Hongyi Wu

Effects of CYP2C19 variant alleles on postclopidogrel platelet reactivity and clinical outcomes in an actual clinical setting in China.

Whether the current pharmacogenetic knowledge of clopidogrel could be translated into Chinese clinical practice is yet to be defined. To address this issue, we assessed the relation of single nucleotide polymorphisms within genes modulating clopidogrel absorption (ABCB1), metabolic activation (CYP2B6, CYP2D6, CYP3A4, CYP2C9, and CYP2C19), and biologic activity (P2RY12) to the response of clopidogrel as measured by ex-vivo platelet reactivity and ischemic events during half a year of follow-up. Only CYP2C19*2 and *3, of the investigated polymorphisms, were associated with postclopidogrel platelet aggregation and the presence of high platelet reactivity. Moreover, the effect of the CYP2C19*2 versus the *3 allele on platelet reactivity did not differ. Although the carriage of one or two CYP2C19 loss-of-function alleles, irrespective of the CYP2C19*2 or *3 allele, increased the propensity for high platelet reactivity, only the two loss-of-function allele carriage was associated with clinical outcome in the first 6 months.

Parity and Cardiovascular Disease Mortality: a Dose-Response Meta-Analysis of Cohort Studies

Parity has been shown to inversely associate with cardiovascular disease (CVD) mortality, but the evidence of epidemiological studies is still controversial. Therefore, we quantitatively assessed the relationship between parity and CVD mortality by summarizing the evidence from prospective studies. We searched MEDLINE (PubMed), EMBASE and ISI Web of Science databases for relevant prospective studies of parity and CVD mortality through the end of March 2015. Fixed- or random-effects models were used to estimate summary relative risks (RRs) and 95% confidence intervals (CIs). Heterogeneity among studies was assessed using the I2 statistics. All statistical tests were two-sided. Ten prospective studies were included with a total of 994,810 participants and 16,601 CVD events. A borderline significant inverse association was observed while comparing parity with nulliparous, with summarized RR = 0.79 (95% CI: 0.60–1.06; I2 = 90.9%, P < 0.001). In dose-response analysis, we observed a significant nonlinear association between parity number and CVD mortality. The greatest risk reduction appeared when the parity number reached four. The findings of this meta-analysis suggests that ever parity is inversely related to CVD mortality. Furthermore, there is a statistically significant nonlinear inverse association between parity number and CVD mortality.

First report of stent thrombosis after a switch therapy resulting from ticagrelor-related dyspnea ☆

Keyword: Acute coronary syndrome Stent thrombosis Ticagrelor Balloon angioplasty and subsequent stenting (a 2.4 mm × 18 mm sirolimus-eluting stent, EXCEL, JW, China) of the right coronary artery (RCA) lesion was performed with good angiographic results (Fig. 1B). He was discharged from the hospital on a regimen of aspirin (100 mg once daily) and ticagrelor (90 mg twice daily). Ten days later, the patients still complained of dyspnea and went to his local clinic. Ticagrelor was switched to clopidogrel 75 mg daily without loading dose. Clopidogrel therapy was commenced at about 12 h after the last dose of ticagrelor. Dyspnea was alleviated by the

Besides CYP2C19, PON1 genetic variant influences post-clopidogrel platelet reactivity in Chinese patients.

patients with chronic heart failure. Heart 2009;95:651–5. [7] Nunain SO, Garratt C, Paul V, et al. Effect of intravenous adenosine on human atrial and ventricular repolarization. Cardiovasc Res 1992;26:939–43. [8] Bertolet BD, Hill JA, Kerensky RA, Belardinelli L. Myocardial infarction related atrial fibrillation: role of endogenous adenosine. Heart 1997;78:88–90. [9] Llach A, Molina CE, Prat-Vidal C, et al. Abnormal calcium handling in atrial fibrillation is linked to up regulation of adenosine A2A receptors. Eur Heart J 2011;32:721–9.

Thrombin induced platelet-fibrin clot strength in relation to platelet volume indices and inflammatory markers in patients with coronary artery disease

Platelet aggregation and inflammation are both implicated in coronary artery disease (CAD). Thrombin induced platelet-fibrin clot strength (MAThrombin) measured by thrombelastography (TEG) has been proved to be a novel marker of platelet aggregation. The aim of this study was to investigate the correlation of MAThrombin to platelet volume indices (PVIs) or to inflammatory markers in different types of CAD. 206 patients with different types of CAD were enrolled. MAThrombin, PVIs, including mean platelet volume (MPV), platelet distribution width (PDW), and platelet-large cell ratio (P-LCR) as well as inflammatory markers, including high-sensitivity C-reactive protein (hs-CRP) and fibrinogen (Fbg) were measured. Multiple linear regression models were used to analyze the association between MAThrombin, PVIs, and inflammatory markers. MAThrombin and inflammatory markers both varied with CAD types (P<0.001). MAThrombin was correlated to PVIs in NSTEMI individuals (MPV, r=0.393, P=0.007; PDW, r=0.334, P=0.023; P-LCR, r=0.382, P=0.008), but had inner-link with inflammatory markers in STEMI cases (hs-CRP, r=0.499, P<0.001; Fbg, r=0.500, P<0.001). These findings may suggest different mechanisms of platelet aggregation in different types of CAD. Moreover, MAThrombin may be used as a potential parameter to evaluate platelet aggregation and inflammation together.Platelet aggregation and inflammation are both implicated in coronary artery disease (CAD). Thrombin induced platelet-fibrin clot strength (MAThrombin) measured by thrombelastography (TEG) has been proved to be a novel marker of platelet aggregation. The aim of this study was to investigate the correlation of MAThrombin to platelet volume indices (PVIs) or to inflammatory markers in different types of CAD. 206 patients with different types of CAD were enrolled. MAThrombin, PVIs, including mean platelet volume (MPV), platelet distribution width (PDW), and platelet-large cell ratio (P-LCR) as well as inflammatory markers, including high-sensitivity C-reactive protein (hs-CRP) and fibrinogen (Fbg) were measured. Multiple linear regression models were used to analyze the association between MAThrombin, PVIs, and inflammatory markers. MAThrombin and inflammatory markers both varied with CAD types (P<0.001). MAThrombin was correlated to PVIs in NSTEMI individuals (MPV, r=0.393, P=0.007; PDW, r=0.334, P=0.023; P-LCR, r=0.382, P=0.008), but had inner-link with inflammatory markers in STEMI cases (hs-CRP, r=0.499, P<0.001; Fbg, r=0.500, P<0.001). These findings may suggest different mechanisms of platelet aggregation in different types of CAD. Moreover, MAThrombin may be used as a potential parameter to evaluate platelet aggregation and inflammation together.

Recurrent ST-segment elevation in infarct-associated leads

Early recurrence of focal ST-segment elevation after acute ST-elevation myocardial infarction (STEMI) usually indicates myocardial reinfarction. However, it can be seen in threatened myocardial rupture, a situation in which administration of potent antithrombotic and thrombolytic therapy may be catastrophic. Herein, we present the case of an 84-year-old woman with STEMI undergoing urgent stenting who had a recurrence of chest pain with cardiogenic shock and new ST elevation in the infarct-related leads mimicking myocardial ischaemia. A patent stent showed by repeated angiography, presence of pericardial effusion and absence of recurrent rise in cardiac marker suggest the diagnosis of a contained left ventricular rupture. The experience of any clinician in dealing with …