810-1 Enhanced Inflammatory Acute Phase Response After Percutaneous Coronary Angioplasty in Patients with Unstable Angina

Elevated levels of C-reactive protein (CRP), a sensitive marker of inflammation, are independent predictors of short-term prognosis in patients (pts) with unstable angina (UA). The causes of the acute phase response in UA, however, are still unknown. Percutaneous transluminal coronary angioplasty (PTCA) is an useful model for the assessment of the effects of plaque disruption and myocardial ischemia on the acute phase response. Serum levels of CRP were measured in 21 pts with chronic stable angina (SA) (G 1) and in 22 pts with UA refractory to maximal medical treatment (G2), undergoing single-vessel PTCA. Venous blood samples were taken immediately before PTCA and 6, 24, 48, 72 hours after the end of the procedure. CRP values are expressed as median and range. Results Before PTCA, CRP was elevated (g 3 mg/l) in 2/21 G1 pts (10%) and in 16/22 G2 pts (73%) (p l 0.001): it was 2.4 (2–4.4) mg/l in Gl and 8 (2.4–29) mg/l in G2 (p l 0.001). After PTCA, CRP increased to a peak value of 2.6 (2–16.4) mg/l 38 ± 13 hrs after the procedure in Gl, and to a peak value of 19.9 (2.8–49.4) mg/l 32 ± 14 hrs after the procedure in G2 (p l 0.001. G1 vs G2). A significant increase in CRP after PTCA, defined as an increase g 50% the basal values, was observed in 8/21 Gl pts and in 16/22 G2 pts (p l 0.05). The percentage increase of CRP after PTCA was higher in G2 than in Gl (180 ± 239%, range 0–925% vs 118 ± 176%, range -13–489%, p l 0.05). No difference in coronary stenosis severity before PTCA (84 ± 9% vs 89 ± 8%), residual stenosis (30 ± 7% vs 29 ± 10%), number of ballon inflations (6 ± 3.4 vs 5.3 ± 3.2), total inflation time (365 ± 202 vs 413 ± 197 sec) and mean inflation pressure (5 ± 0.9 vs 5 ± 1 atm) was found between Gl and G2 pts. Conclusion Our study shows that the plaque disruption and the brief periods of myocardial ischemia caused by PTCA elicit a variable individual inflammatory acute phase response, that is greater in UA compared to SA pts. These data suggest a higher inflammatory responsiveness in patients with UA, that may playa pathogenetic role in acute coronary syndromes, and help explaining the higher rate of acute complications typically observed in patients with unstable angina undergoing PTCA.