Serum amyloid A as a marker and mediator of acute coronary syndromes.

Inflammation promotes acute coronary syndromes and ensuing clinical complications. An emerging downstream marker of inflammation is serum amyloid A (SAA). Elevated plasma SAA levels predict increased cardiovascular risk and portend worse prognosis in patients with acute coronary artery disease (CAD). The pathophysiological role of SAA remains enigmatic. SAA plays a role in host defense, but it might also be atherogenic. SAA affects cholesterol transport, contributes to endothelial dysfunction, promotes thrombosis, evokes recruitment of inflammatory cells, activates neutrophils and suppresses neutrophil apoptosis, key events underlying acute coronary syndromes. These results provide a potential link between SAA and CAD and suggest that reducing SAA levels and/or opposing the actions of SAA may have beneficial effects in patients with acute CAD.