BackgroundNew-onset atrial fibrillation (NOAF) is associated with worse prognostic outcomes in cases diagnosed with ST-segment elevation myocardial infarction (STEMI) patients after percutaneous coronary intervention (PCI). The triglyceride-glucose (TyG) index, as a credible and convenient marker of insulin resistance, has been shown to be predictive of outcomes for STEMI patients following revascularization. The association between TyG index and NOAF among STEMI patients following PCI, however, has not been established to date.ObjectiveTo assess the utility of the TyG index as a predictor of NOAF incidence in STEMI patients following PCI, and to assess the relationship between NOAF and long-term all-cause mortality.MethodsThis retrospective cohort research enrolled 549 STEMI patients that had undergone PCI, with these patients being clustered into the NOAF group and sinus rhythm (SR) group. The predictive relevance of TyG index was evaluated through logistic regression analyses and the receiver operating characteristic (ROC) curve. Kaplan-Meier curve was employed to explore differences in the long-term all-cause mortality between the NOAF and SR group.ResultsNOAF occurred in 7.7% of the enrolled STEMI patients after PCI. After multivariate logistic regression analysis, the TyG index was found to be an independent predictor of NOAF [odds ratio (OR): 8.884, 95% confidence interval (CI): 1.570–50.265, P = 0.014], with ROC curve analyses further supporting the predictive value of this parameter, which exhibited an area under ROC curve of 0.758 (95% CI: 0.720–0.793, P < 0.001). All-cause mortality rates were greater for patients in the NOAF group in comparison with the SR group over a median 35-month follow-up period (log-rank P = 0.002).ConclusionsThe TyG index exhibits values as an independent predictor of NOAF during hospitalization, which indicated a poorer prognosis after a relatively long-term follow-up.

No abstract

Purpose: The purpose of this study was to determine whether ticagrelor, a classic anti-platelet drug, has a therapeutic effect on sepsis-induced myocardial injury. Methods: The C57BL6J mice received oral ticagrelor (10, 25 and 50 mg/kg) for seven days after which cecum ligation and puncture (CLP) were performed. An adenosine-receptor antagonist (CGS15943) was administered two hours before CLP. After 24 h, cardiac function was measured using cardiac echocardiography, then the heart and blood were collected. Hematoxylin and eosin (HE) staining and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL staining) were used to observe pathological changes and cardiomyocyte apoptosis. Plasma concentration of TNF-α, IL-6 and adenosine and myocardial tissue levels of TNF-α and IL-6 were determined. Survival analysis was performed. Western blot was used to determine the expression of a signalling protein in the myocardial tissue. Results: The HE and TUNEL staining showed less inflammatory cell infiltration and less cardiomyocyte apoptosis in the ticagrelor group. Cardiac echocardiography showed preserved heart function in the ticagrelor group. Plasma TNF-α, IL-6 and relative expression of TNF-α and IL-6 in myocardial tissue were significantly lower in the ticagrelor group. Plasma adenosine levels were significantly higher in the ticagrelor group. Adenosine-receptor antagonists significantly blocked the protective effect of ticagrelor. Ticagrelor reduced the mortality of sepsis mice, and this reduction was blocked by the adenosine-receptor antagonist. Western blot showed that ticagrelor activated the phosphorylation of AKT and mTOR. Adenosine-receptor antagonists inhibited the activation of AKT and mTOR. Conclusion: The protective effect of ticagrelor was dependent on adenosine-receptor activation, with downstream upregulation of phosphorylation of AKT and mTOR.

Background Lung tumor embolization leading to acute myocardial infarction (AMI) is rare. Previouscases of lung tumor embolization were reported in the coronary artery. We describe here a case of lung tumor embolization leading to the simultaneous occurrence of AMI and lower extremity arterial embolism. Case presentation A 64-year-old patient was admitted to the emergency department complaining of chest pain and was diagnosed with AMI.An echocardiography showed a mass in the left atrium that was speculated to be a myxoma. An emergency coronary angiography found no evidence of atherosclerosis. On the second day of admission, the patient was diagnosed with lower extremity arterial embolism. Initially, we speculated that the left atrium myxoma caused an embolism resulting in the AMI and lower extremity arterial embolism.However, a lung tumor was the real cause of both conditions. Unfortunately, the patient abandoned treatment when he learned of his disease and died three days later after being discharged from the hospital. Conclusions Lung tumor embolism is an extremely rare cause of AMI. Even rarer is the case presented here, in which a lung tumor embolism caused AMI and lower extremity arterial embolism. Clinicians should recognize lung tumor embolism as a potential cause of AMI.