RESUMO
OBJECTIVES: To examine a relationship between protein C (PC) and antithrombin III (AT III) activities with ejection fraction of left ventricle (EFLV), in the early phase of acute ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI), and to investigate whether PC and AT III are associated with major adverse cardiovascular events (MACE) within 6 months following from pPCI. PATIENTS AND METHODS: The research had a prospective character and included 357 patients who had, following the diagnosis of the STEMI, undergone pPCI at the Clinic of Cardiology and Emergency Internal Medicine, Military Medical Academy, Belgrade, Serbia, from January 2010 until April 2019. RESULTS: The EFLV positively correlated with PC values (rho = 0.229). There was a statistically significant increase in the PC values between patients with MACE compared with those without MACE at 6 months' follow-up evaluation (p < 0.0001). Also, significant difference in PC values between patients who died in hospital and those who were alive at 6 months' follow-up (p < 0.01) was observed. PC values were different across different EFLV groups (p < 0.001), increasing from the 1st to the 4th EFLV quartiles: the median and the interquartile values for the 1st, 2nd, 3rd and 4th quartiles were 1.0400IU/l ± 0.15, 1.1400IU/l ± 0.15, 1.1350IU/l ± 0.16 and 1.2200IU/l ± 0.14, respectively. CONCLUSION: Increased PC activity in the early phase of STEMI is associated with higher EFLV 5 days after the pPCI as well as with MACE at 6 months after the pPCI.
RESUMO
Background: Activity of protein C has important role in the development of early necrosis and no-reflow phenomenon in patients with ST-segment elevation myocardial infarction (STEMI) after successful primary percutaneous coronary intervention (pPCI). Methods: We examined association between plasma activity of protein C, antithrombin, coagulation factors II, VII, VIII and fibrinogen to early formation of new Q-waves (myocardial necrosis) before pPCI and early ST-segment resolution (microcirculatory reperfusion) after pPCI in patients with acute STEMI. According to ischaemic time, patients were considered as early or late presenters. 12-lead ECG was analysed for the presence of new Q-wave at admission and for significant ST-segment resolution 60 minutes after primary PCI. Results: In early presenters' group, protein C activity was significantly lower in patients who did not achieve significant ST-segment resolution after pPCI compared to patients who did (1.11 IU/L vs. 0.99 IU/L, p = .006) and in patients who had new Q-waves compared to group who had not (1.04 UI/l vs. 1.11 IU/L, p = .038). There was significant negative correlation between protein C activity and maximal CK-MB levels (R2 = 0.06, p = .009) and BNP levels (R2 = 0.109, p = .003) and significant positive correlation between protein C activity with LVEF (R2 = 0.065, constant = 33.940, b = 11.968, p = .007) in early STEMI presenters. There were no differences between the activity of other examined haemostasis factors. Conclusion: Therefore we concluded that STEMI patients with early myocardial necrosis and no-reflow phenomenon after pPCI have lower activity of plasma protein C levels.
