In order to explore the possible mechanism of curcumin in the treatment of AF, we focused on the myocardial fibrosis in the pathogenesis of atrial fibrillation to explore whether curcumin could play a role in the treatment of AF by reducing myocardial fibrosis.Rats were given daily gavage of saline (control and AF groups) or curcumin (4 mL/kg, concentration: 50 mg/mL, curcumin groups) during days 4-28. The rat model of AF was induced by Ach - CaCl2, and evaluate the therapeutic effect of curcumin on the duration of AF rhythm, the degree of myocardial fibrosis and the secretion of inflammatory factors in serum. RNA-seq to explore the possible mechanism of curcumin alleviating myocardial fibrosis of AF. curcumin significantly inhibits the duration of AF and reduces the degree of left atrial fibrosis. ELISA results showed curcumin could significantly reduce the secretion of IL-17A, IL-1β, IL -6 and TGF-β1. Bioinformatics analyses revealed that the IL-17 signaling pathway are involved in the therapeutic mechanism of curcumin. Furthermore, The genes encoding Col1a1, Fasn, Pck1, Bmp10, IL33 and Figf were pivotal and possible key genes for the therapeutic mechanisms of curcumin.Curcumin can reduce the degree of left atrial fibrosis of AF and the secretion of inflammatory factors. The therapeutic effect of curcumin on AF was attributed to its effect on the IL-17 signaling pathway. Besides, COL1A1, FASN, PCK1, BMP10, IL33 and FIGF were the pivotal genes associated with mechanisms of action of curcumin on AF.
Objective: Systemic immune-inflammation index (SII) is a novel biomarker that can predict poor outcomes in tumours, nervous system diseases and chronic heart failure. Here, we investigated the predictive value of SII on the poor postoperative outcomes and short-term prognosis of heart valve diseases (HVDs). Design, setting and participants: This retrospective cohort study enrolled all consecutive patients with HVDs (aortic stenosis, aortic regurgitation, mitral stenosis and mitral regurgitation) who underwent surgery (valve replacement or valve repair) at the Affiliated Hospital of North Sichuan Medical College between 2017 and 2020. Main outcomes and measures: Major complications in the perioperative period, all-cause mortality within 30 days and readmission within 30 days. Results: A total of 431 patients with HVDs were enrolled in this study, including 202 males and 229 females, aged 58.9±27.3 years. SII levels of patients in the poor outcomes group were significantly higher than those of patients in the favourable outcomes group (658.40±436.29 vs 335.72±174.76, respectively; p<0.001). Multivariate logistic regression analysis showed that age (OR 1.064, 95% CI 1.026 to 1.104, p=0.025), SII (OR 1.034, 95% CI 1.012 to 1.631, p=0.008) and aortic cross-clamping time (OR 1.013, 95% CI 1.004 to 1.023, p=0.006) were independent risk factors for poor outcomes and short-term prognosis in patients with HVD. The area under the curve of poor outcomes predicted by SII in patients with HVD was 0.806 (95% CI 0.763 to 0.848) and the optimised cut-off value 423.8×10 9 /L, with a sensitivity of 70.3% and specificity of 81.1%. The incidence of poor outcomes (p<0.001), 30-day mortality (p<0.001) and 30-day readmission rate (p=0.026) in the high SII group was significantly higher than that in the low SII group. Conclusions: SII is closely related to poor postoperative outcomes and short-term prognosis of HVD and can serve as an independent predictive factor.
1 July 2013 in International Journal of Cardiology
The World Health Organization announced that COVID-19, with SARS-CoV-2 as its pathogen, had become a pandemic on 11 March 2020. Today, the global epidemic situation is still serious. With the development of research, cardiovascular injury in patients with COVID-19, such as arrhythmia, myocardial injury, and heart failure, is the second major symptom in addition to respiratory symptoms, and cardiovascular injury is related to the prognosis and mortality of patients. The incidence of arrhythmia in COVID-19 patients ranges from 10% to 20%. The potential mechanisms include viral infection-induced angiotensin-converting enzyme 2 expression change, myocarditis, cytokine storm, cardiac injury, electrophysiological effects, hypoxemia, myocardial strain, electrolyte abnormalities, intravascular volume imbalance, drug toxicities and interactions, and stress response caused by virus infection. COVID-19 complicated with arrhythmia needs to be accounted for and integrated in management. This article reviews the incidence, potential mechanisms, and related management measures of arrhythmia in COVID-19 patients.