I. ADVERSE CARDIOVASCULAR EFFECTS
C. Increased Viral Load
There is evidence suggesting a casual role of cytomegalo-virus (CMV) in atherogenesis. CMV infection has been shown to cause progression of atherosclerosis in a murine model of atherosclerosis. Rott et al. demonstrated that selective inhibition of COX-2 increases viral load in apoE-deficient mice. This increase in viral load was paral¬leled by increased anti-CMV antibody titers. Inhibition of COX-2 significantly increased early atherosclerotic lesion areas independent of viral infection.
D. Hypertension and Heart Failure
NSAIDs increase blood pressure and increase the incidence of heart failure because they cause the kidneys to retain sodium and water. COX-2 inhibitors may cause a greater elevation in the blood pressure and the incidence of heart failure. They also interact with antihypertensive agents and drugs used for the management of heart failure.
E. Caution
Caution is required with the use of selective NSAIDs in patients with coronary artery disease. These agents should be avoided in patients at risk for the development of heart failure, hypertension, or acute coronary syndromes. Antiarthritic (nonsteroidal anti-inflammatory) agents including indomethacin, ibuprofen, and pirogxicam and the newer, selective nonsteroidal anti-inflammatory agents (COX-2 inhibitors) such as celecoxib, meloxicam, and rofecoxib retain salt and water in the body and commonly precipitate heart failure in patients with poor heart muscle function.