The renin–angiotensin system (RAS) has been demonstrated to play not only an important role in cardiovascular homeostasis by influencing vascular tone and fluid–electrolyte balance, but is also involved in the atherothrombotic process, cardiac remodelling, and apoptosis.

Agents that inhibit the RAS, such as angiotensin converting enzyme (ACE) inhibitors and angiotensin II type 1 receptor blockers (ARBs), exert considerable benefits in hypertension and heart failure. However, ACE inhibitors may not provide total inhibition of angiotensin II (Ag II) generation, because of non-ACE dependent Ag II producing mechanisms. ARBs are able to exert more specific and complete blockade of the RAS, overcoming some of the ACE inhibitor limitations. In fact they block Ag II effects on catecholamine production, vasoconstriction, aldosterone secretion, low density lipoprotein transport, hypertrophy, and cell growth, without affecting the Ag II mediated positive effects on the type II receptor, such as vasodilatation and inhibition of cell growth.¹

A growing body of data has consistently described an anti-inflammatory action of ARBs. In patients with early atherosclerosis, irbesartan decreases markers of inflammation.² It has also been described that Ag II blockade improves the anti-inflammatory response of aspirin and statins in stable coronary heart disease patients.^3,4 However, a potential anti-inflammatory role of ARBs has not been evaluated in acute coronary syndromes (ACS), a condition in which inflammation is an acknowledged pathophysiological mechanism. In ACS both cellular …