scholarly journals Acute Heart Failure After Reperfused Ischemic Stroke: Association With Systemic and Cardiac Inflammatory Responses

2021 ◽  
Vol 12 ◽  
Author(s):  
Lilian Vornholz ◽  
Fabian Nienhaus ◽  
Michael Gliem ◽  
Christina Alter ◽  
Carina Henning ◽  
...  
Keyword(s):  
Heart Failure ◽  
Flow Cytometry ◽  
Ischemic Stroke ◽  
Inflammatory Response ◽  
Stroke Volume ◽  
Acute Heart Failure ◽  
Inflammatory Responses ◽  
Troponin T ◽  
Systemic Inflammatory Response ◽  
Myocardial Tissue

Patients with acute ischemic stroke (AIS) present an increased incidence of systemic inflammatory response syndrome and release of Troponin T coinciding with cardiac dysfunction. The nature of the cardiocirculatory alterations remains obscure as models to investigate systemic interferences of the brain-heart-axis following AIS are sparse. Thus, this study aims to investigate acute cardiocirculatory dysfunction and myocardial injury in mice after reperfused AIS. Ischemic stroke was induced in mice by transient right-sided middle cerebral artery occlusion (tMCAO). Cardiac effects were investigated by electrocardiograms, 3D-echocardiography, magnetic resonance imaging (MRI), invasive conductance catheter measurements, histology, flow-cytometry, and determination of high-sensitive Troponin T (hsTnT). Systemic hemodynamics were recorded and catecholamines and inflammatory markers in circulating blood and myocardial tissue were determined by immuno-assay and flow-cytometry. Twenty-four hours following tMCAO hsTnT was elevated 4-fold compared to controls and predicted long-term survival. In parallel, systolic left ventricular dysfunction occurred with impaired global longitudinal strain, lower blood pressure, reduced stroke volume, and severe bradycardia leading to reduced cardiac output. This was accompanied by a systemic inflammatory response characterized by granulocytosis, lymphopenia, and increased levels of serum-amyloid P and interleukin-6. Within myocardial tissue, MRI relaxometry indicated expansion of extracellular space, most likely due to inflammatory edema and a reduced fluid volume. Accordingly, we found an increased abundance of granulocytes, apoptotic cells, and upregulation of pro-inflammatory cytokines within myocardial tissue following tMCAO. Therefore, reperfused ischemic stroke leads to specific cardiocirculatory alterations that are characterized by acute heart failure with reduced stroke volume, bradycardia, and changes in cardiac tissue and accompanied by systemic and local inflammatory responses.

scholarly journals Peptide VSAK maintains tissue glucose uptake and attenuates pro-inflammatory responses caused by LPS in an experimental model of the systemic inflammatory response syndrome: a PET study

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ismael Luna-Reyes ◽  
Eréndira G. Pérez-Hernández ◽  
Blanca Delgado-Coello ◽  
Miguel Ángel Ávila-Rodríguez ◽  
Jaime Mas-Oliva
Keyword(s):  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Glucose Uptake ◽  
Inflammatory Responses ◽  
Serum Levels ◽  
Systemic Inflammatory Response ◽  
Positron Emission ◽  
Inflammatory Molecules ◽  
Circulating Levels ◽  
Lps Treatment

AbstractThe present investigation using Positron Emission Tomography shows how peptide VSAK can reduce the detrimental effects produced by lipopolysaccharides in Dutch dwarf rabbits, used to develop the Systemic Inflammatory Response Syndrome (SIRS). Animals concomitantly treated with lipopolysaccharides (LPS) and peptide VSAK show important protection in the loss of radiolabeled-glucose uptake observed in diverse organs when animals are exclusively treated with LPS. Treatment with peptide VSAK prevented the onset of changes in serum levels of glucose and insulin associated with the establishment of SIRS and the insulin resistance-like syndrome. Treatment with peptide VSAK also allowed an important attenuation in the circulating levels of pro-inflammatory molecules in LPS-treated animals. As a whole, our data suggest that peptide VSAK might be considered as a candidate in the development of new therapeutic possibilities focused on mitigating the harmful effects produced by lipopolysaccharides during the course of SIRS.

scholarly journals The Value of Admission Serological Indicators for Predicting 28-Day Mortality in Intensive Care Patients With Acute Heart Failure: Construction and Validation of a Nomogram

2021 ◽  
Vol 8 ◽  
Author(s):  
Xiaoyuan Wei ◽  
Yu Min ◽  
Jiangchuan Yu ◽  
Qianli Wang ◽  
Han Wang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Intensive Care ◽  
Acute Heart Failure ◽  
Sofa Score ◽  
Medical Information ◽  
Troponin T ◽  
Adequate Treatment ◽  
Intensive Care Patients ◽  
Creatine Kinase Mb ◽  
Death Group

Background: Acute heart failure (AHF) is a severe clinical syndrome characterized as rapid onset or worsening of symptoms of chronic heart failure (CHF). Risk stratification for patients with AHF in the intensive care unit (ICU) may help clinicians to predict the 28-day mortality risk in this subpopulation and further raise the quality of care.Methods: We retrospectively reviewed and analyzed the demographic characteristics and serological indicators of patients with AHF in the Medical Information Mart for Intensive Care III (MIMIC III) (version 1.4) between June 2001 and October 2012 and our medical center between January 2019 and April 2021. The chi-squared test and the Fisher's exact test were used for comparison of qualitative variables among the AHF death group and non-death group. The clinical variables were selected by using the least absolute shrinkage and selection operator (LASSO) regression. A clinical nomogram for predicting the 28-day mortality was constructed based on the multivariate Cox proportional hazard regression analysis and further validated by the internal and external cohorts.Results: Age > 65 years [hazard ratio (HR) = 2.47], the high Sequential Organ Failure Assessment (SOFA) score (≥3 and ≤8, HR = 2.21; ≥9 and ≤20, HR = 3.29), lactic acid (Lac) (>2 mmol/l, HR = 1.40), bicarbonate (HCO3-) (>28 mmol/l, HR = 1.59), blood urea nitrogen (BUN) (>21 mg/dl, HR = 1.75), albumin (<3.5 g/dl, HR = 2.02), troponin T (TnT) (>0.04 ng/ml, HR = 4.02), and creatine kinase-MB (CK-MB) (>5 ng/ml, HR = 1.64) were the independent risk factors for predicting 28-day mortality of intensive care patients with AHF (p < 0.05). The novel nomogram was developed and validated with a promising C-index of 0.814 (95% CI: 0.754–0.882), 0.820 (95% CI: 0.721–0.897), and 0.828 (95% CI: 0.743–0.917), respectively.Conclusion: This study provides a new insight in early predicting the risk of 28-day mortality in intensive care patients with AHF. The age, the SOFA score, and serum TnT level are the leading three predictors in evaluating the short-term outcome of intensive care patients with AHF. Based on the nomogram, clinicians could better stratify patients with AHF at high risk and make adequate treatment plans.

Angiopoietin-Like Protein 7 and Short-Term Mortality in Acute Heart Failure

2020 ◽  
Vol 10 (2) ◽  
pp. 116-124 ◽  
Author(s):  
Chongyu Zhang ◽  
Xin He ◽  
Jingjing Zhao ◽  
Yalin Cao ◽  
Jian Liu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Inflammatory Responses ◽  
Statistical Significance ◽  
Serum Levels ◽  
Enzyme Linked Immunosorbent Assay ◽  
Short Term ◽  
Logistic Regression Models ◽  
Increased Risk ◽  
Short Term Mortality

Introduction: Angiopoietin-like protein 7 (ANGPTL7) is involved in extracellular matrix expression and inflammatory responses. However, the prognostic utility of ANGPTL7 among patients with acute heart failure (AHF) remains unclear. Objective: To evaluate the association between ANGPTL7 and short-term mortality due to AHF. Methods and Results: Patients with AHF were prospectively studied. Serum levels of ANGPTL7 were measured by an enzyme-linked immunosorbent assay. Associations between 30- and 90-day mortality and tertiles of ANGPTL7 were assessed by multivariate logistic regression models. The study comprised 142 patients. Median patient age was 68 years, and 69.7% were male. There were 20 deaths within 30 days and 37 deaths within 90 days. Crude rates of 30-day mortality in low, intermediate, and high tertiles of ANGPTL7 were 4.6, 14.6, and 22.9%, respectively. Crude rates of 90-day mortality of corresponding tertiles were 15.2, 25.0, and 37.5%. After adjusting for potential confounders, including NT-proBNP, the high tertile of ANGPTL7 was associated with a significantly increased risk of both 30-day mortality (odds ratio [OR]: 6.77, 95% confidence interval [CI]: 1.41–32.61, p = 0.017) and 90-day mortality (OR: 3.78, 95% CI: 1.38–10.36, p = 0.010) compared with the low tertile of ANGPTL7. Although mortality risk tended to be higher in the intermediate tertile than the low tertile, it did not reach statistical significance (OR: 3.75, 95% CI: 0.73–19.14, p = 0.113 for 30-day mortality; OR: 1.88, 95% CI: 0.66–5.34, p = 0.236 for 90-day mortality). Conclusions: Serum level of ANGPTL7 was independently associated with short-term mortality among patients with AHF.

scholarly journals Association Between Splenic Contraction and the Systemic Inflammatory Response After Acute Ischemic Stroke Varies with Age and Race

2017 ◽  
Vol 9 (5) ◽  
pp. 484-492 ◽  
Author(s):  
Alicia Zha ◽  
Farhaan Vahidy ◽  
Jaskaren Randhawa ◽  
Kaushik Parsha ◽  
Thanh Bui ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Inflammatory Response ◽  
Acute Ischemic Stroke ◽  
Systemic Inflammatory Response

Acute Heart Failure Secondary to Myocardial Tissue Water Changes in Isolated Working Rat Hearts

1995 ◽  
Vol 752 (1 Cardiac Growt) ◽  
pp. 222-226
Author(s):  
A. BARSOTTI ◽  
P. NAPOLI ◽  
F. L. DINI ◽  
E. GIROLAMO ◽  
S. GALLINA ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Myocardial Tissue ◽  
Tissue Water ◽  
Rat Hearts

scholarly journals RhTrx-1 ameliorates miroglial neuroinflammation after cerebral ischemic stroke

2020 ◽  
Author(s):  
Yang Jiao ◽  
Jianjian Wang ◽  
Huixue Zhang ◽  
Yuze Cao ◽  
Yang Qu ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Inflammatory Response ◽  
Inflammatory Responses ◽  
Inflammatory Factors ◽  
Experimental Stroke ◽  
Inflammasome Activation ◽  
Cerebral Ischemic

Abstract Background Microglia are rapidly activated after ischemic stroke and participate in the occurrence of neuroinflammation, which exacerbates the injury of ischemic stroke. Receptor Interacting Serine Threonine Kinase 1 (RIPK1) is thought to be involved in the development of inflammatory responses, but its role in ischemic microglia remains unclear. Here, we applied recombinant human thioredoxin-1 (rhTrx-1), a potential neuroprotective agent, to explore the role of rhTrx-1 in inhibiting RIPK1-mediated neuroinflammatory responses in microglia. Method Middle cerebral artery occlusion (MCAO) and Oxygen and glucose deprivation (OGD) were conducted for in vivo and in vitro experimental stroke models. The expression of RIPK1 in microglia after ischemia was examined. The inflammatory response of microglia was analyzed after treatment with rhTrx-1 and Necrostatin-1 (Nec-1, inhibitors of RIPK1), and the mechanisms were explored. In addition, the effects of rhTrx-1 on neurobehavioral deficits and cerebral infarct volume were examined. Results RIPK1 expression was detected in microglia after ischemia. Molecular docking results showed that rhTrx-1 could directly bind to RIPK1. In vitro experiments found that rhTrx-1 reduced necroptosis, mitochondrial membrane potential damage, Reactive oxygen species (ROS) accumulation and NLR Family, pyrin domain-containing 3 protein (NLRP3) inflammasome activation by inhibiting RIPK-1 expression, and regulated microglial M1/M2 phenotypic changes, thereby reducing the release of inflammatory factors. Consistently, in vivo experiments found that rhTrx-1 treatment attenuated cerebral ischemic injury by inhibiting the inflammatory response. Conclusion Our study demonstrates the role of RIPK1 in microglia-arranged neuroinflammation after cerebral ischemia. Administration of rhTrx-1 provides neuroprotection in ischemic stroke-induced microglial neuroinflammation by inhibiting RIPK1 expression.

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