Association between inflammatory burden index and coronary slow flow phenomenon in patients with chest pain and no obstructive coronary arteries.

BACKGROUND: The inflammatory burden index (IBI), a novel inflammation-based indicator, to is associated with the presence and prognosis of various diseases. However, few studies have focused on exploring the relationship between IBI and the coronary slow flow phenomenon (CSFP). In this study, we aimed to investigate the predictive value of IBI for CSFP in patients with chest pain and no obstructive coronary artery disease. METHODS: A total of 1126 individuals with chest pain and no obstructive coronary arteries were consecutively included in this study. 71 patients developed CSFP were included in the CSFP group. A 1:2 age- and sex-matched patient with normal blood flow and angiographically proven normal coronary arteries was selected as the control group (n = 142). Plasma C-reactive protein (CRP), neutrophil, and lymphocyte counts were measured to determine the value of IBI. RESULTS: The IBI were significantly higher in the CSFP group than in the controls (21.1 ± 6.5 vs. 14.5 ± 6.4, P < 0.001). The IBI increasedelevated with the increase of the numbers of vessels affected by CSFP. Multivariate logistic regression analysis revealed that IBI and body mass index (BMI) were independent predictors of CSFP. Receiver operating characteristic (ROC) curve analysis showed that when IBI was > 15.74, the sensitivity and specificity were 77.5% and 67.6%, respectively, and the area under the ROC curve (AUC) was 0.799 (95% CI: 0.737-0.862, P<0.001). CONCLUSION: The IBI may be an independent predictor of CSFP in patients with chest pain and normal coronary arteries. The IBI could improve the predictive value of CSFP compared with the indicators alone.

Hypertension and its correlation with autonomic nervous system dysfunction, heart rate variability and chronic inflammation.

OBJECTIVE: This study investigates the relationship between hypertension, dysregulation of the autonomic nervous system, heart rate variability (HRV), and chronic inflammation. METHODS: We analysed a cohort of 50 hypertensive patients treated at the affiliated Hospital of Jianghan University. The average systolic and diastolic blood pressures (BPs) in this group were 155.26 and 95.32 mmHg, respectively. A control group of 50 healthy volunteers, undergoing routine physical examinations at the same hospital, was also analysed. RESULTS: The average systolic BP of the control group was 115.64 ± 10.27 mmHg, and the average diastolic BP was 75.33 ± 8.25 mmHg. In contrast, the experimental group exhibited an average systolic BP of 155.26 ± 20.13 mmHg and an average diastolic BP of 95.32 ± 12.16 mmHg. Both systolic and diastolic BPs were significantly higher in the hypertensive group (p < 0.05). The experimental group also demonstrated reduced HRV and skin conductance response, alongside increased BP variability (BPV), urinary epinephrine levels and prolonged pupillary light reaction time compared to controls (p < 0.05). Notably, Standard Deviation of Normal to Normal Intervals (SDNN) and Root Mean Square of Successive Differences (RMSSD) values were significantly lower in the experimental group (p < 0.05). Furthermore, levels of inflammatory markers such as CRP, TNF-α, IL-6 and IL-1ß were markedly elevated in hypertensive patients (p < 0.05). Negative correlations were observed between systolic and diastolic BP with HRV metrics, while positive correlations were found between BP and BPV as well as urinary adrenaline levels. CONCLUSIONS: The findings indicate that hypertension is closely associated with autonomic nervous system dysfunction, reduced HRV and increased chronic inflammation. A comprehensive approach to hypertension management should integrate these interrelated physiological and pathological mechanisms, with potential therapeutic interventions targeting autonomic function and inflammatory states.

Hypertension represents a global health challenge. Autonomic nervous system dysfunction and chronic inflammation assumes a pivotal role in hypertension pathogenesis. Reduced heart rate variability (HRV) is a surrogate marker of autonomic dysfunction. This study endeavours to elucidate the intricate relationship between hypertension and autonomic dysfunction, HRV and chronic inflammation, thereby advancing our comprehension of hypertension pathophysiology.

Inverted U-Shaped relationship Between Systemic Immune-Inflammation Index and Pulmonary Function: A Large Population-Based Study in US Adults.

Background: Systemic immune-inflammation index (SII) is a novel comprehensive inflammatory marker. Inflammation is associated with impaired lung function. We aimed to explore the possible relationship between SII and lung function to examine the potential of SII in predicting lung function decline. Methods: A cross-sectional survey was conducted using the data of the NHANES from 2007 to 2012. Multiple linear regression models were used to analyze the linear relationship between SII and pulmonary functions. Sensitivity analyses, subgroup analyses, and interaction tests were used to examine the robustness of this relationship across populations. Fitted smooth curves and threshold effect analysis were used to describe the nonlinear relationships. Results: A total of 10,125 patients were included in this study. After adjusting for all covariates, multiple linear regression model analysis showed that high Log2-SII level was significantly associated with decreased FVC(ß, -23.4061; 95% CI, -42.2805- -4.5317), FEV1(ß, -46.7730; 95% CI, -63.3371- -30.2089), FEV1%(ß, -0.7923; 95% CI, -1.1635- -0.4211), FEV1/FVC(ß, -0.6366; 95% CI, -0.8328- -0.4404) and PEF(ß, -121.4468; 95% CI,-164.1939- -78.6998). The negative correlation between Log2-SII and pulmonary function indexes remained stable in trend test and stratified analysis. Inverted U-shaped relationships between Log2-SII and FVC, FEV1, FEV1%, and PEF were observed, while a negative linear correlation existed between FEV1/FVC and Log2-SII. The cutoff values of the nonlinear relationship between Log2-SII and FVC, FEV1, FEV1%, PEF were 8.3736, 8.0688, 8.3745, and 8.5255, respectively. When SII exceeded the critical value, the lung function decreased significantly. Conclusion: This study found a close correlation between SII and pulmonary function indicators. This study investigated the SII threshold when lung functions began to decline in the overall population. SII may become a promising serological indicator for predicting lung function decline. However, prospective studies were needed further to establish the causal relationship between these two factors.

Interleukin-15 and high-intensity exercise: relationship with inflammation, body composition and fitness in cancer survivors.

Pre-clinical murine and in vitro models have demonstrated that exercise suppresses tumour and cancer cell growth. These anti-oncogenic effects of exercise were associated with the exercise-mediated release of myokines such as interleukin (IL)-15. However, no study has quantified the acute IL-15 response in human cancer survivors, and whether physiological adaptations to exercise training (i.e. body composition and cardiorespiratory fitness) influence this response. In the present study breast, prostate and colorectal cancer survivors (n = 14) completed a single bout of high-intensity interval exercise (HIIE) [4×4 min at 85-95% heart rate (HR) peak, 3 min at 50-70% HR peak] before and after 7 months of three times weekly high-intensity interval training (HIIT) on a cycle ergometer. At each time point venous blood was sampled before and immediately after HIIE to assess the acute myokine (IL-15, IL-6, IL-10, IL-1ra) responses. Markers of inflammation, cardiorespiratory fitness and measures of body composition were obtained at baseline and 7 months. An acute bout of HIIE resulted in a significant increase in IL-15 concentrations (pre-intervention: 113%; P = 0.013, post-intervention: 102%; P = 0.005). Post-exercise IL-15 concentrations were associated with all other post-exercise myokine concentrations, lean mass (P = 0.031), visceral adipose tissue (P = 0.039) and absolute V ̇ O 2 ${{\dot{V}}_{{{{\mathrm{O}}}_{\mathrm{2}}}}}$ peak (P = 0.032). There was no significant effect of 7 months of HIIT on pre- or post-HIIE IL-15 concentrations (P > 0.05). This study demonstrates HIIE is a sufficient stimulus to increase circulating IL-15 and other myokines including IL-6, IL-10 and IL-1ra which may be clinically relevant in the anti-oncogenic effect of exercise and repetitive exposure to these effects may contribute to the positive relationship between exercise and cancer recurrence. KEY POINTS: Exercise has been demonstrated to reduce the risk of cancer recurrence. Pre-clinical murine and in vitro models have demonstrated that exercise suppresses tumour and cancer cell growth, mediated by exercise-induced myokines (IL-6 and IL-15). High-intensity interval exercise significantly increased myokines associated with the anti-oncogenic effect of exercise and the magnitude of response was associated with lean mass, but training did not appear to influence this response. Given IL-15 has been implicated in the anti-oncogenic effect of exercise and is being explored as an immunotherapy agent, high-intensity interval exercise may improve outcomes for people living beyond cancer through IL-15-mediated pathways. Interventions that increase lean mass may also enhance this response.

The role of thermography in assessment of wounds. A scoping review.

Assessment of wounds based on visual appearance has poor inter- and intra-rater reliability and it is difficult to differentiate between inflammation and infection. Thermography is a user-friendly quantitative image technique that collects the skin surface temperature pattern of the wound area and immediately visualizes the temperatures as a rainbow coloured diagram. The aim of this scoping review is to map and summarize the existing evidence on how thermography has been used to assess signs of inflammation in humans and animals with surgical or traumatic wounds. The method follows the Joanna Briggs Institute methodology. The databases searched were PubMed, Embase, CINAHL and Cochrane Library. 3798 sources were identified, 2666 were screened on title and abstract, 99 on full text and 19 studies were included for review. We found that the literature is diverse and originates from a variety of scientific fields. Thermography has been used to detect and predict inflammation and infection in surgical wounds. Grading systems based on the visual appearance correlate to temperature patterns detected with thermography. The general tendency is that thermography detects the temperature in a wound with inflammation to be warmer than a reference area or the same skin area before surgery. In a surgical wound the temperature is elevated 1-2 weeks after surgery due to natural physiological inflammation that induces healing, after 2 weeks the temperature of the wound area slowly and steady decreases to baseline over 1-3 months. If a secondary temperature peak happens during the healing phase of a surgical wound, it is likely that infection has occurred. Modern handheld thermographic cameras might be a promising tool for the clinician to quickly quantify the temperature pattern of surgical wounds to distinguish between inflammation and infection. However, firm evidence supporting infection thermography surveillance of surgical wounds as a technique is missing.

Heart rate variability and autonomic nervous system imbalance: Potential biomarkers and detectable hallmarks of aging and inflammaging.

The most cutting-edge issue in the research on aging is the quest for biomarkers that transcend molecular and cellular domains to encompass organismal-level implications. We recently hypothesized the role of Autonomic Nervous System (ANS) imbalance in this context. Studies on ANS functions during aging highlighted an imbalance towards heightened sympathetic nervous system (SNS) activity, instigating a proinflammatory milieu, and attenuated parasympathetic nervous system (PNS) function, which exerts anti-inflammatory effects via the cholinergic anti-inflammatory pathway (CAP) and suppression of the hypothalamic-pituitary-adrenal (HPA) axis. This scenario strongly suggests that ANS imbalance can fuel inflammaging, now recognized as one of the most relevant risk factors for age-related disease development. Recent recommendations have increasingly highlighted the need for actionable strategies to improve the quality of life for older adults by identifying biomarkers that can be easily measured, even in asymptomatic individuals. We advocate for considering ANS imbalance as a biomarker of aging and inflammaging. Measures of ANS imbalance, such as heart rate variability (HRV), are relatively affordable, non-invasive, and cost-effective, making this hallmark easily diagnosable. HRV gains renewed significance within the aging research landscape, offering a tangible link between pathophysiological perturbations and age-related health outcomes.

Disease Activity, Inflammation Markers, and Quality of Life Are Associated with Muscle Strength in Croatian Rheumatoid Arthritis Patients-A National-Based Study.

Background and Objectives: Rheumatoid arthritis (RA) patients experience sarcopenia and decreased muscle mass and handgrip strength, leading to decreased quality of life and disability. The prevalence of RA varies across regions. This study aimed to evaluate the factors associated with RA in Croatian regional centres and explore correlations between clinical parameters and muscle strength. Materials and Methods: Included in this study were 267 stable RA patients from four Croatian clinical centres. The patients' mean age was 60.4 ± 12.0 years, with 12.7% of them being male. For each study participant, information was gathered on their anthropometric characteristics, clinical and laboratory indicators, quality of life, disease activity, and sociodemographics. Results: The main results showed that in the female RA participants, the significant positive predictors are weight, height, exercise, VAS, and haemoglobin level. The negative predictors are the use of conventional synthetic disease-modifying anti-rheumatic drugs, the use of biological disease-modifying anti-rheumatic drugs, the number of tender joints, the number of swollen joints, the estimated sedimentation rate, the C-reactive protein, the disease activity score, the parameters of the EQ5D, and being prescribed with three or more medications. In the male RA participants, significant predictors of muscle strength are only weight, height, and anxiety/depression difficulties, according to the EQ5D. Conclusions: This study showed correlations between muscle strength and the parameters of disease activity, inflammation parameters, health-related quality of life, therapy, and exercise in the female RA participants in Croatia.

Association between the pan-immune-inflammation value and coronary collateral circulation in chronic total coronary occlusive patients.

BACKGROUND: Inflammation and immunity play important roles in the formation of coronary collateral circulation (CCC). The pan-immune-inflammation value (PIV) is a novel marker for evaluating systemic inflammation and immunity. The study aimed to investigate the association between the PIV and CCC formation in patients with chronic total occlusion (CTO). METHODS: This retrospective study enrolled 1150 patients who were diagnosed with CTO through coronary angiographic (CAG) examinations from January 2013 to December 2021 in China. The Cohen-Rentrop criteria were used to catagorize CCC formation: good CCC formation (Rentrop grade 2-3) and poor CCC formation group (Rentrop grade 0-1). Based on the tertiles of the PIV, all patients were classified into three groups as follows: P1 group, PIV ≤ 237.56; P2 group, 237.56< PIV ≤ 575.18; and P3 group, PIV > 575.18. RESULTS: A significant relationship between the PIV and the formation of CCC was observed in our study. Utilizing multivariate logistic regression and adjusting for confounding factors, the PIV emerged as an independent risk factor for poor CCC formation. Notably, the restricted cubic splines revealed a dose-response relationship between the PIV and risk of poor CCC formation. In terms of predictive accuracy, the area under the ROC curve (AUC) for PIV in anticipating poor CCC formation was 0.618 (95% CI: 0.584-0.651, P < 0.001). Furthermore, the net reclassification index (NRI) and integrated discrimination index (IDI) for PIV, concerning the prediction of poor CCC formation, were found to be 0.272 (95% CI: 0.142-0.352, P < 0.001) and 0.051 (95% CI: 0.037-0.065, P < 0.001), respectively. It's noteworthy that both the NRI and IDI values were higher for PIV compared to other inflammatory biomarkers, suggesting its superiority in predictive capacity. CONCLUSIONS: PIV was associated with the formation of CCC. Notably, PIV exhibited potential as a predictor for poor CCC formation and showcased superior predictive performance compared to other complete blood count-based inflammatory biomarkers.

Effects of Nutritional Status and Foods Consumed on Inflammation and Disease Activity in Patients with Rheumatoid Arthritis.

Background and Objectives: This study investigated the impact of nutritional status and foods consumed on inflammation and disease activity in patients with rheumatoid arthritis (RA). Materials and Methods: We designed a cross-sectional observational study, involving 110 patients diagnosed with RA. The patients included were between 18 and 75 years old, diagnosed with rheumatoid arthritis two years ago or earlier, with stable treatment for the last 8 weeks. Data on anthropometric parameters, body mass composition, nutritional status, individual food consumption records, inflammation, disease activity, quality of life, clinical, and laboratory parameters were collected for each study participant. The evaluation parameters of the patients were the simple disease activity index (SDAI), clinical disease activity index (CDAI), systemic immune-inflammation index (SII) and individual food consumption records. A bioimpedance device and measuring tape were used to take body composition and anthropometric measurements of the patients. Results: According to the body mass index, waist circumference and waist-to-height ratio, in our study, we found that 60% of the patients were obese, 80% were at a very high health risk, and approximately 91% were in need of nutritional treatment. There was a significant negative correlation between the dietary intake of total energy, total fat, omega 3, calcium, zinc, cobalamin and the disease activity (SDAI, CDAI). There was a significant negative correlation between polyunsaturated fatty acids, omega 3, carotene, vitamin E, selenium and the SII. Additionally, there was a positive correlation between omega 6 and the SII, SDAI, CDAI (p < 0.05). Conclusions: The results of this study show that the foods consumed in the nutrition of RA patients may have effects on their inflammation and disease activity.

Inflammation-related abnormal dynamic brain activity correlates with cognitive impairment in first-episode, drug-naïve major depressive disorder.

BACKGROUND: Cognitive impairment is common in major depressive disorder (MDD) and potentially linked to inflammation-induced alterations in brain function. However, the relationship between inflammation, dynamic brain activity, and cognitive impairment in MDD remains unclear. METHODS: Fifty-seven first-episode, drug-naïve MDD patients and sixty healthy controls underwent fMRI scanning. Dynamic amplitude of low-frequency fluctuations (dALFF) and dynamic functional connectivity (dFC) were measured using the sliding window method. Plasma IL - 6 levels and cognitive function were assessed using enzyme-linked immunosorbent assay (ELISA) and the Repeated Battery for Assessment of Neuropsychological Status (RBANS), respectively. RESULTS: MDD patients exhibited decreased dALFF in the bilateral inferior temporal gyrus (ITG), right inferior frontal gyrus, opercular part (IFGoperc), and bilateral middle occipital gyrus (MOG). Regions of dALFF associated with IL-6 included right ITG (r = -0.400/p = 0.003), left ITG (r = -0.381/p = 0.004), right IFGoperc (r = -0.342/p = 0.011), and right MOG (r = -0.327/p = 0.016). Furthermore, IL-6-related abnormal dALFF (including right ITG: r = 0.309/p = 0.023, left ITG: r = 0.276/p = 0.044) was associated with attention impairment. These associations were absent entirely in MDD patients without suicidal ideation. Additionally, IL-6 levels were correlated with dFC of specific brain regions. LIMITATIONS: Small sample size and cross-sectional study design. CONCLUSIONS: Inflammation-related dALFF was associated with attention impairment in MDD patients, with variations observed among MDD subgroups. These findings contribute to the understanding of the intricate relationship between inflammation, dynamic brain activity and cognitive impairments in MDD.

Salience network resting state functional connectivity during airway inflammation in asthma: A feature of mental health resilience?

BACKGROUND: Inflammation is an established contributor to the pathophysiology of depression and the prevalence of depression in those with chronic inflammatory disease is two- to four-fold higher than the general population. Yet little is known about the neurobiological changes that confer depression or resilience to depression, that occur when episodes of heightened inflammation are frequent or span many years. METHODS: We used an innovative combination of longitudinal resting state functional magnetic resonance imaging coupled to segmental bronchial provocation with allergen (SBP-Ag) to assess changes in resting state functional connectivity (rsFC) of the salience network (SN) caused by an acute inflammatory exacerbation in twenty-six adults (15 female) with asthma and varying levels of depressive symptoms. Eosinophils measured in bronchoalveolar lavage fluid and blood provided an index of allergic inflammation and the Beck Depression Inventory provided an index of depressive symptoms. RESULTS: We found that in those with the highest symptoms of depression at baseline, SN rsFC declined most from pre- to post-SBP-Ag in the context of a robust eosinophilic response to challenge, but in those with low depressive symptoms SN rsFC was maintained or increased, even in those with the most pronounced SBP-Ag response. CONCLUSIONS: Thus, the maintenance of SN rsFC during inflammation may be a biomarker of resilience to depression, perhaps via more effective orchestration of large-scale brain network dynamics by the SN. These findings advance our understanding of the functional role of the SN during inflammation and inform treatment recommendations for those with comorbid inflammatory disease and depression.

Insomnia and circadian rhythms dysregulation in people who have attempted suicide: correlations with markers of inflammation and suicidal lethality.

INTRODUCTION: Suicide is a widespread problem, with risk factors still a challenge. The aim was to assess correlations among insomnia, circadian rhythm, and inflammatory markers in individuals who attempted suicide. MATERIALS AND METHODS: Consecutive patients hospitalised following an attempted suicide, were assessed. Psychiatric diagnosis (DSM-5-TR Criteria), lethality of the suicide attempt (Suicide Intent Scale-SIS), and inflammatory parameters NLR (neutrophil-lymphocyte ratio) PLR (platelet-lymphocyte ratio), and SII (systemic inflammation index/neutrophil-to-platelet ratio on lymphocytes), were computed. Depressive and manic symptoms (Beck Depression Inventory-BDI-II, Young Mania Rating Scale- YMRS), circadian rhythms disturbances (Biological Rhythms Interview of Assessment in Neuropsychiatry-BRIAN), insomnia symptoms (Insomnia Severity Index-ISI) were assessed together with socio-demographic, clinical and pharmacological data. RESULTS: The final sample included 52 individuals. Patients who experienced insomnia during the preceding two weeks utilised high lethality methods, reported heightened dysregulation of chronobiological rhythms, heightened severity of depression, and elevated levels of inflammatory markers. High lethality was best predicted by insomnia symptoms (OR = 20.1, CI-95% 4.66-87.25, p = 0.001), by disturbances of circadian rhythms (OR = 6.97, CI-95% 1.82-26.66, p = 0.005), and by NLR indices (OR 4.00, CI-95% 1.14-13.99, p = 0.030). CONCLUSIONS: Sleep disturbances may be a risk factor for suicidal lethality, along with markers of inflammation. It is plausible that insomnia and circadian sleep dysregulation may contribute to inflammation, thereby promoting suicidal risk.

Current perspective on e-cigarette use and respiratory outcomes: mechanisms and messaging.

INTRODUCTION: There has been an increasing amount of research on the consequences of e-cigarette use for respiratory outcomes, which is significant for public health and respiratory medicine. We discuss recent findings and lay out implications for prevention and treatment. AREAS COVERED: Based on literature searches using several databases (PubMed, Web of Science, Google Scholar) for keywords, including synonyms, 'e-cigarettes,' with 'pulmonary function,' 'oxidative stress,' and 'inflammation,' we review studies on acute effects of e-cigarette use for measures of pulmonary function and discuss selected laboratory studies on mechanisms of effect, focusing on processes with known relation to respiratory disease; oxidative stress and inflammation. We discuss available studies that have tested the effectiveness of communication strategies for prevention of e-cigarette use oriented to different audiences, including nonsmoking adolescents and adult smokers. EXPERT OPINION: We conclude that the evidence presents a mixed picture. Evidence is found for adverse consequences of e-cigarette use on measures of lung function and two disease-related biological processes, sometimes but not always less than for cigarette smoking. How to best communicate these results to a complex audience of users, from younger susceptible adolescents to long-term adult smokers interested in quitting, is a question of significant interest and empirically validated communication strategies are greatly needed.

A MULTI-HIT MODEL OF LONG COVID PATHOPHYSIOLOGY: THE INTERACTION BETWEEN IMMUNE TRIGGERS AND NERVOUS SYSTEM SIGNALING.

Early in the pandemic, clinicians recognized an overlap between Long COVID symptoms and dysautonomia, suggesting autonomic nervous system (ANS) dysfunction. Our clinical experience at Johns Hopkins with primary dysautonomia suggested heritability of sympathetic dysfunction, manifesting primarily as hyperhidrosis and as other dysautonomia symptoms. Whole exome sequencing revealed mutations in genes regulating electrical signaling in the nervous system, thus providing a genetic basis for the sympathetic overdrive observed. We hypothesize that dysautonomia in Long COVID requires two molecular hits: a genetic vulnerability to prime the ANS and a SARS-CoV-2 infection, as an immune trigger, to further disrupt ANS function resulting in increased sympathetic activity. Indeed, Long COVID patients show signs of chronic inflammation and autoimmunity. We have translated this two-hit concept to the clinic using ion channel inhibitors to target genetic susceptibility and immunomodulators to treat inflammation. This multi-hit hypothesis shows promise for managing Long COVID and merits further study.

Aerobic exercise effects on systolic blood pressure and endothelial inflammation in obese and non-obese elderly women with isolated systolic hypertension.

OBJECTIVES: This study aimed to investigate the effects of a 16-week aerobic exercise program on systolic blood pressure, intracellular cell adhesion molecule-1, vascular cell adhesion molecule-1, and oxidized low-density lipoprotein of obese and nonobese elderly women with isolated systolic hypertension. METHODS: Elderly women aged 70-85 years were recruited and grouped into the normal isolated systolic hypertension ( n  = 12) and obese isolated systolic hypertension groups ( n  = 13). The participants followed an aerobic exercise program, using a wireless heart rate monitor to maintain an appropriate heart rate reserve based on the American College of Sports Medicine exercise guidelines. The two-way repeated measures analysis of variance tested group × time interaction. Pearson's correlation and simple regression assessed the influence of each variable, which showed significant differences. RESULTS: An interaction effect for systolic blood pressure, intracellular cell adhesion molecule-1, and vascular cell adhesion molecule-1 ( P  < 0.05) and a main time effect for oxidized low-density lipoprotein ( P  < 0.05) were observed. A correlation between the rates of change in systolic blood pressure and vascular cell adhesion molecule-1 ( P  < 0.05) with a 42.8% influence ( P  < 0.001) and in intracellular cell adhesion molecule-1 and vascular cell adhesion molecule-1 ( P  < 0.05) with a 21.6% influence ( P  < 0.05) was observed. CONCLUSIONS: These findings collectively showed that the 16-week aerobic exercise program effectively lowered blood pressure in patients with isolated systolic hypertension, particularly in the normal group compared to the obese group. Thus, regular aerobic exercise for 16 weeks or more enhances vascular health, potentially improving the healthy life expectancy of elderly women.

Cardiorenal Syndrome and Inflammation: A Forgotten Frontier Resolved by Sorbents?

Cardiorenal syndrome (CRS) describes the maladaptive relationship between heart and kidney dysfunction, with different pathways perpetuating the pathophysiology. Inflammation is one of these mechanisms. It contributes to the final nonhemodynamic pathways of organ dysfunction in the heart-kidney cross-talk. It may be a mediator and amplifier of this pathological communication, playing a vital role in both acute and chronic cardiorenal dysfunction. Current therapeutic strategies are not satisfactory in mitigating the inflammatory pathway in CRS. Hemoadsorption overcomes this limitation, and the soluble mediators of inflammation are potentially amenable to removal by hemoadsorption. This perspective article describes the inflammatory mechanisms in CRS and the rationality of using hemoadsorption in this scenario.

Dapagliflozin, inflammation and left ventricular remodelling in patients with type 2 diabetes and left ventricular hypertrophy.

BACKGROUND AND AIMS: Sodium-glucose co-transporter 2 (SGLT2) inhibitors have beneficial effects in heart failure (HF), including reverse remodelling, but the mechanisms by which these benefits are conferred are unclear. Inflammation is implicated in the pathophysiology of heart failure (HF) and there are some pre-clinical data suggesting that SGLT2 inhibitors may reduce inflammation. There is however a lack of clinical data. The aim of our study was to investigate whether improvements in cardiac remodelling caused by dapagliflozin in individuals with type 2 diabetes (T2D) and left ventricular hypertrophy (LVH) were associated with its effects on inflammation. METHODS: We measured C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α), interleukin-1ß (IL-1ß), interleukin 6 (IL-6), and interleukin 10 (IL-10) and neutrophil-to-lymphocyte ratio (NLR) in plasma samples of 60 patients with T2D and left ventricular hypertrophy (LVH) but without symptomatic HF from the DAPA-LVH trial in which participants were randomised dapagliflozin 10 mg daily or placebo for 12 months and underwent cardiac magnetic resonance imaging (CMR) at baseline and end of treatment. The primary analysis was to investigate the effect of dapagliflozin on inflammation and to assess the relationships between changes in inflammatory markers and LV mass and global longitudinal strain (GLS) and whether the effect of dapagliflozin on LV mass and GLS was modulated by baseline levels of inflammation. RESULTS: Following 12 months of treatment dapagliflozin significantly reduced CRP compared to placebo (mean difference of -1.96; 95% CI -3.68 to -0.24, p = 0.026). There were no significant statistical changes in other inflammatory markers. There were modest correlations between improvements in GLS and reduced inflammation (NLR (r = 0.311), IL-1ß (r = 0.246), TNF-α (r = 0.230)) at 12 months. CONCLUSIONS: Dapagliflozin caused a significant reduction in CRP compared to placebo. There were correlations between reductions in inflammatory markers including IL-1ß and improvements in global longitudinal strain (but not reduced LV mass). Reductions in systemic inflammation might play a contributory role in the cardiovascular benefits of dapagliflozin. TRIAL REGISTRATION: Clinicaltrials.gov NCT02956811 (06/11/2016).

Bioelectrical impedance-derived phase angle (PhA) in people living with obesity: Role in sarcopenia and comorbidities.

BACKGROUND AND AIM: Obesity is characterized by alterations in fat and muscle mass. Phase angle (PhA) is considered an index of muscle mass, and is related to comorbidities in SO. This work aimed to assess the relationship between PhA, muscle mass, inflammation, and comorbidities in obesity. METHODS AND RESULTS: We included 198 outpatients with obesity (BMI≥30) divided into tertiles according to PhA distribution (<5°, 5°-6°, >7°). Body composition was analyzed using bioimpedance (Tanita MC-780P Multi-Frequency Segmental Body Composition Analyzer). Quantitative variables were compared using the Kruskal-Wallis test and qualitative variables using the chi-square test. A correspondence analysis was built to show the influence of qualitative variables on subjects in each tertile. Patients in the lowest tertile had the lowest skeletal muscle mass and appendicular skeletal muscle mass index (ASMI); the highest inflammatory index (albumin and derived neutrophil-to-lymphocyte ratio, Alb-dNLR); and the highest percentage of individuals with a history of type 2 diabetes mellitus (T2DM), chronic kidney disease (CKD), and heart failure (HF). The correspondence analysis showed an association between the lowest tertile and presence of HF with preserved ejection fraction (HFpEF) and CKD. On the logistic regression model, ASMI (OR 0.9, 95%CI 0.85-0.95, p = 0.0004), Alb-dNLR (OR 1.04, 95%CI 1.04-16.4, p = 0.04) and HFpEF and T2DM were significantly associated with the lowest PhA. CONCLUSIONS: Identifying high-risk individuals living with obesity is a priority. These results show that lower PhA is related to inflammation, poorer skeletal muscle mass and consequently, their impact on obesity-related comorbidities and clinical outcomes.

Enthesopathies - Mechanical, inflammatory or both?

Entheses have the challenging task of transferring biomechanical forces between tendon and bone, two tissues that differ greatly in composition and mechanical properties. Consequently, entheses are adapted to withstand these forces through continuous repair mechanisms. Locally specialized cells (mechanosensitive tenocytes) are crucial in the repair, physiologically triggering biochemical processes to maintain hemostasis. When repetitive forces cause "material fatigue," or trauma exceeds the entheses' repair capacity, structural changes occur, and patients become symptomatic. Clinical assessment of enthesopathies mainly depends on subjective reports by the patient and lacks specificity, especially in patients with central sensitization syndromes. Ultrasonography has been increasingly used to improve the diagnosis of enthesopathies. In this article, the literature on how biomechanical forces lead to entheseal inflammation, including factors contributing to differentiation into a "clinical enthesitis" state and the value of ultrasound to diagnose enthesopathies will be reviewed, as well as providing clues to overcome the pitfalls of imaging.

Role of inflammation in diabetic macular edema and neovascular age-related macular degeneration.

Diabetic macular edema (DME) and neovascular age-related macular degeneration (nAMD) are multifactorial disorders that affect the macula and cause significant vision loss. Although inflammation and neoangiogenesis are hallmarks of DME and nAMD, respectively, they share some biochemical mediators. While inflammation is a trigger for the processes that lead to the development of DME, in nAMD inflammation seems to be the consequence of retinal pigment epithelium and Bruch membrane alterations. These pathophysiologic differences may be the key issue that justifies the difference in treatment strategies. Vascular endothelial growth factor inhibitors have changed the treatment of both diseases, however, many patients with DME fail to achieve the established therapeutic goals. From a clinical perspective, targeting inflammatory pathways with intravitreal corticosteroids has been proven to be effective in patients with DME. On the contrary, the clinical relevance of addressing inflammation in patients with nAMD has not been proven yet. We explore the role and implication of inflammation in the development of nAMD and DME and its therapeutical relevance.