The triglyceride glucose (TyG) index is a marker of insulin resistance. However, the prognostic value thereof in patients with chronic heart failure (CHF) and type 2 diabetes remains unclear.Methods: This study included patients diagnosed with CHF and type 2 diabetes in Fuwai Hospital of Chinese Academy of Medical Sciences, Shenzhen, from January 2017 to July 2019. The primary endpoint was cardiovascular death or rehospitalization for heart failure. Results:The study included 546 patients with CHF and type 2 diabetes. We divided the patients into three groups (T1 [TyG index < 8.55], T2 [TyG index ! 8.55 and < 9.06], and T3 [TyG index ! 9.06]) according to the TyG index level. The incidence of the primary outcome in the T3 group was significantly higher than that in the T1 group. There was no significant difference between the T1 and T2 groups. The trend test revealed a positive correlation between the TyG index and the incidence of the primary outcome (P = 0.001). Conclusions:There is a positive correlation between the TyG index and the prognosis of patients with CHF and type 2 diabetes.
Background Inflammatory cells infiltrate into the ischemic and hypoxic myocardial tissue after myocardial infarction. B cells gather at the site of myocardial injury and secrete cytokines to regulate immune inflammation and fiber repair processes. Methods The animal experiment used ligation of the left anterior descending (LAD) artery of C57BL/6 mice to establish a mouse acute myocardial infarction (AMI) model to observe changes in activated B cells and cytokines at different time points. Twelve-week-old C57BL/6 male mice were randomly divided into the Sham group (24 mice) (thread under the LAD artery without ligation) and the AMI group (64 mice). In addition, C57BL/6 B-cell knockout (BKO) mice and C57BL/6 wild-type (WT) mice were used to establish AMI models to observe the expression levels of cardiomyocyte cytokines, such as TNF-α IL-1β, IL-6, TGF-β1, COL1-A1, COL3-AIII, TIMP, and MMP9. Moreover, pathological and collagen changes in the myocardium were analysed. One-way ANOVA and LSD method was used for comparisons of multiple and pairwise groups respectively. P < 0.05 indicated significant differences. Results An AMI model of C57BL/6 mice was established successfully. The ratio of activated B cells and the expression of TNF-α, IL-1β, IL-6, TGF-β1, and B cell activating factor (BAFF) in the 5-day subgroup were the highest in the myocardium, spleen and peripheral blood with the most obvious myocardial inflammatory cell infiltration. The cytokines mRNA expression levels in the 5-day subgroup of the BKO group were decreased compared with those in the WT group (P < 0.05). Among the 2-week subgroups of the Sham, WT and BKO groups, the the LVEDd and LVESd of the BKO group were lower than those of the WT group (P < 0.05), and the left ventricular ejection fraction was higher than that of the WT group (P < 0.05). Conclusion Activated B cells participate in the sustained state of myocardial inflammation and immune system activation after AMI, and may affect the metabolism of myocardial collagen after AMI by secreting cytokines. Moreover, B cells promote the expression of myocardial collagen Type I and Type III and damage the left ventricular ejection function.
BackgroundDual antiplatelet therapy is a standard protocol for secondary prevention after acute coronary syndrome, but despite a variety of new dual antithrombotic strategies, there is a dearth of studies evaluating the effects and safety of some popular therapies. This study used a network meta-analysis to compare the efficacy and safety of all available antithrombotic therapies.MethodsPubMed, MEDLINE, and Cochrane library databases were searched for randomized controlled trials, published up to July 1, 2017, that evaluated the efficacy of antithrombotic therapy in acute coronary syndrome treatment. The primary endpoints were clinically significant bleeding and major bleeding and secondary endpoints were major cardiovascular events, all-cause deaths, cardiac deaths, and myocardial infarction.ResultsCompared with treatment with aspirin + new P2Y12 inhibitor, treatment with aspirin + new P2Y12 inhibitor converted to clopidogrel clinically reduced the risk of major cardiovascular events or significant bleeding (OR: 0.30, 95% credibility interval: 0.12–0.75). Both myocardial infarction risk (OR: 0.82, 95% credibility interval: 0.62–1.09) and major bleeding risk (OR: 0.18, 95% credibility interval: 0.01–1.68) were not significantly different between treatment regimens. There were no significant differences in major cardiovascular events, all-cause deaths, cardiac deaths, myocardial infarction, clinically significant bleeding, and major bleeding risk with rivaroxaban + new P2Y12 inhibitor therapy when compared with aspirin + new P2Y12 inhibitor. Compared with aspirin + clopidogrel, the conversion therapy further reduced the risk of myocardial infarction (OR: 1.81, 95%, credibility interval: 1.01–1.34) without an increased clinical risk of significant bleeding (OR: 0.41, 95%, credibility interval: 0.15–1.07). Treatment with aspirin + new P2Y12 inhibitors reduced all-cause deaths (OR: 0.91, 95% credibility interval: 0.84–0.98) and cardiac death risk (OR: 0.86, 95% credibility interval: 0.79–0.93).ConclusionWe concluded the following from our study: 1) an aspirin + new P2Y12 inhibitor/ clopidogrel conversion treatment strategy was not inferior to aspirin + new P2Y12 inhibitor; 2) compared with aspirin + clopidogrel, the conversion strategy may further reduce the risk of myocardial infarction without increasing the risk of bleeding; and 3) compared with aspirin + clopidogrel, treatment with aspirin + new P2Y12 inhibitors may result in reduced risk of death.
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