Enhanced inflammatory response to coronary angioplasty in patients with severe unstable angina

Background-Systemic markers of inflammation have been found in unstable ang ina. Disruption of culprit coronary stenoses may cause a greater inflammato ry response in patients with unstable than those with stable angina. We ass essed the time course of C-reactive protein (CRP), serum amyloid A protein (SAA), and interleukin-6 (IL-6) after single-vessel PTCA in 30 patients wit h stable and 56 patients with unstable angina (protocol A). We also studied 12 patients with stable and 15 with unstable angina after diagnostic coron ary angiography (protocol B). Methods and Results-Peripheral blood samples were taken before and 6, 24, 4 8, and 72 hours after PTCA or angiography, In protocol A, baseline CRP, SAA , and LL-6 levels were normal in 87% of stable and 29% of unstable patients . After PTCA, CRP, SAA, and IL-6 did not change in stable patients and unst able patients with normal baseline levels but increased in unstable patient s with raised baseline levels (all P<0.001). In protocol B, CRP, SAA, and I L-6 did not change in stable angina patients after angiography but increase d in unstable angina patients (all P<0.05), Baseline CRP and SAA levels cor related with their peak values after PTCA and angiography tall P<0.001). Conclusions-Our data suggest that plaque rupture per se is not the main cau se of the acute-phase protein increase in unstable angina and that increase d baseline levels of acute-phase proteins are a marker of the hyperresponsi veness of the inflammatory system even to small stimuli. Thus, an enhanced inflammatory response to nonspecific stimuli may be involved in the pathoge nesis of unstable angina.