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Comparative effects of AT1-antagonism and angiotensin-converting enzyme inhibition on markers of inflammation and platelet aggregation in patients with coronary artery disease

Bernhard Schieffer, MD^*,*, Christoph Bünte, MS^*, Jana Witte, MS^*, Kirsten Hoeper, RN^*, Rainer H. Böger, MD, Edzard Schwedhelm, PhD and Helmut Drexler, MD^*

^* Department of Cardiology and Angiology, Medizinische Hochschule Hannover, Germany
Clinical Pharmacology Unit, Institute of Experimental and Clinical Pharmacology, University Hospital Hamburg-Eppendorf, Germany

View larger version (13K): [in a new window]   Figure 1 Impact of renin-angiotensin system inhibition on interleukin-10 (IL-10). Patients were treated for 3 months with either 20 mg enalapril (ENAL, white bars) or 300 mg of irbesartan (IRB, black bars); IL-10 serum concentrations were determined by enzyme-linked immunosorbent assay technique at baseline and at 3 months. Data represent mean ± SEM.

View larger version (15K): [in a new window]   Figure 2 Renin-angiotensin system inhibition and metalloprotease 9 (MMP9). Concentration of serum MMP9 protein was determined by enzyme-linked immunosorbent assay and its serum activity was fluorometrically analyzed by enzyme immunosorbent assay zymography. Patients were treated for 3 months with either 20 mg enalapril (white bars) or 300 mg of irbesartan (black bars) and blood samples were drawn at baseline and at 3 months. Bar graphs summarize individual -changes in serum MMP9 and MMP9 activity over a three-month observation period. Data are given as mean ± SEM.

View larger version (13K): [in a new window]   Figure 3 Impact of renin-angiotensin system inhibition on surrogate markers of inflammation. Bar graphs summarize individual -changes in serum high-sensitivity C-reactive protein (hsCRP) and interleukin-6 levels over a three-month observation period in patients with coronary artery disease and hypertension. Patients were treated with either 20 mg of enalapril (white bars) or 300 mg Irbesartan (black bars) and interleukin-6 serum levels were determined by enzyme-linked immunosorbent assay. Data are given as mean ± SEM.

View larger version (16K): [in a new window]   Figure 4 Renin-angiotensin system inhibition and platelet aggregation. Platelet-rich plasma from patients treated with either 20 mg enalapril (white bars) or 300 mg irbesartan (black bars) was isolated (all received 100 mg acetyl salicylic acid). Platelet aggregation was determined turbimetrically after U46619 stimulation (a synthetic thromboxane A2-analog). Bar graph summarizes individual -changes of platelet aggregation in patients with coronary artery disease and hypertension. Data represent mean ± SEM.

View larger version (12K): [in a new window]   Figure 5 Renin-angiotensin system inhibition and urine bicyclo-prostaglandin E2 (PGE2). High-sensitivity C-reactive protein was determined in urine samples from patients treated with either 20 mg enalapril or 300 mg irbesartan and normalized to serum creatinine levels. All patients received 100 mg acetyl salicylic acid. Prostaglandin E2 was determined by enzyme-linked immunosorbent assay. Both treatment regimens had no significant impact on urine bicyclo-PGE2, which is predominantly secreted by platelets, indicating a cyclo-oxygenase-independent mechanism. White bars = enalapril; black bars = irbesartan.