• Artificial intelligence (AI)
• emergency medical services
• machine learning (ML)
• prognosis
• sepsis

• intensive care unit
• pulmonary hypertension
• right heart failure
• right ventricle

• Humans
• Critical Care/methods
• Heart Failure/therapy
• Heart Failure/etiology
• Heart Failure/physiopathology
• Heart Failure/diagnosis
• Heart-Assist Devices
• Hemodynamics
• Intensive Care Units
• Ventricular Dysfunction, Right/etiology
• Ventricular Dysfunction, Right/therapy
• Ventricular Dysfunction, Right/physiopathology
• Ventricular Dysfunction, Right/diagnosis

• heart failure
• influenza
• morbidity
• mortality

• Humans
• Influenza, Human/mortality
• Influenza, Human/complications
• Influenza, Human/epidemiology
• Heart Failure/mortality
• Heart Failure/epidemiology
• Hospitalization/statistics & numerical data
• Denmark/epidemiology
• Seasons
• Male
• Female
• Aged
• Middle Aged

• Lactate
• Metabolism
• Mitochondria
• Pyruvate
• Sepsis

• Sepsis/metabolism
• Humans
• Pyruvic Acid/metabolism
• Animals
• Mitochondria/metabolism
• Glycolysis
• Oxidative Phosphorylation

• 11M3122N Fonds Wetenschappelijk Onderzoek (FWO)
• 1220924N Fonds Wetenschappelijk Onderzoek (FWO)
• S003122N Fonds Wetenschappelijk Onderzoek (FWO)
• 3G014921 Fonds Wetenschappelijk Onderzoek (FWO)
• 01M00121 Universiteit Gent (UGent)

• ATP5
• S100A9
• SICM
• bioinformatics analysis
• mitochondrial dysfunction

• was supported by Scientific Research Fund of Zhejiang Provincial Education Department (Y202250204), the Key R&D Program Projects of Zhejiang Province (2021C03072), the National Natural Science Foundation of China (82272201 and 82272202), Zhejiang Province Clinical Key Specialized Emergency Medicine Department, and the

• Cedrol
• Fibrosis
• Heart
• Inflammation
• Lipopolysaccharide
• Oxidative stress

• ALM
• Coagulopathy
• Infection
• Inflammation
• Intra-abdominal
• Sepsis

• Humans
• Sepsis/therapy
• Adenosine/metabolism
• Lidocaine/therapeutic use
• Magnesium/therapeutic use
• Fluid Therapy/methods

• BNP
• NT-proBNP
• acute ischemic stroke
• brain natriuretic peptide
• stroke biomarkers
• stroke etiology
• thrombus

• 13/RC/2073_2 Science Foundation Ireland (SFI)

• Cardiomyocytes
• Exosome
• Inflammation
• MAPK pathway
• MiRNA-412-5p

• Antibiotic stewardship
• Cardiovascular
• Immunology
• Personalised medicine
• Pregnancy
• Sepsis

• vagus nerve stimulation
• septic shock
• cardiac injury
• inflammatory response

• Female
• Rats
• Animals
• Rats, Sprague-Dawley
• Shock, Septic/complications
• Shock, Septic/therapy
• Shock, Septic/pathology
• Vagus Nerve Stimulation
• Myocardium/pathology
• Heart
• Heart Injuries/pathology
• NF-kappa B

• complication
• infection
• multi-target treatment
• programmed cell death (PCD)
• sepsis induced myocardial injury (SIMI)

• biomarkers
• cardiovascular disease
• exosome function
• exosome therapeutics
• intracellular communication

• Humans
• Exosomes/metabolism
• Cardiovascular Diseases/metabolism
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Myocardial Infarction/metabolism
• Coronary Artery Disease/metabolism

• 82171871 National Natural Science Foundation of China
• None Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)

• SIRS
• cTnI
• cardiac damage
• cat
• systemic inflammatory response syndrome

• COVID-19
• Heart failure
• Liver cirrhosis

• chorioamnionitis
• fetal growth restriction
• interleukin-1
• perinatal inflammation
• transitional circulation

• cardiac dysfunction
• dog
• myocardial damage
• systemic inflammatory response syndrome (SIRS)

• IL-12p40 deletion
• LPS
• cardiac dysfunction
• monocytes
• sepsis

• Kawasaki disease
• Kawasaki disease shock syndrome
• coronary artery aneurysm
• intravenous immunoglobulin

The objective of this work is to develop a fusion artificial intelligence (AI) model that combines patient electronic medical record (EMR) and physiological sensor data to accurately predict early risk of sepsis. The fusion AI model has two components—an on-chip AI model that continuously analyzes patient electrocardiogram (ECG) data and a cloud AI model that combines EMR and prediction scores from on-chip AI model to predict fusion sepsis onset score. The on-chip AI model is designed using analog circuits for sepsis prediction with high energy efficiency for integration with resource constrained wearable device. Combination of EMR and sensor physiological data improves prediction performance compared to EMR or physiological data alone, and the late fusion model has an accuracy of 93% in predicting sepsis 4 h before onset. The key differentiation of this work over existing sepsis prediction literature is the use of single modality patient vital (ECG) and simple demographic information, instead of comprehensive laboratory test results and multiple vital signs. Such simple configuration and high accuracy makes our solution favorable for real-time, at-home use for self-monitoring.

• bioenergetics
• cardiomyopathy
• citric acid cycle
• mitochondria
• oxidative phosphorylation
• proteomics
• sepsis

• Animals
• Cardiomyopathies/etiology
• Cardiomyopathies/metabolism
• Male
• Mice
• Mitochondria/metabolism
• Mitochondrial Proteins
• Myocardium/metabolism
• Oxidative Phosphorylation
• Proteome/metabolism
• Pyruvate Dehydrogenase Complex/metabolism
• Pyruvic Acid/metabolism
• Sepsis/complications
• Sepsis/metabolism

• R35 GM124775 NIGMS NIH HHS
• R01 NS110567 NINDS NIH HHS
• R35 GM140822 NIGMS NIH HHS
• R01 AR071618 NIAMS NIH HHS
• R01 GM117233 NIGMS NIH HHS
• R01 GM122908 NIGMS NIH HHS
• R01 HL142290 NHLBI NIH HHS
• U01 HL116321 NHLBI NIH HHS
• R01 HL140934 NHLBI NIH HHS

Prior studies have shown that septic shock survivors had a normal cardiac index (CI) and systemic vascular resistance index (SVRI). However, this feature seems to be questionable in other-caused shock, since several factors are associated with the hemodynamic profile. This study aims to describe hemodynamic profiles (preload, inotropy, afterload, stroke volume, and cardiac output) after fluid resuscitation and vasoactive therapy in children with shock.

Children aged 1 month to 18 years old with shock conditions were included in this study. Fluid resuscitation was administered following the American College of Critical Care Medicine (ACCM) protocol. Hemodynamic profiles were assessed at 1 and 6 h from the start of fluid resuscitation. Grouping of the subjects was determined by the USCOM examination in 1st hour until the end of the study and we divided into 3 groups.

At 1 h, group 1 (low CI) was 14% (CI:2.5[1.2–3.2]L/min/m²), group 2 (normal CI) was 66% (CI:4.2[3.4–5.8]L/min/m²), and group 3 (high CI) was 20% (CI:7.1[6.1–9.4]L/min/m²). SVRI was higher in groups 1 and 2 compared to group 3 (p < 0.05). Group 1 and 2 revealed fluid-refractory shock (SVV:25[12–34]% and 29(13–58)%, respectively), lower Smith-Madigan Inotropy Index (SMII) and higher Potential to Kinetic Ratio (PKR) compared to group 3 (p < 0.05). Group 3 revealed fluid-responsive shock (Stroke Volume Variation (SVV):32[18–158]%), higher SMII and lower PKR. At 6th hour, CI in all groups were normal (group 1:3.5[1.2–7.5]; group 2:4.0[1.7–6.1]; group 3:6.0[3.1–6.2]). However, 71.4% and 54.5% of subjects in groups 1 and 2, respectively, still revealed low inotropy. Group 3 revealed a significant increase in SVRI and PKR (p < 0.01).

Most pediatric shock patients were hypodynamic. Even when the CI was normal, the preload, inotropy, and afterload may still be abnormal. It represented the inotropy as a key to hemodynamic.

•

Describe the macrocirculation parameter (preload, inotropy, afterload) in children with shock.

• Risk factors
• Septic shock
• Severe sepsis
• Urolith
• Urosepsis

• Aged
• Cross-Sectional Studies
• Humans
• Retrospective Studies
• Risk Factors
• Sepsis/complications
• Shock, Septic/complications

The coronavirus pandemic has crippled healthcare system since its outbreak in 2020, and has led to over 2.6 million deaths worldwide. Clinical manifestations of COVID-19 range from asymptomatic carrier to severe pneumonia, to life-threatening acute respiratory distress syndrome (ARDS). The early efforts of the pandemic surrounded treating the pulmonary component of COVID-19, however, there has been robust data surrounding the cardiac complications associated with the virus. This is suspected to be from a marked inflammatory response as well as direct viral injury. Arrhythmias, acute myocardial injury, myocarditis, cardiomyopathy, thrombosis, and myocardial fibrosis are some of the observed cardiac complications. There have been high morbidity and mortality rates in those affected by cardiac conditions associated with COVID-19. Additionally, there have been documented cases of patients presenting with typical cardiac symptoms who are subsequently discovered to have COVID-19 infection. In those who test positive for COVID-19, clinical awareness of the significant cardiac components of the virus is pertinent to prevent morbidity and mortality. Unfortunately, treatment and preventative measures developed for COVID-19 have been shown to be also be associated with cardiac complications. This is a comprehensive review of the cardiac complications and manifestations of COVID-19 infection in addition to those associated with both treatment and vaccination.

Supplemental Digital Content is available in the text.

Angiotensin II (ATII) was approved for septic or other distributive shock due to its property of increasing blood pressure within 3 hours. Limited data exist regarding its effectiveness when used in real-world clinical practice.

This study sought to assess the predictive value of H₂FPEF score in patients with COVID-19.

Retrospective study.

Rush University Medical Center.

A total of 1682 patients had an echocardiogram in the year preceding their COVID-19 admission with a preserved ejection fraction (≥50%). A total of 156 patients met inclusion criteria.

Patients were divided into H₂FPEF into low (0–2), intermediate (3–5), and high (6–9) score H₂FPEF groups and outcomes were compared.

Adjusted multivariable logistic regression models evaluated the association between H₂FPEF score group and a composite outcome for severe COVID-19 infection consisting of (1) 60-day mortality or illness requiring (2) intensive care unit, (3) intubation, or (4) non-invasive positive pressure ventilation.

High H₂FPEF scores were at increased risk for severe COVID-19 infection when compared intermediate to H₂FPEF score groups (OR 2.18 [CI: 1.01–4.80]; p = 0.049) and low H₂FPEF score groups (OR 2.99 [CI: 1.22–7.61]; p < 0.05). There was no difference in outcome between intermediate H₂FPEF scores (OR 1.34 [CI: 0.59–3.16]; p = 0.489) and low H₂FPEF score.

Patients with a high H₂FPEF score were at increased risk for severe COVID-19 infection when compared to patients with an intermediate or low H₂FPEF score regardless of regardless of coronary artery disease and chronic kidney disease.

• 3D bioprinting
• COVID-19
• Irreversible heart tissue damage
• Regenerative medicine

• Apoptosis
• Endotoxemic shock
• Lipopolysaccharide
• Oxidative stress
• Topiroxostat

• Altitude sickness
• Energy metabolism
• Free radical metabolism
• Hypoxia
• Mice
• Octacosan
• Petroleum ether extract of

• H9c2 cells
• LPS
• heart sepsis
• miR-21-5p
• programmed cell death protein 4

Sepsis is a life-threatening organ dysfunction and a major healthcare burden worldwide. Although sepsis is a medical emergency that requires immediate management, screening for the occurrence of sepsis is difficult. Herein, we propose a deep learning-based model (DLM) for screening sepsis using electrocardiography (ECG).

This retrospective cohort study included 46,017 patients who were admitted to two hospitals. A total of 1,548 and 639 patients had sepsis and septic shock, respectively. The DLM was developed using 73,727 ECGs from 18,142 patients, and internal validation was conducted using 7774 ECGs from 7,774 patients. Furthermore, we conducted an external validation with 20,101 ECGs from 20,101 patients from another hospital to verify the applicability of the DLM across centers.

During the internal and external validations, the area under the receiver operating characteristic curve (AUC) of the DLM using 12-lead ECG was 0.901 (95% confidence interval, 0.882–0.920) and 0.863 (0.846–0.879), respectively, for screening sepsis and 0.906 (95% confidence interval (CI), 0.877–0.936) and 0.899 (95% CI, 0.872–0.925), respectively, for detecting septic shock. The AUC of the DLM for detecting sepsis using 6-lead and single-lead ECGs was 0.845–0.882. A sensitivity map revealed that the QRS complex and T waves were associated with sepsis. Subgroup analysis was conducted using ECGs from 4,609 patients who were admitted with an infectious disease, and the AUC of the DLM for predicting in-hospital mortality was 0.817 (0.793–0.840). There was a significant difference in the prediction score of DLM using ECG according to the presence of infection in the validation dataset (0.277 vs. 0.574, p < 0.001), including severe acute respiratory syndrome coronavirus 2 (0.260 vs. 0.725, p = 0.018).

The DLM delivered reasonable performance for sepsis screening using 12-, 6-, and single-lead ECGs. The results suggest that sepsis can be screened using not only conventional ECG devices but also diverse life-type ECG machines employing the DLM, thereby preventing irreversible disease progression and mortality.

• Artificial intelligence
• Deep learning
• Electrocardiography
• Infections
• Sepsis
• Shock, Septic

• energy metabolism
• hemostasis
• metabolic resuscitation
• mitochondrial dysfunction
• myocardial dysfunction
• sepsis

Myocardial injury resulting from sepsis is the leading cause of death worldwide. Micro RNA miR-122-5p is involved in various physiological and pathological processes and is highly expressed in the heart of septic rats. However, its function in sepsis-caused myocardial injury remains elusive. Herein, a rat model of septic myocardial injury was established by intraperitoneal injection of lipopolysaccharide (LPS), and cardiomyocyte H9c2 was exposed to LPS to induce sepsis-related inflammatory injury in vitro. Inhibition of miR-122-5p suppressed LPS-triggered myocardial injury evidenced by decreased heart weight index (HWI), reduced inflammatory cell infiltration and cell rupture, and reduced cardiac marker enzymes cTnI and LDH. MiR-122-5p inhibition inhibited ROS production and enhanced the activities of antioxidant enzymes CAT, SOD and GSH-px in LPS-treated rats and H9c2 cells. MiR-122-5p inhibition reduced the production of pro-inflammatory cytokines TNF-α, IL-6 and IL-1β, and inhibited cell apoptosis along with decreased cleaved-caspase 3 induced by LPS. Moreover, increased GIT1 expression was found following miR-122-5p inhibition. We further verified GIT1 as a target of miR-122-5p, and silencing GIT1 partially reversed the benefits of miR-122-5p loss in LPS-injured H9c2 cells. The HO-1 and NQO-1 expression and Nrf-2 activation were enhanced by miR-122-5p inhibition, which was reversed by GIT1 depletion, indicating the involvement of Nrf-2/HO-1 signaling in regulating miR-122-5p/GIT1-mediated cardioprotection. Taken together, our data suggest that inhibition of miR-122-5p may mitigate sepsis-triggered myocardial injury through inhibiting inflammation, oxidative stress and apoptosis via targeting GIT1, which provides a possible therapeutic target for sepsis.

• GIT1
• miR-122-5p
• myocardial injury
• sepsis

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Sepsis-induced circulatory and cardiac dysfunction is associated with high mortality rates. Mitophagy, a specific form of autophagy, is excessively activated in lipopolysaccharide-induced myocardial injury. The present study investigated whether aldehyde dehydrogenase 2 (ALDH2) regulates mitophagy in sepsis-induced myocardial dysfunction. After lipopolysaccharide administration, cardiac dysfunction, inflammatory cell infiltration, biochemical indicators of myocardial cell injury, and cardiomyocyte apoptosis were ameliorated in mice by ALDH2 activation or overexpression. In contrast, cardiac dysfunction and cardiomyocyte apoptosis were exacerbated in mice followed ALDH2 inhibition. Moreover, ALDH2 activation or overexpression regulated mitophagy by suppressing the expression of phosphatase and tensin homolog-induced putative kinase 1 (PINK1)/Parkin, by preventing the accumulation of 4-hydroxy-trans-nonenal. Conversely, ALDH2 inhibition promoted the expression of LC3B by increasing 4-hydroxy-trans-2-nonenal accumulation. Consequently, ALDH2 may protect the heart from lipopolysaccharide-induced injury by suppressing PINK1/Parkin-dependent mitophagy.

• ALDH2
• PINK1/parkin
• lipopolysaccharide
• mitophagy
• myocardium
• oxidative stress

High morbidity and mortality are the most typical characteristics of septic cardiomyopathy. We aimed to reveal the role of miR-22 in septic cardiomyopathy and to explore the underlying mechanisms. miR-22 cardiac-specific knockout (miR-22^cKO) mice and miR-22 cardiac-specific transgenic (miR-22^cOE) mice were subjected to a cecal ligation and puncture (CLP) operation, while a sham operation was used in the control group. The echocardiogram results suggested that miR-22^cKO CLP mice cardiac dysfunction was alleviated. The serum LDH and CK-MB were reduced in the miR-22^cKO CLP mice. As expected, there was reduced apoptosis, increased autophagy and alleviated mitochondrial dysfunction in the miR-22^cKO CLP mice, while it had contrary role in the miR-22^cOE group. Inhibiting miR-22 promoted autophagy by increasing the LC3II/GAPDH ratio and decreasing the p62 level. Additionally, culturing primary cardiomyocytes with lipopolysaccharide (LPS) simulated sepsis-induced cardiomyopathy in vitro. Inhibiting miR-22 promoted autophagic flux confirmed by an increased LC3II/GAPDH ratio and reduced p62 protein level under bafilomycin A1 conditions. Knocking out miR-22 may exert a cardioprotective effect on sepsis by increasing autophagy and decreasing apoptosis via sirt1. Our results revealed that targeting miR-22 may become a new strategy for septic cardiomyopathy treatment.

• apoptosis
• autophagy
• miR-22
• septic cardiomyopathy
• sirt1

• EPAC
• OXPHOS
• PKA
• apoptosis
• cAMP
• mitochondrial biogenesis
• mitochondrial dynamics
• mitophagy
• soluble adenylyl cyclase

• COVID-19
• Cardiac biomarkers
• Heart failure
• Hemodynamics

• COVID-19/epidemiology
• COVID-19/physiopathology
• Comorbidity
• Disease Progression
• Heart Failure/epidemiology
• Heart Failure/physiopathology
• Heart Failure/therapy
• Heart Transplantation
• Heart-Assist Devices
• Hemodynamic Monitoring
• Hemodynamics
• Humans
• Immunosuppression Therapy
• SARS-CoV-2
• Self Care
• Telemedicine
• COVID-19 Drug Treatment

Shikonin (SHI) is an anti-inflammatory agent extracted from natural herbs. It is still unknown whether SHI ameliorates lipopolysaccharide (LPS)-induced cardiac dysfunction. This study aims to explore the protective effects of SHI on LPS-induced myocardial injury and its mechanism. The LPS-induced cardiac dysfunction mouse model was employed to investigate the protective effects of SHI. In the present study, we found that SHI treatment improved the survival rate and cardiac function and remarkably ameliorated the release of inflammatory cytokines and macrophage infiltration in heart tissue of LPS-treated mice. SHI also reduced lactate dehydrogenase (LDH) and cardiac troponin (cTn) release, cell inflammation, and apoptosis in LPS plus adenosine triphosphate (ATP)-treated H9c2 cells. In addition, SHI significantly upregulated silent information regulator 1 (SIRT1) expression and suppressed the upregulation of NOD-like receptor protein 3 (NLRP3), cleaved caspase-1, and caspase-1 activity in heart tissues induced by LPS. Meanwhile, we got the same results in LPS plus ATP-treated H9c2 cells in vitro. Further, SIRT1 inhibitor or siRNA partially blocked SHI-mediated upregulation of SIRT1 expression and downregulation of NLRP3, cleaved caspase-1, and caspase-1 activity in heart tissues induced by LPS. Therefore, we conclude that SHI ameliorates LPS-induced cardiac dysfunction by inhibiting SIRT1-dependent activation of NLRP3 inflammasomes and might be a promising therapeutic strategy for the treatment of LPS-induced cardiac dysfunction.

• NLRP3
• SIRT1
• cardiac dysfunction
• lipopolysaccharide
• shikonin

• B cell
• antibodies
• influenza
• pregnancy
• vaccine

• charity number 1167073 Borne Charity
• Charity No.1169897 CW+ charity
• Charity number: 247808 Westminster Medical School Research Trust

• Animals
• Antineoplastic Agents/adverse effects
• Antineoplastic Agents/therapeutic use
• Arrhythmias, Cardiac/etiology
• Arrhythmias, Cardiac/physiopathology
• Arrhythmias, Cardiac/prevention & control
• Cardiotoxicity/etiology
• Cardiotoxicity/physiopathology
• Cardiotoxicity/prevention & control
• Humans
• Mice
• Neoplasms/drug therapy
• Neoplasms/radiotherapy
• Radiotherapy/adverse effects

• K08 HL116952 NHLBI NIH HHS
• R01 CA233610 NCI NIH HHS

• Cerebral palsy
• Chorioamnionitis
• Congenital dermatitis
• Cytokines
• FIRS
• Fetal cytokine release syndrome
• Fetal cytokine storm
• Fetal hematophagocytic syndrome
• Fetal macrophage activation-like syndrome
• Funisitis
• Interleukin-6
• Intra-amniotic infection
• Intra-amniotic inflammation
• Neonatal encephalopathy
• Neonatal morbidity
• Neonatal sepsis
• Neuroinflammation perinatal morbidity
• Premature birth
• Prematurity
• Preterm labor
• Preterm prelabor rupture of the membranes (preterm PROM)
• Retinopathy of prematurity
• Sensorineuronal hearing loss

• Adult
• Chorioamnionitis/diagnosis
• Chorioamnionitis/immunology
• Chorioamnionitis/physiopathology
• Chorioamnionitis/therapy
• Cytokines/blood
• Female
• Fetus
• Humans
• Infant, Newborn
• Infant, Premature, Diseases/immunology
• Infant, Premature, Diseases/physiopathology
• Interleukin-6/blood
• Obstetric Labor, Premature/physiopathology
• Pregnancy
• Systemic Inflammatory Response Syndrome/diagnosis
• Systemic Inflammatory Response Syndrome/immunology
• Systemic Inflammatory Response Syndrome/physiopathology

• HHSN275201300006C NICHD NIH HHS
• Z01 HD002400 Intramural NIH HHS

It is well known that cardiac dysfunction in sepsis is associated with significantly increased mortality. The pathophysiology of sepsis-induced cardiac dysfunction can be summarized as involving impaired myocardial circulation, direct myocardial depression, and mitochondrial dysfunction. Impaired blood flow to the myocardium is associated with microvascular dysfunction, impaired endothelium, and ventriculo-arterial uncoupling. The mechanisms behind direct myocardial depression consist of downregulation of β-adrenoceptors and several myocardial suppressants (such as cytokine and nitric oxide). Recent research has highlighted that mitochondrial dysfunction, which results in energy depletion, is a major factor in sepsis-induced cardiac dysfunction. Therefore, the authors summarize the pathophysiological process of cardiac dysfunction in sepsis based on the results of recent studies.

• heart
• mitochondria
• pathophysiology
• sepsis

• Immunity
• Inflammation
• Influenza
• Skeletal muscle
• Vaccination

• COVID-19
• cardiovascular
• heart

• ABSI score
• Major burn
• Tp-e interval
• Tp-e/QT ratio
• Ventricular arrhythmia

To investigate the effects of adalimumab pretreatment on the lipopolysaccharide-mediated myocardial injury.

Twenty-eight Wistar rats were randomized into four groups (n=7). Control (C) group animals were injected once a day with intraperitoneal (i.p) 0.9 % saline for two days. In the Adalimumab (Ada) group, adalimumab was injected at a dose of 10 mg/kg/ day (i.p) for two days. Lipopolysaccharide (Lps) group rats were injected with a dose of 5 mg/kg (i.p) lipopolysaccharide. Lipopolysaccharide + Adalimumab (Lps+Ada) group rats received adalimumab before the administration of lipopolysaccharide. The animals were sacrificed 24 h after the last injection and blood samples were obtained for determination of biochemical cardiac injury markers and circulating levels of TNF-α and interleukin-6 (IL-6). Hearts were harvested for histological examination.

Endotoxin exposure resulted in significant increases in serum cardiac injury markers, serum cytokines and histological myocardial injury scores in the Lps group. The levels of circulating cytokines, cardiac injury markers and histological injury scores for myocardial necrosis, perivascular cell infiltration, and inflammation were significantly reduced in Lps+Ada as compared to Lps group (p<0.05).

Adalimumab pretreatment reduces endotoxin-induced myocardial damage in rats. This beneficial effect is thought to be related to the reduction of cytokine release.