Increased levels of acute phase proteins (APP) in serum are associated with vulnerability of atherosclerotic plaques and acute manifestations of coronary heart disease (CHD). APP have been viewed as indexes of active vascular inflammation or as mediators of atherothrombosis. In the present study we tested the hypothesis that individuals who develop stable or unstable forms of CHD might have different innate responses to an inflammatory stimulus. We compared changes in plasma C-reactive protein (CRP) and serum amyloid A (SAA) concentrations 48 h after a standardized inflammatory stimulus (adjuvanted influenza vaccination) in patients with quiescent CHD that had been manifested at onset as inducible myocardial ischemia (Group 1, n=26) or as acute coronary syndromes (ACS) (Group 2, n=34). Selected patients were free from inflammatory or other conditions that might affect the immune response. CRP concentration increased significantly after vaccination in both groups (Group 1: 0.47 [0.21-0.86] to 0.56 [0.32-1.17]mg/L, p=0.005; Group 2: 0.64 [0.21-1.09] to 0.75 [0.33-1.48]mg/L, p=0.003), without significant differences between groups in absolute or percentage changes. By contrast, SAA did not change after vaccination in Group 1 (14.4 [8.9-19.5] to 14.8 [10.3-18.8]mg/L, p=0.88) but increased significantly in Group 2 (16.9 [10.0-21.5] to 19.2 [11.3-29.1]mg/L, p=0.002), with significant differences between the groups in absolute and percentage terms (p=0.015 and 0.019, respectively). Changes in CRP and SAA, both absolute and percentage, were significantly correlated in Group 2 (r=0.60 and 0.66, both p<0.001). The responsiveness of plasma SAA to an inflammatory stimulus in Group 2 alone suggests a pro-inflammatory status in patients prone to acute coronary syndrome but not in those with inducible myocardial ischemia.