Coronary angioplasty and angiography significantly increased inflammatory markers in unstable angina patients with raised baseline levels (P<0.001), but not in stable angina patients.
Observational (n=113)
Does the inflammatory response to PTCA or diagnostic angiography differ between patients with stable versus unstable angina?
Patients with unstable angina and elevated baseline inflammatory markers exhibit a hyperresponsive inflammatory reaction to both PTCA and diagnostic angiography, suggesting systemic inflammation plays a role in the pathogenesis of unstable angina.
p-value: p=<0.001
BACKGROUND: Systemic markers of inflammation have been found in unstable angina. Disruption of culprit coronary stenoses may cause a greater inflammatory response in patients with unstable than those with stable angina. We assessed 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 with stable and 56 patients with unstable angina (protocol A). We also studied 12 patients with stable and 15 with unstable angina after diagnostic coronary angiography (protocol B). METHODS AND RESULTS: Peripheral blood samples were taken before and 6, 24, 48, and 72 hours after PTCA or angiography. In protocol A, baseline CRP, SAA, and IL-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 unstable patients with normal baseline levels but increased in unstable patients with raised baseline levels (all P<0.001). In protocol B, CRP, SAA, and IL-6 did not change in stable angina patients after angiography but increased in unstable angina patients (all P<0.05). Baseline CRP and SAA levels correlated with their peak values after PTCA and angiography (all P<0.001). CONCLUSIONS: Our data suggest that plaque rupture per se is not the main cause of the acute-phase protein increase in unstable angina and that increased baseline levels of acute-phase proteins are a marker of the hyperresponsiveness of the inflammatory system even to small stimuli. Thus, an enhanced inflammatory response to nonspecific stimuli may be involved in the pathogenesis of unstable angina.
Liuzzo et al. (Tue,) conducted a observational in Stable and unstable angina (n=113). Single-vessel PTCA or diagnostic coronary angiography vs. Stable angina was evaluated on Time course of CRP, SAA, and IL-6 after procedure (p=<0.001). Coronary angioplasty and angiography significantly increased inflammatory markers in unstable angina patients with raised baseline levels (P<0.001), but not in stable angina patients.