Inflammation in acute coronary syndromes.

Inflammation is becoming an intriguing focus of research as a possible pathogenetic component and therapeutic target in ischaemic heart disease. However, the potential links between inflammation and ischaemic heart disease are present at three levels at least. First, the inflammatory response has been known for many years to play a major role in ischaemia/reperfusion injury, and its reduction can limit myocardial damage[1]. Second, inflammation is a very common feature of the chronic atherosclerotic process, as first described by Virchow in 1856[2] and recently comprehensively reviewed by Ross[3]. Finally, inflammation may be an acute pathogenetic component of instability in approximately half of patients with acute coronary syndromes (ACS), independently of the atherosclerotic and ischaemic burdens[4]. There may be several actual triggers of inflammation, the individual inflammatory response may vary, and the mechanisms through which inflammation correlates with the development of cardiovascular events in epidemiological studies may be multiple and not necessarily the same in all patients. The inflammatory response may influence prognosis through modulating the consequences of ischaemia and necrosis in some individuals, through sudden development of instability, or through atherogenesis in others. The present review focuses on the independent role of inflammation in ACS and on the short-term and mid-term prognostic value of inflammatory markers. The final common pathway through which instability precipitates ACS is represented by a variable combination of coronary thrombosis and vasoconstriction in epicardial arteries and in resistive coronary vessels, superimposed on a variable atherosclerotic background (Fig. 1)[5]. Thrombosis is the most obvious acute component, because its frequent persistence makes it detectable at autopsy, angioscopy and angiography. Spasm and vasoconstriction are transient, however, and can only be detected by chance, when critical stenoses are relieved by nitrates[6], or by design, when provocative tests are used[7,8]; coronary microvascular constriction can only be inferred and revealed by special studies[9]. Thrombosis is also a much more effective therapeutic target as compared with vasoconstriction, because vasodilator drugs, when given systemically, usually do not counter the constrictor effect of substances released by thrombi locally[6]. European Heart Journal Supplements (2002) 4 (Supplement B), B8–B13