Tag: Inflammation

IL-6 and D-dimer Levels at Admission Predict Cardiac Injury and Early Mortality during SARS-CoV-2 Infection

Announcing a new article publication for Cardiovascular Innovations and Applications journal. The activation of immune and thrombotic biomarkers at admission, and their ability to predict cardiac injury and mortality patterns in COVID-19, remains unclear.

This retrospective cohort study included 170 patients with COVID-19 with cardiac injury at the time of admission to Tongji Hospital in Wuhan between January 29, 2020, and March 8, 2020. The temporal evolution of inflammatory cytokines, coagulation markers, clinical treatment, and mortality were analyzed. Continuous variables are expressed as median (interquartile range). The Mann-Whitney test was used for two-group comparisons, whereas the Kruskal-Wallis test was used for comparisons among three groups. Categorical variables are expressed as proportions and percentages, and Fisher’s exact test was used to compare differences. A multivariate regression model was used to predict in-hospital death. A simple linear regression analysis was applied to examine the correlation between baseline biomarkers and peak cTnI levels.

Of the 170 patients, 60 (35.3%) died early (<21 d), and 61 (35.9%) died after a prolonged stay. The admission laboratory findings correlating with early death were elevated interleukin 6 (IL-6) (P < 0.0001), tumor necrosis factor-α (P = 0.0025), and C-reactive protein (P < 0.0001). We observed the trajectory of biomarker changes in patients after admission hospitalization, and determined that early mortality was associated with a rapidly increasing D-dimer level, and gradually decreasing platelet and lymphocyte counts. Multivariate and simple linear regression models indicated that the risk of death was associated with immune and thrombotic pathway activation. Elevated admission cTnI levels were associated with elevated IL-6 (P = 0.03) and D-dimer (P = 0.0021) levels.

In patients with COVID-19 with cardiac injury, IL-6 and D-dimer levels at admission predicted subsequently elevated cTnI levels and early death, thus highlighting the need for early inflammatory cytokine-based risk stratification in patients with cardiac injury.

https://www.scienceopen.com/hosted-document?doi=10.15212/CVIA.2024.0009

CVIA is available on the ScienceOpen platform and at Cardiovascular Innovations and Applications. Submissions may be made using ScholarOne Manuscripts. There are no author submission or article processing fees. Cardiovascular Innovations and Applications is indexed in the EMBASE, EBSCO, ESCI, OCLC, Primo Central (Ex Libris), Sherpa Romeo, NISC (National Information Services Corporation), DOAJ, Index Copernicus, Research4Life and Ulrich’s web Databases. Follow CVIA on Twitter @CVIA_Journal; or Facebook.

Kexin Peng, Beibei Du and Daoyuan Si et al. IL-6 and D-dimer Levels at Admission Predict Cardiac Injury and Early Mortality during SARS-CoV-2 Infection. CVIA. 2024. Vol. 9(1). DOI: 10.15212/CVIA.2024.0009

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Inhibition of Stimulator of Interferon Genes Protects Against Myocardial Ischemia-Reperfusion Injury in Diabetic Mice

Announcing a new article publication for Cardiovascular Innovations and Applications journal.  Although the past decade has witnessed substantial scientific progress with the advent of cardioprotective pharmacological agents, most have failed to protect against myocardial ischemia/reperfusion (I/R) injury in diabetic hearts. This article investigates the role of stimulator of interferon genes (STING) in I/R injury in diabetic mice and further exploring the underlying mechanisms.

Type 2 diabetic mice were subjected to I/R or sham operation to investigate the role of STING. STING knockout mice were subjected to 30 minutes of ischemia followed by reperfusion for 24 hours. Finally, myocardial injury, cardiac function, and inflammation levels were assessed.

STING pathway activation was observed in diabetic I/R hearts, as evidenced by increased p-TBK and p-IRF3 expression. STING knockout significantly decreased the ischemic area and improved cardiac function after I/R in diabetic mice. STING knockout also elicited cardio-protective effects by decreasing serum cardiac troponin T and lactate dehydrogenase levels, thus diminishing the inflammatory response in the heart after I/R in diabetic mice. In vitro, STING inhibition decreased the expression of hypoxia-re-oxygenation-induced inflammatory cytokines.

Targeting STING inhibits inflammation and prevents I/R injury in diabetic mice. Thus, STING may be a potential novel therapeutic target against myocardial I/R injury in diabetes.

https://www.scienceopen.com/hosted-document?doi=10.15212/CVIA.2023.0020

CVIA is available on the ScienceOpen platform and at Cardiovascular Innovations and Applications. Submissions may be made using ScholarOne Manuscripts. There are no author submission or article processing fees. Cardiovascular Innovations and Applications is indexed in the EMBASE, EBSCO, ESCI, OCLC, Primo Central (Ex Libris), Sherpa Romeo, NISC (National Information Services Corporation), DOAJ, Index Copernicus, Research4Life and Ulrich’s web Databases. Follow CVIA on Twitter @CVIA_Journal; or Facebook.

Yuce Peng, Guoxiang Zhou and Mingyu Guo et al. Inhibition of Stimulator of Interferon Genes Protects Against Myocardial Ischemia-Reperfusion Injury in Diabetic Mice. CVIA. 2023. Vol. 8(1). DOI: 10.15212/CVIA.2023.0020

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