Experimental studies suggest that systemic inflammation leads to endothelial dysfunction and atherosclerosis. This study will examine the effects of the anti-inflammatory drug sulfasalazine on endothelial function in patients with coronary artery disease. Subjects will be treated with sulfasalazine or to placebo for six weeks. After a two-week rest period, subjects will cross over to the alternative treatment. Endothelium-dependent flow-mediated dilation of the brachial artery will be studied before and after each drug. We hypothesize that anti-inflammatory therapy will reverse endothelial dysfunction in patients with coronary artery disease.

Inclusion Criteria:

• History of coronary artery disease

Exclusion Criteria:

• G6PD deficiency defined by red blood cell G6PD activity assay
• Sulfa allergy
• Aspirin allergy
• Allergy to furosemide (lasix), hydrochlorthiazide, sulfonylureas, acetazolamide (Diamox) or other carbonic anhydrase inhibitors
• SGOT, SGPT, alkaline phosphatase, total bilirubin greater than 2 times the upper limit of normal
• WBC less than 4.0 or greater than 11.0 K/UL
• Platelet count less than 150 K or greater than 450K
• Hematocrit less than 30% 7
• Serum creatinine greater than 1.5 mg/dl
• Unstable angina or acute MI within 2 weeks
• Warfarin treatment
• Immunosuppressive treatment (methotrexate, cyclosporine, etc.)
• Digoxin treatment
• Phenytoin (Dilantin) treatment
• Methenamine (Mandelamine, Urex) treatment
• Probenecid or sulfinpyrazone (Anturane, Aprazone) treatment
• Porphyria
• Symptomatic GI obstruction
• GU obstruction (not including clinical evidence of benign prostatic hypertrophy)
• Pregnancy