AN OVERVIEW ON NON STEROIDAL ANTI-INFLAMMATORY DRUG AS A TRIGGER OF CARDIOVASCULAR DISEASE

Nonsteroidal anti inflammatory drugs which are widely used by elderly patients. It have undesirable side effect including ulcers, bleeding, kidney failure and raised risk of heart and stroke. Mechanism of action, prolonged exposure to any class of non steroidal anti inflammatory drugs has been shown to have potential adverse effects on cardiovascular events in patients with or without pre existing cardiovascular conditions, depending on the duration and dosage of these drugs. Patient which having pre-existing coronary artery disease, hypertension, and history of stroke are at the higher risk of cardiovascular disease after taking non steroidal anti inflammatory drugs. The use of non steroidal anti inflammatory drugs with other antiplatelet drugs (except aspirin) increased the rate of cardiovascular events.Cyclooxygenase-2 inhibition results in a reduction of prostaglandin synthesis and is associated with both anti natriuretic and vasoconstrictor effects. Inhibition of cyclooxygenase-2 may lead to reductions in both prostagladinE2 and prostacyclin. Inhibition of ProstaglandinE2 may promote an acute relative reduction in daily urinary sodium excretion. The kidneys in patients with normal kidney function will tend to increase sodium excretion to compensate for the antinatriuretic effects of the Cyclooxygenase-2 selective inhibitor or Non steroidal anti inflammatory drug to maintain homeostasis of sodium balance. This phenomenon occurs in lack of a elevation in blood pressure or sustained rise in plasma volume. Suppression of the Cyclooxygenase -2?dependent formation of prostaglandinI2 by the coxibs might influence in patients to myocardial infarction or thrombotic stroke. Thus, reduction in prostaglandinI2 formation, lead to a expected elevation of blood pressure, accelerate atherogenesis, patients receiving coxibs to an exaggerated thrombotic response to the rupture of an atherosclerotic plaque.