Background: To assess whether dipyridamole therapy exerts a significant anti-inflammatory effect in heart failure patients.
Methods: We performed a retrospective analysis of the stored bio-samples of 3 groups of patients: 1) 25 normal healthy controls (N); 2) 25 heart failure patients (HF) under standard optimal therapy, including aspirin; 3) 17 HF patients with previous stroke and under clinically-driven therapy with A (Aggrenox, long-acting dipyridamole 200 mg + aspirin 25 mg, twice daily) for at least 1 month (HF-A). In all, we evaluated interleukin (IL)-6, adiponectin and C-reactive protein (CRP) as well as NT-proBNP. The same laboratory measurements were performed in the 17 HF patients with recent or previous stroke, both before and 1-month after clinically driven administration of A.
Results: All laboratory inflammatory indices were significantly higher in HF patients compared to N: IL-6 (N = 0.68 (0.3 - 12.7) vs. HF = 3.10 (0.5 - 16.7) vs. HF-A = 1.24 (0.3 - 3.3) pg/mL; p < 0.001 N vs. HF, p < 0.01 N vs. HFA, p = ns HF vs. HF-A); CRP (N = 0.12 (0.01 - 0.45) vs. HF = 0.58 (0.04 - 2.7) vs. HF-A = 0.72 (0.02 - 4.8) mg/dL; p = ns N vs. HF, p = 0.05 N vs. HF-A, p = ns HF vs. HF-A); Adiponectin (N = 8.8 (3.0 - 31.4) vs. HF = 12.16 (4.9 - 27.3) vs. HF-A = 10.0 (4.8 - 15.6) μg/mL; p < 0.05 N vs. HF, p = ns N vs. HF-A p = ns HF vs. HF-A). NT-proBNP was also increased (N = 42.2 (13 - 93) vs. HF = 1907 (18.1 - 8038) vs. HF-A = 497.9 (7.8 - 3686) pg/mL; p < 0.001 N vs. HF, p = 0.01 N vs. HF-A, p = ns HF vs. HF-A). In 17 subjects, the intra-patient assessment (before and 1-month after starting of Aggrenox therapy) did not show a decrease in inflammation markers.
Conclusions: HF patients show an increase in inflammatory indices independently of underlying A therapy.