Despite patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI) and receiving clopidogrel therapy, some patients still experience major adverse cardiovascular events (MACEs). Clopidogrel resistance, which may be regulated by genetic and epigenetic factors, may play a role in MACEs. This study aimed to determine the association between genetic (CYP2C19 and P2Y12 polymorphisms) and epigenetic (DNA methylation of CYP2C19 and P2Y12 and miRNA-26a expression) factors and their effects on MACEs among post-PCI patients. Post-PCI patients who received a standard dosage of clopidogrel at Harapan Kita Hospital between September 2018 and June 2020 were included in this study. MACEs were observed in patients within 1 year after PCI. Platelet aggregation was assessed using light transmission aggregometry (LTA). DNA methylation of CYP2C19 and P2Y12 was assessed using the bisulfite conversion method. CYP2C19 and P2Y12 polymorphisms and miRNA-26a expression were evaluated using quantitative real-time polymerase chain reaction (qRT-PCR). Among a total of 201 subjects, 49.8% were clopidogrel-resistant, and 14.9% experienced MACEs within 1 year after PCI (death was 7.5%). Hypomethylation of CYP2C19 (p = 0.037) and miRNA-26a upregulation (p = 0.020) were associated with clopidogrel resistance. CYP2C19*2/*3 polymorphisms (p = 0.047) were associated with MACEs in 1 year. This study demonstrated that hypomethylation of CYP2C19 and miRNA-26a upregulation increased the risk of clopidogrel resistance in post-PCI patients, but there was no correlation between clopidogrel resistance and MACEs. However, CYP2C19*2/*3 polymorphisms were the factors that predicted MACEs within 1 year.
Background: PV and ET have high predisposition to thrombosis and recurrence of thrombosis. We determined VEGF, D-dimer and coagulation activation markers in clinically stable patients and recurrence of thrombosis. Methods: Thirty-five Indonesian patients diagnosed with PV and ET and under treatment for the disease were recruited. The following assays were performed: VEGF, D-dimer, fibrinogen, TAT-complex, vWF, β-TG and JAK2 V617F mutation. Data between patients who were clinically stable (n=20) and those with recurrent thrombosis (n=15) at the time of study was analysed. Results: The mean age for PV/ET was 51.7 ± 14.9 years. Thrombosis episode was recorded for 94.3% (33/35) patients. Twenty (57.1%) clinically stable and 15 (42.9%) patients had recurrence of thrombosis. D-dimer (P=<0.001), fibrinogen (P=0.005) were statistically significant and VEGF (P=0.06) were seen in recurrence of thrombosis compared to clinically stable patients who had normal D-dimer. Elevated D-dimer seen in recurrence thrombosis was significantly correlated with VEGF (P=0.002) levels. Elevated VEGF were seen in 45% of clinically stable patients and 73.3% in recurrence of thrombosis.
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