PENTOXIFYLLINE AND INFLAMMATION MARKERS IN PATIENTS WITH ACUTE CORONARY SYNDROME

In 500 consecutive patients with acute coronary syndrome, we added pentoxifylline 400 mg TID to standard therapy (group B) vs. placebo (group A). Blood was harvested for inflammatory markers (hsCRP, IL-6, TNF alpha) after admission, named T0, and at 48 h and 15 days after the acute event, called T1 and T2. We find that at 48 h (T1) was an attenuation of rise in hsCRP and TNF alpha level in group B compared with group A. Patients who received pentoxifylline (group B) attenuated the increase of hsCRP from baseline (1.25 +/- 1.2 mg/L) to 48 hours (5.3 +/- 1.6 mg/L), but not in group A patients who received a placebo (baseline 1.35 +/- 1.2 mg/L and 48 hours 8.9 +/- 2.2 mg/L, p < 0.001). The results were the same regarding TNF alpha level (administration of pentoxifylline reduced level in group B at 48 hours (at admission 33.4 +/- 14.2 pg/L and 23 +/- 19.3 pg/L at 48 hours), but not in group A (p < 0.001). However, the IL-6 level was not modified by the administration of pentoxifylline (group A, T0-7.3 +/- 5.1 pg/L and T1 24.4 +/- 8.6 pg/L; group B, T0- 7.2 +/- 4.8 pg/L and T1- 24.4 +/- 8.6 pg/L, p = NS). At 15 days (T2) administration of pentoxifylline in group B normalized earlier the hsCRP and TNF alpha levels compared with group A (hsCRP -group A, T2-4.4 +/- 2.5 mg/L vs. group B, T2-1.2 +/- 1 mg/L, p < 0.001; TNF alpha- group A, T2-10.2 +/- 7.3 pg/L vs. group B, T2-6.2 +/- 3.4 pg/L, p < 0.001). This do not apply to IL-6 level at T2 (IL -6-group A, T2-12.5 +/- 6.5 pg/L vs. group B, T2-11.3 +/- 7.2 pg/L, p = NS). No correlation was found between the reduced level of inflammatory marker (hsCRP and TNF alpha) by adding pentoxifylline 400 mg TID to standard therapy.