ABC | Volume 113, Nº3, September 2019

Original Article Dracoulakis et al. High platelet activity during ASA use in ACS Arq Bras Cardiol. 2019; 113(3):357-363 Figure 2 – Correlation between the variation of CRP and VFN (acute/late). CRP: C-reactive protein; VFN: VerifyNow™; r: Spearman’s coefficient. 250 200 100 –100 –200 –150 –250 150 50 –50 –60 –80 –40 –20 20 40 60 0 0 Variation of VFN Variation of CRP r = 0.342 p = 0.010 (including CRP), markers of hypercoagulability and platelet function in different CAD spectra (asymptomatic, stable CAD and ACS). However, contrary to these findings, Ziegler et al. 30 demonstrated that in patients with peripheral arterial disease, there was no significant correlation between CRP and platelet aggregation measured by PFA-100 ® . These conflicting results can be attributed, at least in part, to methodological differences. In our study, different methods of determining platelet function were used simultaneously. The correlation between the tests during the acute phase was significant, but the magnitude of these correlations was only weak or moderate. Unexpectedly, even the methods classified as COX‑1‑specific showed medium to low correlation with each other. These findings are consistent with findings fromprevious studies: Lordkipanidzé et al. 19 studied 201 patients with stable CAD undergoing aspirin therapy 19 using six different tests. The prevalence of HPR varied from 4% when analyzed by optical aggregometry with AA, to 59.5%, when analyzed by PFA-100 ® (COL/EPI). In this study, as in ours, there wereweak correlations betweenmethods for determining platelet function, including COX-1 specific methods. The present study was the first to analyze different methods of platelet aggregation during the acute and late phases, in the same population of patients with NSTE ACS. In summary, our findings may have important therapeutic implications in demonstrating that one-third of the patients showed HPR in the acute phase, leading to the hypothesis that new dosing regimens should be tested in this population. In addition, despite the fact that there is a significant decrease in the incidence of HPR during the chronic phase, a significant percentage of the population still presents HPR at this stage. Study limitations Firstly, our study had a relatively small sample size, but it was adequate to assess the primary outcome. However, the secondary results should be considered as hypothesis generators and interpreted with caution. Secondly, all patients were on chronic ASA use at a dose of 100 mg/day to 200 mg/day, but individual doses were not collected and may have influenced the results obtained. 25 Lastly, in recent times, the role of young (immature) platelets has been valued; if they had been assessed in the present study (which was not done), they could have added important information. Conclusion In conclusion, the prevalence of HPR during ASA therapy measured by COX-1-specific methods is higher during the acute phase than in the late phase of patients with non-ST segment elevation ACS. However, the relationship between inflammation as indicated by CRP and IL-6 and platelet reactivity in these two phases is weak, suggesting that the variability in the inflammation state may not play a role in the temporal changes in platelet reactivity in this population. Author contributions Conception and design of the research and Analysis and interpretation of the data: Dracoulakis MDA, Martins HS, Nicolau JC; Acquisition of data: Dracoulakis MDA; Statistical analysis, Obtaining financing and Writing of the manuscript: Dracoulakis MDA, Nicolau JC; Critical revision of the manuscript for intellectual content: Dracoulakis MDA, Gurbel P, Cattaneo M, Martins HS, Nicolau JC, Kalil Filho R. Potential Conflict of Interest No potential conflict of interest relevant to this article was reported. Sources of Funding This study was funded by Abbot Vascular. Study Association This article is part of the thesis of Doctoral submitted by Marianna Deway Andrade Dracoulakis, from Instituto do Coração - HCFMUSP. 361