Jiabei Li

Tailored antiplatelet therapy and clinical adverse outcomes

Objective The clinical evidence regarding the influence of tailored antiplatelet strategy on adverse outcomes has been controversial. The aim of the study was to evaluate the significance of tailored antiplatelet therapy with respect to clinical adverse events in antiplatelet-resistant patients. Methods Randomised studies that assess clinical relevance of personalised antiplatelet treatment in antiplatelet-resistant patients were identified through a literature search: PubMed, EMBASE, Web of Science and the Cochrane Library. The primary endpoint was the composite of death from any cause and stent thrombosis. All total clinical adverse events and bleeding complications were evaluated. Results Data were combined across seven randomised studies comprising 12 048 subjects, of whom 3738 (31.0%) were found to be antiplatelet-resistant. Antiplatelet-resistant patients provided with tailored antiplatelet therapy showed less risk of death or stent thrombosis than those assigned conventional antiplatelet treatment (0.5% vs 2.2%; OR (95% CI) 0.25 (0.13 to 0.49), p<0.0001). A significant benefit in terms of total adverse event risk reduction was observed during follow-up for tailored vs conventional antiplatelet therapy (5.5% vs 10.0%; OR (95% CI) 0.40 (0.20 to 0.77), p=0.006). No statistical difference in bleeding complications was observed between these two groups (p=0.08). Conclusions In the study, personalised antiplatelet treatment for antiplatelet resistance was found to be associated with less occurrence of death or stent thrombosis and the less risk of total clinical adverse events than conventional treatment, without increasing the risk of bleeding complications.

Bivalirudin Anticoagulant Therapy With or Without Platelet Glycoprotein IIb/IIIa Inhibitors During Transcatheter Coronary Interventional Procedures: A Meta-Analysis

AbstractThe safety and effectiveness of using the direct thrombin inhibitor bivalirudin during transcatheter coronary interventional procedures remains uncertain.This study aimed to systematically assess anticoagulation with bivalirudin alone or bivalirudin plus glycoprotein (GP) IIb/IIIa inhibitors (bivalirudin-based anticoagulant therapy) in patients undergoing percutaneous coronary intervention (PCI) procedures by a meta-analysis of randomized controlled trials (RCTs).Systematical searches of the MEDLINE, EMBASE, and Cochrane databases were conducted. RCTs comparing bivalirudin-based anticoagulant therapy with a comparable heparin therapy in patients undergoing PCI were eligible. Risk ratios (RRs) with 95% confidence intervals (CIs) served as summary statistics.A total of 38,096 patients from 17 RCTs were randomized to the bivalirudin group (n = 18,878) or heparin group (n = 19,218) in the meta-analysis. No significant differences in death, myocardial infarction or reinfarction, ischemia-driven revascularization, or in-stent thrombosis were observed between the 2 groups (all P > 0.05). Notably, bivalirudin-based therapy showed a highly significant 34% decrease in the incidence of major bleeding (RR = 0.66; 95% CI 0.54–0.81; P < 0.001) and a 28% reduction in the need for blood transfusion (RR = 0.72; 95% CI 0.56–0.91; P < 0.01). Meta-regression analyses demonstrated that additional administration of GP IIb/IIIa receptor inhibitors (P = 0.01), especially eptifibatide (P = 0.001) and tirofiban (P = 0.002), was likely to increase the major bleeding risk associated with bivalirudin.Bivalirudin, in comparison to heparin, is associated with a markedly lower risk of major bleeding, and the additional use of GP IIb/IIIa inhibitors may weaken this benefit.

Down-regulation of mir-542-3p promotes neointimal formation in the aging rat.

AIM To explore mir-542-3p mediated inhibition of vascular smooth muscle cell (VSMC) proliferation through the inhibition of Syk activation. METHODS AND RESULTS MicroRNA (mir)-542-3p was selected for analysis based on miRNA microarray and qRT-PCR results. In vitro mir-542-3p expression was significantly downregulated in old (o)VSMCs compared with young (y)VSMCs under serum stimulation conditions. Upregulation of mir-542-3p in oVSMCs significantly inhibited VSMC proliferation, whereas downregulation of mir-542-3p in yVSMCs increased VSMC proliferation. We identified spleen tyrosine kinase (Syk) as a direct target of mir-542-3p by database search, and showed that its expression and phosphorylation were higher in oVSMCs than in yVSMCs after serum stimulation. Luciferase assays confirmed that Syk is a direct target of miR-3542-3p. Knock-down of mir-542-3p in yVSMCs inhibited the activation of the Syk downstream effectors STAT3 and STAT5, whereas mir-542-3p overexpression enhanced STAT3 and STAT5 activities. In a rat balloon injury model, mir-542-3p inhibited neointima formation and proliferating cell nuclear antigen (PCNA) protein expression. CONCLUSION Mir-542-3p modulates VSMC proliferation via the Syk/STAT3-STAT5 axis. Downregulation of mir-542-3p may explain age-related neointimal hyperplasia in rats.

Left Ventricular Function during Acute High-Altitude Exposure in a Large Group of Healthy Young Chinese Men

Objective The purpose of this study was to observe left ventricular function during acute high-altitude exposure in a large group of healthy young males. Methods A prospective trial was conducted in Szechwan and Tibet from June to August, 2012. By Doppler echocardiography, left ventricular function was examined in 139 healthy young Chinese men at sea level; within 24 hours after arrival in Lhasa, Tibet, at 3700 m; and on day 7 following an ascent to Yangbajing at 4400 m after 7 days of acclimatization at 3700 m. The resting oxygen saturation (SaO2), heart rate (HR) and blood pressure (BP) were also measured at the above mentioned three time points. Results Within 24 hours of arrival at 3700 m, the HR, ejection fraction (EF), fractional shortening (FS), stroke volume (SV), cardiac output (CO), and left ventricular (LV) Tei index were significantly increased, but the LV end-systolic dimension (ESD), end-systolic volume (ESV), SaO2, E/A ratio, and ejection time (ET) were significantly decreased compared to the baseline levels in all subjects. On day 7 at 4400 m, the SV and CO were significantly decreased; the EF and FS Tei were not decreased compared with the values at 3700 m; the HR was further elevated; and the SaO2, ESV, ESD, and ET were further reduced. Additionally, the E/A ratio was significantly increased on day 7 but was still lower than it was at low altitude. Conclusion Upon acute high-altitude exposure, left ventricular systolic function was elevated with increased stroke volume, but diastolic function was decreased in healthy young males. With higher altitude exposure and prolonged acclimatization, the left ventricular systolic function was preserved with reduced stroke volume and improved diastolic function.

Short-term high-altitude pre-exposure improves neurobehavioral ability.

This study aims to evaluate the effect of the duration of high-altitude (HA) pre-exposure on human neurobehavioral parameters including mood states and cognitive performance at HA. One hundred and eleven healthy individuals (ranging in age from 18 to 35 years) were recruited to participate in this study. They were divided into two groups: a 4-day short-term HA pre-exposure group (n=57) and a 3-month long-term HA pre-exposure group (n=54). All participants lived in the area at 400 m altitude above sea level before pre-exposure to HA. They were then transported to 3700 m plateau for either a 4-day or a 3-month HA pre-exposure, and finally delivered to 4400 m plateau. On the last day of pre-exposure at 3700 m and on the 10th day at 4400 m, neurobehavioral parameters of the participants in the two groups were evaluated. At the end of pre-exposure and on the 10th day of HA exposure, participants in the short-term group had significantly lower negative mood states, better cognitive performance with higher sensorimotor, attention, and psychomotor abilities, and less acute mountain sickness in comparison with the participants in the long-term pre-exposure group. Our field study with large samples showed that in comparison with 3-month long-term pre-exposure, 4-day short-term HA pre-exposure at 3700 m has a better effect in improving human neurobehavioral parameters including mood states and cognitive performance and reducing acute mountain sickness when exposed to a HA at 4400 m.

Sleep quality changes in insomniacs and non-insomniacs after acute altitude exposure and its relationship with acute mountain sickness.

Objective We aimed to observe the changes in subjective sleep quality among insomniacs and non-insomniacs after acute ascending to 3,700 m and its possible relationship with acute mountain sickness (AMS). Methods A total of 600 adult men were recruited. Subjects’ subjective sleep quality was evaluated by the Athens Insomnia Scale. AMS was assessed using the Lake Louise scoring system. Arterial oxygen saturation was measured. Results Despite insomnia resolution in only a few subjects, the prevalence of insomnia among insomniacs remained stable at 90% after rapid ascent to 3,700 m. However, among non-insomniacs, the prevalence of insomnia sharply increased to 32.13% in the first day of altitude exposure and progressively reduced to 4.26% by the 60th day of altitude stay. Moreover, the prevalences of insomnia symptoms decreased more markedly from day 1 to day 60 at 3,700 m among non-insomniacs than among insomniacs. At 3,700 m, the prevalence of AMS among insomniacs was 79.01%, 60.49%, and 32.10% on the first, third, and seventh days, respectively, which was significantly higher than that among non-insomniacs. Multivariate regression revealed that elevated Athens Insomnia Scale scores are an independent risk factor for AMS (adjusted odds ratio 1.388, 95% confidence interval: 1.314–1.464, P<0.001), whereas high arterial oxygen saturation and long duration of altitude exposure are protective factors against AMS. Conclusion Our results suggest that the effect of high-altitude exposure on subjective sleep quality is more marked, but disappears more quickly, among non-insomniacs than among insomniacs, whereas AMS is especially common among insomniacs. Moreover, poor subjective sleep quality is a risk factor for AMS.

Responsiveness to aspirin in patients with unstable angina pectoris by whole blood aggregometry.

Aims:  To evaluate aspirin responsiveness in patients with unstable angina pectoris (UAP) by whole blood aggregometry. Another goal was to differentiate aspirin‐resistant patients into pharmacokinetic or pharmacodynamic type.

Comparison of collagen versus adenosine diphosphate in detecting antiplatelet effect in patients with coronary artery disease.

Widely varying methods of assessing platelet aggregation have resulted in the absence of an established standard approach to assess the effects of antiplatelet drugs. The objective of this study was to compare the roles of collagen and adenosine diphosphate (ADP) in the assessment of effects of aspirin or clopidogrel on platelet aggregation. Sixty patients with documented coronary artery disease were assigned to receive aspirin alone (ASA 100 mg/d) (n=30) or aspirin-plus-clopidogrel (ASA 100 mg/d+C 75 mg/d) (n=30). Platelet aggregation assessment by the use of whole blood aggregation tests with collagen or ADP was performed in these patients and 30 age- and gender-matched normal volunteers. When compared with the control group, therapy with ASA or ASA+C resulted in significant inhibition of collagen-induced platelet aggregation (P<0.001 for each), but there was no statistically significant difference in the results between the ASA and ASA+C groups. When platelet aggregation was induced by ADP, the combined therapy with aspirin and clopidogrel decreased platelet aggregation significantly when compared with aspirin alone (P<0.001), and no significant difference in the results between the ASA and normal groups was observed. In conclusion, collagen may prove useful to study the effect of aspirin and ADP may be appropriate for assessing the inhibitory effect of clopidogrel.

Association between Low Free Triiodothyronine Levels and Poor Prognosis in Patients with Acute ST-Elevation Myocardial Infarction

Background Low free triiodothyronine (fT3) levels are generally associated with poor prognosis in patients with heart diseases, but this is controversial and there is a lack of data about ST-elevation myocardial infarction (STEMI) in Chinese patients. Objective To assess the association between fT3 levels and the prognosis of patients with STEMI. Methods This was a prospective observational study of 699 consecutive patients with STEMI treated at the Xinqiao Hospital between January 1, 2013, and December 31, 2014. The patients were divided into the low fT3 (fT3 < 3.1 pmol/L; n = 179, 27.5%) and normal fT3 (fT3 ≥ 3.1 pmol/L; n = 473, 72.5%) groups according to fT3 levels at admission. Patients were followed up at 1, 3, 6, and 12 months for all-cause death and major adverse cardiac events (MACE). Results During the 1-year follow-up, there were 70 all-cause deaths (39.1%) in the low fT3 group and 40 (8.5%) in the normal fT3 group (P < 0.001). MACE occurred in 105 patients (58.7%) in the low fT3 group and 74 (15.6%) in the normal fT3 group (P < 0.001). Multivariate Cox proportional hazards regression analysis indicated that fT3 levels were independently associated with 30-day and 1-year all-cause death [30-day: hazard ratio (HR) = 0.702, 95% confidence interval (95% CI): 0.501–0.983, P = 0.04; 1-year: HR = 0.557, 95% CI: 0.411–0.755, P < 0.001] and MACE (30-day: HR = 0.719, 95% CI: 0.528–0.979, P = 0.036; 1-year: HR = 0.557, 95% CI: 0.445–0.698, P < 0.001). Conclusion Low fT3 levels were strongly associated with poor prognosis in patients with STEMI. Measurement of fT3 levels may be a valuable and simple way to identify high-risk STEMI patients.