studies, clinical studies investigating the role of inflammatory biomarkers in hypertension have been undertaken. High-sensitivity C-reactive protein (hsCRP) and blood pressure were found to be independent determinants of cardiovascular risk with additive predictive value (1), and hsCRP was found to predict the future risk of developing hypertension in normotensive individuals (2).

Angiotensin II is a potent pro-inflammatory mediator (3), and the Val-MARC trial sought to investigate whether blood pressure therapy with the angiotensin receptor blocker (ARB) valsartan, alone or in combination with the diuretic hydrochlorothiazide (HCTZ), would reduce plasma hsCRP levels and whether any effects of ARB or ARB/HCTZ on hsCRP are dependent or independent of blood pressure reduction. This was an investigator-initiated, community-based, prospective, randomized trial of 1,668 patients with stage II hypertension, conducted in the U.S. between January 2004 and June 2005.

Dr. Ridker reviews the 6-week primary blood pressure endpoint data and primary inflammation endpoint data (4). Of interest is that there was minimal evidence of correlation between change in blood pressure and change in hsCRP, and these data raise the hypothesis that angiotensin receptor blockade with valsartan monotherapy may lower inflammation independently of its blood pressure reducing effect.

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After viewing this presentation the participant will be able to discuss:

- Six-week data from the Val-MARC trial: Effects of ARB monotherapy vs ARB/HCTZ combination therapy on blood pressure and hsCRP levels
- Implications for future BP trials

1. Gavin J. Blake, MD, MPH, MRCPI; Nader Rifai, PhD; Julie E. Buring, ScD; Paul M Ridker, MD, MPH Blood Pressure, C-Reactive Protein, and Risk of Future Cardiovascular Events Circulation. 2003;108:2993.

2. Howard D. Sesso, ScD, MPH; Julie E. Buring, ScD; Nader Rifai, PhD; Gavin J. Blake, MD, MPH; J. Michael Gaziano, MD, MPH; Paul M. Ridker, MD, MPH C-Reactive Protein and the Risk of Developing Hypertension JAMA. 2003;290:2945-2951.

3. Peter Libby, MD Current Concepts of the Pathogenesis of the Acute Coronary Syndromes Circulation. 2001;104:365.

4. Paul M. Ridker, Eleanor Danielson, Nader Rifai, Robert J. Glynn; for the Val-MARC Investigators. Valsartan, Blood Pressure Reduction, and C-Reactive Protein: Primary Report of the Val-MARC Trial Hypertension 2006, doi:10.1161/01.HYP.0000226046.58883.32.