BackgroundThe aim of this study was to observe the effects of genetic polymorphism of CYP2C19 on inhibitory effects of ticagrelor (Tic) and clopidogrel (Clo) towards post-percutaneous coronary intervention (PCI) platelet aggregation (IPA) and major cardiovascular events (MACE) in patients with acute coronary syndromes (ACS).Material/MethodsFrom August 2013 to March 2014, 166 patients with ACS undergoing PCI were selected. The patients were randomly grouped into the Tic group and the Clo group. IPA was detected by thromboelastography (TEG) at 1 week after taking the pills. Genotyping of CYP2C19 gene was determined by analysis of gene sequence detection. Patients were followed up for 1 month and MACE was observed.ResultsThe total IPA in the Clo group was significantly increased compared with the Tic group (P<0.05). The IPAs in the 3 subgroups of Clo group were all significantly increased compared with the 3 subgroups of the Tic group (all P<0.05). MACE was not significantly different between Clo and Tic groups (P>0.05). MACE had no significant difference among the 3 subgroups of the Tic group (P>0.05). MACE in the low metabolism subgroup of the Clo group was significantly increased compared with the fast metabolism subgroup and middle metabolism subgroup of Clo group (P<0.05). MACE was not significant different between the fast metabolism subgroup and the middle metabolism subgroup of the Clo group (P>0.05). MACE in the low metabolism subgroup of the Tic group was significantly decreased compared with the low metabolism subgroup of the Clo group (P<0.05).ConclusionsTicagrelor has a better effect on inhibition platelet aggregation than Clopidogrel in ACS patients undergoing PCI.

Objectives Both increased arterial stiffness and hyperuricaemia are associated with elevated cardiovascular risks. Little is known about the relations of serum uric acid (UA) level to regional arterial stiffness and wave reflection. The aim of the study was to investigate the gender-specific association of serum UA and indices of arterial function in a community-based investigation in China. Methods Cross-sectional data from 2374 adults (mean age 58.24 years) who underwent routine laboratory tests, regional pulse wave velocity (PWV) and pulse wave analysis measurements were analysed in a gender-specific manner. None of the participants had atherosclerotic cardiovascular disease, chronic renal failure, systemic inflammatory disease, gout, or were under treatment which would affect serum UA level. Results Mean ages were 58.24±12.38 years for all participants (range 35 to 96 years). Mean serum UA was 293.93±75.52 mmol/l. Men had higher serum UA level than women (326.76 ±72.96 mmol/l vs 263.68±64.4 mmol/l, p<0.001). Subjects with hyperuricaemia had significantly higher carotid-femoral PWV (PWVc-f ) in women (12.8±3.32 m/s vs 10.96±2.75 m/s, p<0.001), significantly higher carotid-ankle PWV in both gender (men: 9.85 ±3.08 m/s vs 9.29±1.64 m/s, p=0.001; women: 9.62±1.91 m/s vs 9.04±1.7 m/s, p=0.003), while marginally lower augmentation index in men (log AIx-75, 1.24±0.32% vs 1.3±0.24%, p=0.049). Multiple regression analysis showed that serum UA was an independent determinant only for PWVc-f in women (β=0.104, p=0.027), when adjusted for atherogenic confounders. No other independent relationship was found between UA level and other surrogates of arterial stiffness. Conclusions Serum UA levels are associated with alterations in systemic arterial stiffness that differ in men and women. Women might be more susceptible to vascular damage associated with hyperuricaemia.Heart 2012;98(Suppl 2): E1-E319 E139 ABSTRACTS on 12 May 2018 by guest. Protected by copyright.