Serum Amyloid a as a Marker and Mediator of Acute Coronary Syndromes

Abstract

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.

Keywords: :

• acute coronary artery disease
• atherosclerosis
• cardiovascular risk prediction
• endothelial cells
• inflammation
• leukocytes
• serum amyloid A

Financial & competing interests disclosure

This work was supported by grant MOP-64283 (to János G Filep) from the Canadian Institutes of Health Research. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.