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Acute myocardial infarction (AMI) has a significant impact on the health-related quality of life (HRQoL) and is influenced by unfavorable socioeconomic factors. We aimed to evaluate the association between adverse socioeconomic factors including low educational level, low occupational qualification and financial hardship with presenting symptoms and HRQoL in patients hospitalized for an AMI. We hypothesized a detectable effect on a spatial level and therefore assessed the HRQoL in 298 patients with AMI using the EQ-5D-5L generic measure for health status. Sociodemographic characteristics, clinical data, medical history, and prevalence of cardiovascular risk factors were obtained. Self-reported HRQoL was determined upon hospital admission and after 12 months. Patients with lower educational attainment were more likely to report dyspnea at hospital admission, had a worse renal function and more frequently hypertension. One year post-AMI the health state of the cohort worsened in terms of the mobility, activity, pain, and anxiety/depression domains but not the self-care domain. Patients with a lower education level or a poor financial situation reported a worse HRQoL and health state at baseline and follow-up (change in EQ VAS baseline—follow-up − 7.7 and − 11.0, respectively, lowest category). In contrast, the health state of patients with a higher education level or better financial situation improved (change in EQ VAS baseline—follow-up + 4.0 and + 2.6, highest category). Our study demonstrates a substantially widening gap in the health state and HRQoL between patients with lower and higher educational attainment within the first year after AMI, already measurable on a spatial level.

Background Type 2 diabetes mellitus (T2DM) represents a significant risk factor for cardiovascular disease, particularly heart failure with preserved ejection fraction (HFpEF). HFpEF predominantly affects elderly individuals and women, and is characterized by dysfunctions associated with metabolic, inflammatory, and oxidative stress pathways. Despite HFpEF being the most prevalent heart failure phenotype in patients with T2DM, its underlying pathophysiological mechanisms remain inadequately elucidated. Objective This study aims to investigate the effects of diabetes mellitus on myocardial inflammation, oxidative stress, and protein quality control (PQC) mechanisms in HFpEF, with particular emphasis on insulin signaling, autophagy, and chaperone-mediated stress responses. Methods We conducted an analysis of left ventricular myocardial tissue from HFpEF patients, both with and without diabetes, employing a range of molecular, biochemical, and functional assays. The passive stiffness of cardiomyocytes (Fpassive) was assessed in demembranated cardiomyocytes before and after implementing treatments aimed at reducing inflammation (IL-6 inhibition), oxidative stress (Mito-TEMPO), and enhancing PQC (HSP27, HSP70). Inflammatory markers (NF-κB, IL-6, TNF-α, ICAM-1, VCAM-1, NLRP3), oxidative stress markers (ROS, GSH/GSSG ratio, lipid peroxidation), and components of signaling pathways (PI3K/AKT/mTOR, AMPK, MAPK, and PKG) were evaluated using western blotting, immunofluorescence, and ELISA techniques. Results Hearts from diabetic HFpEF patients exhibited significantly heightened inflammation, characterized by the upregulation of NF-κB, IL-6, and the NLRP3 inflammasome. This increase in inflammation was accompanied by elevated oxidative stress, diminished nitric oxide (NO) bioavailability, and impaired activation of the NO-sGC-cGMP-PKG signaling pathway. Notably, dysregulation of insulin signaling was observed, as indicated by decreased AKT phosphorylation and impaired autophagy regulation mediated by AMPK and mTOR. Additionally, PQC dysfunction was evidenced by reduced expression levels of HSP27 and HSP70, which correlated with increased cardiomyocyte passive stiffness. Targeted therapeutic interventions effectively reduced Fpassive, with IL-6 inhibition, Mito-TEMPO, and HSP administration leading to improvements in cardiomyocyte mechanical properties. Conclusion The findings of this study elucidate a mechanistic relationship among diabetes, inflammation, oxidative stress, and PQC impairment in the context of HFpEF. Therapeutic strategies that target these dysregulated pathways, including IL-6 inhibition, mitochondrial antioxidants, and chaperone-mediated protection, may enhance myocardial function in HFpEF patients with T2DM. Addressing these molecular dysfunctions could facilitate the development of novel interventions specifically tailored to the diabetic HFpEF population. Graphical abstract

Acute lung injury is a life threatening condition often requiring mechanical ventilation. Lung-protective ventilation with tidal volumes of 6 mL/kg predicted body weight (PBW, calculated on the basis of a patient's sex and height), is part of current recommended ventilation strategy. Hence, an exact height is necessary to provide optimal mechanical ventilation. However, it is a common practice to visually estimate the body height of mechanically ventilated patients and use these estimates as a reference size for ventilator settings. We aimed to determine if the common practice of estimating visual height to define tidal volume reduces the possibility of receiving lung-protective ventilation. In this prospective observational study, 28 mechanically ventilated patients had their heights visually estimated by 20 nurses and 20 physicians. All medical professionals calculated the PBW and a corresponding tidal volume with 6 ml/kg/PBW on the basis of their visual estimation. The patients' true heights were measured and the true PBW with a corresponding tidal volume was calculated. Finally, estimates and measurements were compared. 1033 estimations were undertaken by 153 medical professionals. The majority of the estimates were imprecise and resulting data comprised taller body heights, higher PBW and higher tidal volumes (all p≤0.01). When estimates of patients´ heights are used as a reference for tidal-volume definition, patients are exposed to mean tidal volumes of 6.5 ± 0.4 ml/kg/PBW. 526 estimation-based tidal volumes (51.1%) did not provide lung-protective ventilation. Shorter subjects (<175cm) were a specific risk group with an increased risk of not receiving lung protective ventilation (OR 6.6; 95%CI 1.2-35.4; p = 0.02), while taller subjects had a smaller risk of being exposed to inadequately high tidal volumes (OR 0.15; 95%CI 0.02-0.8; p = 0.02). Furthermore, we found an increased risk of overestimating if the assessor was a female (OR 1.74; 95%CI 1.14-2.65; p = 0.01). The common practice of visually estimating body height and using these estimates for ventilator settings is imprecise and potentially harmful because it reduces the chance of receiving lung-protective ventilation. Avoiding this practice increases the patient safety. Instead, height should be measured as a standard procedure.

Background The triglyceride-glucose (TyG) index and its obesity-related derivatives have emerged as surrogate markers of insulin resistance associated with cardiovascular outcomes. However, whether these indicators influence atrial fibrillation (AF) risk through cardiac structural and functional remodeling remains unclear. Methods This is a post-hoc analysis of a prospective cohort study of 32,500 UK Biobank participants free of AF who underwent baseline cardiac magnetic resonance (CMR) imaging. The TyG index and its obesity-related derivatives (TyG-body mass index (BMI), TyG-waist circumference (WC), and TyG-waist-to-height ratio (WHtR)) were calculated at baseline. Multivariable Cox regression models were used to assess associations with incident AF, and mediation analyses quantified the contribution of CMR-derived cardiac parameters to these associations. Results Over a median follow-up of 13.61 years, 1,288 incident AF cases occurred. The TyG index alone showed no independent association with AF risk. In contrast, all TyG obesity-related derivatives were significantly associated with incident AF, with TyG-WC demonstrating the strongest association (HR = 1.245, 95% CI 1.169–1.325), followed by TyG-BMI (HR = 1.223, 95% CI 1.158–1.293) and TyG-WHtR (HR = 1.190, 95% CI 1.122–1.262). Mediation analyses identified left atrial maximum volume (LAVmax) as the predominant mediator, accounting for 70.63%, 47.83%, and 40.79% of the associations for TyG-BMI, TyG-WHtR, and TyG-WC, respectively. Conclusions TyG obesity-related derivatives, particularly TyG-WC, were independently associated with incident AF. Cardiac structural remodeling, especially LA enlargement, appeared to be a key mediating pathway. These findings support the importance of early metabolic intervention to prevent adverse atrial remodeling and reduce AF susceptibility. Graphical Abstract

Background Patients diagnosed with both aortic stenosis (AS) and diabetes mellitus (DM) encounter a distinctive set of challenges due to the interplay between these two conditions. This study aimed to investigate the effects of DM on the left ventricle in AS patients, specifically focusing on the inflammatory response, oxidative stress, and their implications for cardiomyocyte function, titin phosphorylation, and the nitric oxide (NO)-soluble guanylyl cyclase (sGC)-cyclic guanosine monophosphate (cGMP)-protein kinase G (PKG) signaling pathway. Methods and results Left ventricular myocardial biopsies (in total: n  = 28) were obtained from patients with diabetic AS ( n  = 11) and compared with those from non-diabetic AS patients ( n  = 17). Enzyme-linked immunosorbent assay (ELISA) demonstrated significantly elevated levels of pro-inflammatory mediators, including high mobility group box protein 1 (HMGB1) and calprotectin, as well as receptors associated with the inflammatory response, such as Toll-like receptor 2 (TLR2), 4 (TLR4), and receptor for advanced glycation endproducts (RAGE). These were correlated with an enhanced NOD-like receptor protein 3 (NLRP3) inflammasome and the release of interleukins (IL) 1, 6, and 18 in diabetic AS patients compared to their non-diabetic counterparts. Additionally, in the diabetic AS cohort, there was an increase in oxidative stress markers (hydrogen peroxide (H 2 O 2 ), 3-nitrotyrosine, lipid peroxidation (LPO), oxidative glutathione (GSSG)/reduced glutathione (GSH) ratio) within the myocardium and mitochondria, accompanied by impaired NO-sGC-cGMP-PKG signaling, decreased titin phosphorylation, and increased passive stiffness (F passive ) of cardiomyocytes relative to non-diabetic AS patients. In vitro anti-inflammatory treatment with an IL-6 inhibitor and antioxidant treatment with GSH effectively normalized the elevated F passive observed in AS patients with DM to levels comparable to the non-diabetic group. Furthermore, treatment with PKG and the sodium-glucose cotransporter 2 (SGLT2) inhibitor empagliflozin also resulted in a reduction of F passive in cardiomyocytes from diabetic AS patients, although not to the levels observed in non-diabetic AS patients. Conclusion DM exacerbates inflammation and oxidative stress in AS patients, leading to impaired NO-sGC-cGMP-PKG signaling and increased cardiomyocyte F passive . These conditions are reminiscent of the pathophysiology of heart failure with preserved ejection fraction (HFpEF). These alterations can be ameliorated through anti-inflammatory and antioxidant therapies, indicating potential therapeutic strategies for diabetic patients suffering from AS. Graphical abstract

Microbiome has been linked to the pathogenesis of coronary artery disease (CAD) but data providing direct evidence for an association of short-chain fatty acids (SCFA) with CAD are lacking. This study aimed to evaluate the role of propionate, the most important SCFA in patients with CAD. We performed a cross-sectional study enrolling patients admitted for invasive coronary angiography in two university hospitals in Germany. Patients with known or suspected CAD and risk factors for cardiovascular disease were prospectively recruited. Blood sampling was performed after overnight fasting and before invasive procedures. Measurement of propionate was performed by liquid chromatography. The study included 1,253 patients (median [IQR], 67 [58-76] years; 799 men [64%]). A total of 739 had invasively confirmed CAD with at least one coronary artery stenosis ≥50% and 514 had exclusion of CAD. CAD patients had significant lower levels of propionate (median 5.75 μM, IQR, 4.1-7.6) compared to the non-CAD groups 6.53 μM (4.6-8.6,  < 0.001). Multivariate linear regression analysis revealed an odds ratio of 0.94 (CI 0.90-0.98,  = 0.002) for propionate as predictor of CAD. The odds ratio was further decreased to 0.45 (CI 0.31-0.65,  < 0.001) when comparing patients in the lowest quartile of propionate with those with higher levels of propionate. The study provides large-scale data for the association of propionate to manifest coronary artery disease, independent of other traditional cardiovascular risk factors.

Background Ambient air pollution has been linked to atrial fibrillation (AF), yet the underlying metabolic mechanisms remain poorly understood. Methods We analyzed 227,324 UK Biobank participants without baseline AF. We constructed an air pollution score by aggregating all four pollutants (PM 2.5 , PM 10 , NO 2 , NO x ). Nuclear magnetic resonance metabolomics identified a pollution-related metabolic signature through elastic net regression. Associations between air pollutants, the metabolic signature and AF were analyzed using Cox models. Mediation analysis was employed to examine the role of the metabolic signature in the association between air pollutants and AF. Results During follow-up, 16,235 participants (7.14%) developed AF. We identified 65-metabolite signature significantly associated with air pollution, predominantly comprising lipoprotein lipid concentrations (32.31%), lipoprotein subclasses (15.38%), fatty acids (13.85%), and amino acids (12.31%). Each standard deviation increase in this metabolic signature was associated with 18% higher AF risk (HR = 1.18, 95%CI:1.03–1.35). The metabolic profile mediated 15.45% of the relationship between air pollution and AF, with lipoprotein parameters showing the strongest mediation effects. Conclusion Air pollution-related metabolic signature was independently associated with AF risk and mediated a significant portion of pollution’s arrhythmogenic effects. These findings provide novel insights into biological mechanisms linking environmental exposures to AF. Graphical abstract

IntroductionAcute myocardial infarction (AMI) is a major public health issue in Germany with considerable regional differences in morbidity and mortality. Possible reasons for regional differences include a higher prevalence of cardiovascular risk factors, infrastructural deficits, different levels of healthcare quality or social determinants. We aim to study associations of social determinants and of rural infrastructure with the quality of medical care (eg, time to reperfusion or medication adherence) and on the long-term outcome after myocardial infarction.Methods and analysisWe will employ a prospective cohort study design. Patients who are admitted with AMI will be invited to participate. We aim to recruit a total of 1000 participants over the course of 5 years. Information on outpatient care prior to AMI, acute healthcare of AMI, healthcare-related environmental factors and social determinants will be collected. Baseline data will be assessed in interviews and from the electronic data system of the hospital. Follow-up will be conducted after an observation period of 1 year via patient interviews. The outcomes of interest are cardiac and all-cause mortality, changes in quality of life, changes in health status of heart failure, major adverse cardiovascular events and participation in rehabilitation programmes.Ethics and disseminationEthical approval was obtained from the Ethics Committee of Brandenburg Medical School (reference: E-01-20200923). Research findings will be disseminated and shared in different ways and include presenting at international and national conferences, publishing in peer-reviewed journals and facilitating dissemination workshops within local communities with patients and healthcare professionals.Trials registration numberDRKS00024463.

Abstract Background  Left atrial appendage (LAA) closure with the WATCHMAN device is an alternative to anticoagulation therapy for the prevention of stroke in selected patients with atrial fibrillation (AF). Infrequently, left atrial (LA) device-related thrombus formation occurs and it is poorly understood. Thrombus formation due to incomplete covering of the LAA is even rarer and may occur within the first few months after device implantation. Case summary  Here, we present a case of a 68-year-old male patient with permanent AF, drug- and hepatitis induced liver cirrhosis (CILD Score B), and prior aortic valve replacement. The patient had a history of percutaneous LAA closure using a WATCHMAN device. He developed massive peri-device leak and thrombus arising from the space between the device and appendage cleft 2 years after implantation. Because of the high bleeding risk with a HAS-BLED score of 5 points, surgery was chosen as the therapy of choice instead of long-term anticoagulation. The patient was discharged in good clinical condition and has been scheduled for a yearly follow-up. Discussion  This case emphasizes the importance of choosing appropriately sized LAA occluder devices and planning for regular post-interventional follow-ups to minimize the risk of per-device leaks and thrombi.

Introduction: Evidence on the association of socioeconomic deprivation with occurrence of acute myocardial infarction (AMI) is available from international studies and urban settings in western Germany. This study aimed to assess this association based on small geographical areas in a rural setting in eastern Germany. Methods: This study used routine data of all patients with AMI who were treated in the Hospital Brandenburg in the city of Brandenburg, Germany, between May 2019 and May 2020. Hospitalisation rates of AMI were calculated for postal code regions that were located within the catchment area of the Hospital Brandenburg. Poisson regression was used to compare hospitalisation rates in areas with medium socioeconomic deprivation to areas with high deprivation, controlling for age group, sex and period (before or during COVID-19 pandemic). Publicly available social, infrastructure and healthcare-related features were mapped to characterise the study region. Results: In total, 265 cases of AMI were registered in the study area, which comprised 116,126 inhabitants. The city of Brandenburg was characterised by the highest level of socioeconomic deprivation, while neighbouring areas showed a rural settlement structure and medium levels of deprivation. The number of general practitioners per 10 000 inhabitants did not differ between both areas. The adjusted rate ratio comparing hospitalisations due to AMI in areas with medium socioeconomic deprivation to areas with high socioeconomic deprivation was 0.71 (95%CI 0.56-0.91, p=0.01). Conclusion: This study adds evidence about the association of socioeconomic deprivation and AMI occurrence from a rural area in eastern Germany. Further research about the relationship of socioeconomic deprivation and cardiovascular health is needed from heterogeneous contexts.