Background: The Shexiang Baoxin Pill (MUSKARDIA) has been used for treating coronary artery disease (CAD) and angina for more than 30 years in China. Nevertheless, methodologically sound trials on the use of MUSKARDIA in CAD patients are scarce. The aim of the study is to determine the effects of MUSKARDIA as an add-on to optimal medical therapy (OMT) in patients with stable CAD. Methods: A total of 2674 participants with stable CAD from 97 hospitals in China were randomized 1:1 to a MUSKARDIA or placebo group for 24 months. Both groups received OMT according to local tertiary hospital protocols. The primary outcome was the occurrence of a major adverse cardiovascular event (MACE), defined as a composite of cardiovascular death, non-fatal myocardial infarction (MI), or non-fatal stroke. Secondary outcomes included all-cause mortality, non-fatal MI, non-fatal stroke, hospitalization for unstable angina or heart failure, peripheral revascularization, angina stability and angina frequency. Results: In all, 99.7% of the patients were treated with aspirin and 93.0% with statin. After 2 years of treatment, the occurrence of MACEs was reduced by 26.9% in the MUSKARDIA group (MUSKARDIA: 1.9% vs. placebo: 2.6%; odds ratio = 0.80; 95% confidence interval: 0.45–1.07; P  = 0.2869). Angina frequency was significantly reduced in the MUSKARDIA group at 18 months (P = 0.0362). Other secondary endpoints were similar between the two groups. The rates of adverse events were also similar between the two groups (MUSKARDIA: 17.7% vs. placebo: 17.4%, P = 0.8785). Conclusions: As an add-on to OMT, MUSKARDIA is safe and significantly reduces angina frequency in patients with stable CAD. Moreover, the use of MUSKARDIA is associated with a trend toward reduced MACEs in patients with stable CAD. The results suggest that MUSKARDIA can be used to manage patients with CAD. Trial registration chictr.org.cn, No. ChiCTR-TRC-12003513

Background:The efficacy and safety of ticagrelor following percutaneous coronary intervention for patients with acute coronary syndrome remains unclear. This study sought to evaluate clinical outcomes of ticagrelor as part of dual-antiplatelet treatment for these patients. Methods: PubMed, MEDLINE, Embase, and other Internet sources were searched for eligible citations. The primary end point was major adverse cardiovascular and cerebrovascular events, consisting of cardiovascular death, myocardial infarction, and stroke. The secondary end point was the occurrence of definite/probable stent thrombosis (ST). The risk of bleeding was chosen to be the safety end point. Results: Eleven clinical trials -six randomized trials and five observational trials -were finally analyzed. A tendency toward reduction in the risk of major adverse cardiovascular and cerebrovascular events was observed only with respect to ticagrelor (OR 0.83, 95% CI 0.66-1.03; P=0.091), which might have resulted from the lower risk of cardiovascular death (OR 0.78, 95% CI 0.68-0.89; P,0.001). The overall incidence of ST differed significantly between the ticagrelor group and the clopidogrel group (OR 0.74, 95% CI 0.59-0.93; P=0.009), but the risk of bleeding, regardless of major or minor bleeding, increased significantly. Conclusion: As part of dual-antiplatelet treatment following percutaneous coronary intervention, ticagrelor significantly reduced the risk of cardiovascular death and ST in acute coronary syndrome patients, but at the cost of bleeding. More powerful relevant randomized trials are still warranted to guide clinical decision-making.

Avian hepatitis E virus (HEV) is a single-stranded, positive-sense RNA virus with a complete genome of approximately 6.6 kb in size. To date, four major genotypes of avian HEV have been identified and classified into the Orthohepevirus B genus of the family Hepeviridae . The avian HEV associated with hepatitis-splenomegaly syndrome, big liver and spleen disease or hepatic rupture hemorrhage syndrome in chickens is genetically and antigenically related to mammalian HEV. With the increased genotypes of avian HEV identified, a broader host tropism is also notable in the epidemiological studies. Due to the lack of an efficient cell culture system, the mechanisms of avian HEV replication and pathogenesis are still poorly understood. The recent identification and characterization of animal strains of avian HEV has demonstrated the virus’ ability of cross-species infection. Although it has not yet been detected in humans, the potential threat of a zoonotic HEV capable of transmission to humans needs to be taken into consideration. This review article focuses on the current knowledge regarding avian HEV in virology, epidemiology, pathogenesis, clinical presentation, transmission, diagnosis and prevention. HIGHLIGHTS - The mechanisms of avian HEV replication and pathogenesis are still poorly understood due to the lack of an efficient cell culture system. - A broader host tropism is also notable in the epidemiological studies with the increased genotypes of avian HEV identified. - The recent identification and characterization of animal strains of avian HEV has demonstrated the virus’ ability of cross-species infection. - The potential threat of a zoonotic HEV capable of transmission to humans needs to be taken into consideration.

Background The triglyceride glucose-body mass index (TyG-BMI index) has been considered a reliable surrogate measure of insulin resistance; however, its ability to predict the incidence of cardiovascular disease in individuals with coronary artery disease (CAD) remains uncertain. The aim of this study was to demonstrate the correlation between the TyG-BMI index and cardiovascular incidence. Methods A total of 2533 consecutive participants who underwent percutaneous coronary intervention (PCI) and drug-eluting stent (DES) implantation were included. Data from 1438 patients was analyzed in the study. The endpoint was defined as a composite of acute myocardial infarction, repeat revascularization, stroke, and all-cause mortality (major adverse cardiac and cerebrovascular events, MACCEs) at 34-month follow-up. The formula for calculating the TyG-BMI index is ln [fasting triglyceride (mg/dL) × fasting blood glucose (mg/dL)/2] × BMI. Results Among the 1438 participants, 195 incident patient cases of MACCEs were ascertained. The incidence of MACCEs showed no statistically significant differences in the TyG-BMI index tertiles in the overall population. Further exploratory subgroup analysis and multivariable logistic regression analysis revealed a linear relationship between the TyG-BMI index (per 1 SD increased) and MACCEs in the elderly patients (OR = 1.22, 95% CI 1.011–1.467, p = 0.038) and in the female patients (OR = 1.33, 95% CI 1.004–1.764, p = 0.047). The addition of the TyG-BMI index to traditional risk factor models in elderly and female patients did not improve risk prediction for MACCEs. Conclusion A higher TyG-BMI index was proportionally related to an increased incidence of MACCEs in the elderly or female patients. However, the inclusion of the TyG-BMI index did not provide better predictive performance for MACCEs in the elderly, specifically in female patients.