Irbesartan, an angiotensin type 1 receptor inhibitor, regulates markers ofinflammation in patients with premature atherosclerosis

Objectives This study assessed the role of angiotensin II type 1 (AT(1)) re ceptor antagonists on inflammatory mechanisms involved in atherogenesis. Sp ecific inflammatory markers included solubilized tumor necrosis factor-alph a receptor II (sTNF-alpha RII), vascular cell adhesion molecule-1 (VCAM-1) and superoxide. In addition, the AT(1) receptor blocker irbesartan was eval uated for its ability to suppress these markers in individuals with atheros clerosis. Background Mechanisms involved in the complex process of atherogenesis incl ude alterations in the inflammatory responses. The use of compounds that su ppress these responses may reduce the degree of damage seen in atherosclero sis. Methods With a cross-sectional study design, 33 normotensive patients with stable coronary artery disease (CAD) were treated with irbesartan for a 24- week period. These patients were compared against a control population with no known coronary atherosclerosis. Marker levels were measured by enzyme-l inked immunosorbent assay technique and lucigenin chemiluminescence assay a nd statistically evaluated by two-way repeated measures analysis of varianc e. Results All patients with coronary artery disease had increased levels of i nflammatory molecules over those of control patients. Treatment with irbesa rtan in these patients significantly reduced levels of inflammatory molecul es measured. Soluble VCAM-1 levels were reduced by 36%; soluble TNF-alpha l evels were reduced by 54% and superoxide level decreased by 52%. Maximal su ppression of inflammatory markers by irbesartan therapy in patients with CA D was seen at 12 weeks. Conclusions The effect of irbesartan on each inflammatory marker is signifi cant. Our results show that use of irbesartan may retard the inflammatory p rocess seen in premature forms of atherosclerosis. (C) 2001 by the American College of Cardiology.