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Background The percentage of women

Background From a large observational acute coronary syndrome registry in Côte d'Ivoire, we aimed to assess incidence, clinical presentation, management, and in‐hospital outcomes for type 2 myocardial infarction (T2MI) compared with type 1 MI. Methods and Results We conducted a cross‐sectional monocentric study using data from REACTIV (Registre des Infarctus de Côte d'Ivoire) at the Abidjan Heart Institute. All patients hospitalized with MI between 2018 and 2022 who underwent coronary angiography were included. For each patient, sociodemographic data, cardiovascular risk factors and history, and clinical and paraclinical presentation were collected at admission. In‐hospital outcomes, including major adverse cardiovascular events and mortality, were reported. Among 541 consecutive patients hospitalized with MI, 441 met the definition of type 1 MI or T2MI. T2MI accounted for 14.1% of cases. Patients with T2MI showed a trend toward slightly younger age (54 versus 58 years, P=0.09). Patients with T2MI seemed to have less severe coronary artery disease, with less frequent multivessel disease (P

BackgroundThere is increasing evidence regarding the association between endotoxemia and the pathogenesis of atherosclerosis and myocardial infarction (MI). During the acute phase of MI, endotoxemia might increase inflammation and drive adverse cardiovascular (CV) outcomes. We aimed to explore the risk factors and prognostic value of endotoxemia in patients admitted for acute MI.MethodsPatients admitted to the coronary care unit of Dijon University Hospital for type 1 acute MI between 2013 and 2015 were included. Endotoxemia, assessed by plasma lipopolysaccharide (LPS) concentration, was measured by mass spectrometry. Major adverse CV events were recorded in the year following hospital admission.ResultsData from 245 consecutive MI patients were analyzed. LPS concentration at admission markedly increased with age and diabetes. High LPS concentration was correlated with metabolic biomarkers (glycemia, triglyceride, and total cholesterol) but not with CV (troponin Ic peak and N-terminal pro-brain natriuretic peptide) or inflammatory biomarkers (C-reactive protein, IL6, IL8, and TNFα). LPS concentration was not associated with in-hospital or 1-year outcomes.ConclusionsIn patients admitted for MI, higher levels of endotoxins were related to pre-existing conditions rather than acute clinical severity. Therefore, endotoxins measured on the day of MI could reflect metabolic chronic endotoxemia rather than MI-related acute gut translocation.

A 66-year-old man with a history of catheter ablation for atrial fibrillation presented with purulent cardiac tamponade, revealing an atrio-oesophageal fistula. He underwent successful endoscopic management. A few days later, the patient fell into a sudden coma due to multiple cerebral air embolisms, resulting from a fistula between the esophagus and the right superior pulmonary vein.

Summary: Background: Smoking cigarettes produces carbon monoxide (CO), which can reduce the oxygen-carrying capacity of the blood. We aimed to determine whether elevated expiratory CO levels would be associated with a worse prognosis in smokers presenting with acute cardiac events. Methods: From 7 to 22 April 2021, expiratory CO levels were measured in a prospective registry including all consecutive patients admitted for acute cardiac event in 39 centres throughout France. The primary outcome was 1-year all-cause death. Initial in-hospital major adverse cardiac events (MAE; death, resuscitated cardiac arrest and cardiogenic shock) were also analysed. The study was registered at ClinicalTrials.gov (NCT05063097). Findings: Among 1379 patients (63 ± 15 years, 70% men), 368 (27%) were active smokers. Expiratory CO levels were significantly raised in active smokers compared to non-smokers. A CO level >11 parts per million (ppm) found in 94 (25.5%) smokers was associated with a significant increase in death (14.9% for CO > 11 ppm vs. 2.9% for CO ≤ 11 ppm; p 11 ppm was associated with a significant increase in MAE in smokers during initial hospitalisation after adjustment for comorbidities (odds ratio [OR] 15.75, 95% CI [5.56–44.60]) or parameters of in-hospital severity (OR 10.67, 95% CI [4.06–28.04]). In the overall population, CO > 11 ppm but not smoking was associated with an increased rate of all-cause death (HR 4.03, 95% CI [2.33–6.98] and 1.66 [0.96–2.85] respectively). Interpretation: Elevated CO level is independently associated with a 6-fold increase in 1-year death and 10-fold in-hospital MAE in smokers hospitalized for acute cardiac events. Funding: Grant from Fondation Coeur & Recherche.

Background and aims: Heterozygous familial hypercholesterolemia (HeFH) is increasingly better diagnosed and treatments can improve the cardiovascular prognosis. We evaluated the long-term cardiovascular risk of HeFH using the French REgistry of Familial hypERCHOLesterolemia (REFERCHOL). Methods: We studied HeFH patients diagnosed genetically and clinically by the Dutch Lipid Clinic Network (DLCN) criteria in all lipid clinics across the country and their 5-year risk of cardiovascular events (all fatal and non-fatal acute coronary, cerebral and peripheral arterial disease events, aortic valve replacement surgery) using the French national health data system. Results: The database comprised 3202 individuals, 2010 (62.8%) with genetically verified HeFH and 1192 (37.2%) a DLCN score ≥6. Of these individuals, 2485 (77.6%) were in primary prevention and 717 (22.4%) in secondary prevention. The incidence of cardiovascular events was 24.58 per 1000 person-years for the overall sample, 19.15 in primary prevention and 43.40 in secondary prevention. The incidence of myocardial infarction, cerebral infarction and death was 16.32 per 1000 person-years for the overall sample, 12.93 in primary prevention and 28.08 in secondary prevention. The incidence of aortic valve replacement was 1.78 per 1000 person-years. In the overall sample, at inclusion, 41% were not treated for LDL cholesterol, 48% of these in primary prevention and 20% in secondary prevention and high-dose statins were used by only 24% of individuals, 15% of these in primary prevention and 45% in secondary prevention. Conclusions: The incidence of cardiovascular events in HeFH is high and lipid-lowering treatment is far from optimal. The cardiovascular risk of HeFH is underestimated and patients are inadequately treated.

Introduction The ongoing ageing population is associated with an increase in the number of patients suffering a stroke, transient ischaemic attack (TIA) or myocardial infarction (MI). In these patients, implementing secondary prevention is a critical challenge and new strategies need to be developed to close the gap between clinical practice and evidence-based recommendations. We describe the protocol of a randomised clinical trial that aims to evaluate the efficiency and effectiveness of an intensive multidisciplinary follow-up of patients compared with standard care.Methods and analysis The DiVa study is a randomised, prospective, controlled, multicentre trial including patients >18 years old with a first or recurrent stroke (ischaemic or haemorrhagic) or TIA, or a type I or II MI, managed in one of the participating hospitals of the study area, with a survival expectancy >12 months. Patients will be randomised with an allocation ratio of 1:1 in two parallel groups: one group assigned to a multidisciplinary, nurse-based and pharmacist-based 2-year follow-up in association with general practitioners, neurologists and cardiologists versus one group with usual follow-up. In each group for each disease (stroke/TIA or MI), 430 patients will be enrolled (total of 1720 patients) over 3 years. The primary outcome will be the incremental cost–utility ratio at 24 months between intensive and standard follow-up in a society perspective. Secondary outcomes will include the incremental cost–utility ratio at 6 and 12 months, the incremental cost-effectiveness ratio at 24 months, reduction at 6, 12 and 24 months of the rates of death, unscheduled rehospitalisation and iatrogenic complications, changes in quality of life, net budgetary impact at 5 years of the intensive follow-up on the national health insurance perspective and analysis of factors having positive or negative effects on the implementation of the project in the study area.Ethics and dissemination Ethical approval was obtained and all patients receive information about the study and give their consent to participate before randomisation. Results of the main trial and each of the secondary analyses will be submitted for publication in a peer-reviewed journal.Trial registration number ClinicalTrials.gov Identifier: NCT04188457. Registered on 6 December 2019.

Abstract There is growing evidence that environmental noise exposure could increase the risk of atherothrombotic events, including acute myocardial infarction (MI). We analysed the burden of environmental noise on atherothrombotic risk in MI patients. From the RICO survey, 879 consecutive MI patients included from 2004 to 2008 and living in an urban unit of > 237,000 inhabitants were analysed. Atherothrombotic risk was calculated using the TRS-2P score. TRS-2P categories were split into low (TRS-2P = 0/1) (40.8%), medium–low (TRS-2P = 2) (25.7%), medium–high (TRS-2P = 3) (21.8%) and high risk (TRS-2P ≥ 4) (11.6%). Noise exposure was associated with atherothrombotic risk, with the LAeq,24 h (OR (95% CI): 1.165 (1.026–1.324)) and Lnight (OR (95CI): 1.157 (1.031–1.298)), for each 10 dB(A) increase. After adjustment, noise exposure remained a predictor of atherothrombotic risk, with LAeq,24 h (OR (95% CI): 1.162 (1.011–1.337)) and with Lnight (OR (95% CI): 1.159 (1.019–1.317)). The relationship with transportation Lnight was significant for men (OR (95% CI): 1.260 (1.078–1.472)) but not for women (OR (95% CI): 0.959 (0.763–1.205)). We found a significant association between residential traffic noise exposure and atherothrombotic risk in men but not in women. These results could have major consequences for secondary prevention.

BackgroundIn acute cardiovascular disease management, the delay between the admission in a hospital emergency department and the assessment of the disease from a Delayed Enhancement cardiac MRI (DE-MRI) scan is one of the barriers for an immediate management of patients with suspected myocardial infarction or myocarditis.ObjectivesThis work targets patients who arrive at the hospital with chest pain and are suspected of having a myocardial infarction or a myocarditis. The main objective is to classify these patients based solely on clinical data in order to provide an early accurate diagnosis.MethodsMachine learning (ML) and ensemble approaches have been used to construct a framework to automatically classify the patients according to their clinical conditions. 10-fold cross-validation is used during the model's training to avoid overfitting. Approaches such as Stratified, Over-sampling, Under-sampling, NearMiss, and SMOTE were tested in order to address the imbalance of the data (i.e. proportion of cases per pathology). The ground truth is provided by a DE-MRI exam (normal exam, myocarditis or myocardial infarction).ResultsThe stacked generalization technique with Over-sampling seems to be the best one providing more than 97% of accuracy corresponding to 11 wrong classifications among 537 cases. Generally speaking, ensemble classifiers such as Stacking provided the best prediction. The five most important features are troponin, age, tobacco, sex and FEVG calculated from echocardiography.ConclusionOur study provides a reliable approach to classify the patients in emergency department between myocarditis, myocardial infarction or other patient condition from only clinical information, considering DE-MRI as ground-truth. Among the different machine learning and ensemble techniques tested, the stacked generalization technique is the best one providing an accuracy of 97.4%. This automatic classification could provide a quick answer before imaging exam such as cardiovascular MRI depending on the patient's condition.

Antioxidants in cancer therapy have been a hot topic in the medical field for 20 years. Antioxidants are able to reduce the risk of cancer formation by neutralizing free radicals. Protons (H+) and molecular hydrogen (H2) interact in the cell and are essential in a wide variety of processes. The antioxidant, anti-inflammatory, and antiapoptotic effects of H2 have been studied in numerous experimental and clinical studies. Experimental data indicate that H2 is an antitumor agent in the treatment of glioblastoma (GBM). In vivo H2 inhalation could suppress the growth of GBM tumors, thereby extending the survival of mice with GBM. The sphere-forming ability of glioma cells was suppressed by hydrogen treatment. In addition, H2 treatment also suppressed the migration, invasion, and colony-forming ability of glioma cells. Proton therapy and proton beam radiotherapy offer some advantages over other modern conformal photon-based therapies when used in the treatment of central nervous system malignancies.

Abstract Background Although patients with familial heterozygous hypercholesterolemia (FH) have a high risk of early myocardial infarction (MI), the coronary artery disease (CAD) burden in FH patients with acute MI remains to be investigated. Methods The data for all consecutive patients hospitalized in 2012–2019 for an acute MI and who underwent coronary angiography were collected from a multicenter database (RICO database). FH (n = 120) was diagnosed using Dutch Lipid Clinic Network criteria (score ≥ 6). We compared the angiographic features of MI patients with and without FH (score 0–2) (n = 234) after matching for age, sex, and diabetes (1:2). Results Although LDL-cholesterol was high (208 [174–239] mg/dl), less than half of FH patients had chronic statin treatment. When compared with non-FH patients, FH increased the extent of CAD (as assessed by SYNTAX score; P = 0.005), and was associated with more frequent multivessel disease (P = 0.004), multiple complex lesions (P = 0.022) and significant stenosis location on left circumflex and right coronary arteries. Moreover, FH patients had more multiple lesions, with an increased rate of bifurcation lesions or calcifications (P = 0.021 and P = 0.036, respectively). In multivariate analysis, LDL-cholesterol levels (OR 1.948; 95% CI 1.090–3.480, P = 0.024) remained an independent estimator of anatomical complexity of coronary lesions, in addition to age (OR 1.035; 95% CI 1.014–1.057, P = 0.001). Conclusions FH patients with acute MI had more severe CAD, characterized by complex anatomical features that are mainly dependent on the LDL-cholesterol burden. Our findings reinforce the need for more aggressive preventive strategies in these high-risk patients, and for intensive lipid-lowering therapy as secondary prevention.

Aim: The SAMe-TT2R2 score helps identify patients with atrial fibrillation (AF) likely to have poor anticoagulation control during anticoagulation with vitamin K antagonists (VKA) and those with scores >2 might be better managed with a target-specific oral anticoagulant (NOAC). We hypothesized that in clinical practice, VKAs may be prescribed less frequently to patients with AF and SAMe-TT2R2 scores >2 than to patients with lower scores. Methods and results: We analyzed the Phase III dataset of the Global Registry on Long-Term Oral Antithrombotic Treatment in Patients with Atrial Fibrillation (GLORIA-AF), a large, global, prospective global registry of patients with newly diagnosed AF and ≥1 stroke risk factor. We compared baseline clinical characteristics and antithrombotic prescriptions to determine the probability of the VKA prescription among anticoagulated patients with the baseline SAMe-TT2R2 score >2 and ≤ 2. Among 17,465 anticoagulated patients with AF, 4,828 (27.6%) patients were prescribed VKA and 12,637 (72.4%) patients an NOAC: 11,884 (68.0%) patients had SAMe-TT2R2 scores 0-2 and 5,581 (32.0%) patients had scores >2. The proportion of patients prescribed VKA was 28.0% among patients with SAMe-TT2R2 scores >2 and 27.5% in those with scores ≤2. Conclusions: The lack of a clear association between the SAMe-TT2R2 score and anticoagulant selection may be attributed to the relative efficacy and safety profiles between NOACs and VKAs as well as to the absence of trial evidence that an SAMe-TT2R2-guided strategy for the selection of the type of anticoagulation in NVAF patients has an impact on clinical outcomes of efficacy and safety. The latter hypothesis is currently being tested in a randomized controlled trial. Clinical trial registration: URL: https://www.clinicaltrials.gov//Unique identifier: NCT01937377, NCT01468701, and NCT01671007.

Abstract Pharmacovigilance reports of cerebral and cardiovascular events in those who use decongestants have triggered alerts related to their use. We aimed to assess the risk of stroke and myocardial infarction (MI) associated with the use of decongestants. We conducted a nested case-crossover study of patients with incident stroke and MI identified in France between 2013 and 2016 in two systematic disease registries. Decongestant use in the three weeks preceding the event was assessed using a structured telephone interview. Conditional logistic multivariable models were used to estimate the odds of incident MI and stroke, also accounting for transient risk factors and comparing week 1 (index at-risk time window, immediately preceding the event) to week 3 (reference). Time-invariant risk factors were controlled by design. In total, 1394 patients with MI and 1403 patients with stroke, mainly 70 years old or younger, were interviewed, including 3.2% who used decongestants during the three weeks prior to the event (1.0% definite exposure in the index at-risk time window, 1.1% in the referent time window; adjusted odds ratio (aOR), 0.78; 95%CI, 0.43–1.42). Secondary analysis yielded similar results for individual events (MI/stroke). We observed no increased risk of MI or stroke for patients 70 years of age and younger without previous MI or stroke who used decongestants.

Abstract Aims Cardiovascular co‐morbidities like congestive heart failure (CHF) alter the course of coronavirus disease 2019. Factors associated with the outbreak and lockdown can exacerbate CHF. Methods and results We analysed the answers of 124 randomly selected CHF outpatients (mean age 71.0 ± 14.0 years, 60.5% male) interviewed by phone during the sixth and seventh weeks of the lockdown. Most patients were treated for New York Heart Association class II (38.7%) and reduced ejection fraction HF (70.2%). Psychological distress (Kessler 6 score ≥ 5) was common (18.5%), and 21.8% felt worse than before the lockdown. Few patients (n = 10) adjusted their intake of HF medications, always on medical prescription. Decreased physical activity was common (41.9%) and more frequent in women (P = 0.025) and urban dwellers (P = 0.009). Almost half of respondents (46.0%) declared increased screen time, but only few declared more alcohol intake (4.0%). Weight gain was common (27.4%), and 44.4% of current smokers increased tobacco consumption. Adherence to recommended salt or fluid intake restrictions was reduced in 14.5%. Increase in HF symptoms was commonly reported (21.8%) and tended to be higher in women than in men (P = 0.074). Of the 23 patients who had a phone teleconsultation during the pandemic, 16 had initially planned an in‐person consultation that they switched for teleconsultation. Conclusions During the lockdown, psychological distress and decreased well‐being were common in CHF outpatients, and there was an increase in unhealthy lifestyle behaviours. These changes may negatively impact short‐term and long‐term prognoses. Medication adherence was maintained, and limitations in access to care were partly counterbalanced by use of telehealth.

Abstract Aims In the older population, acute heart failure is a frequent, life‐threatening complication of COVID‐19 that requires urgent specific care. We aimed to explore the impact of point‐of‐care chest ultrasound (CUS) use in older bedridden inpatients during the COVID‐19 pandemic as a tool to distinguish between cardiogenic pulmonary oedema and isolated viral pneumonia‐related dyspnoea. Methods and results This prospective series included 16 patients aged 75 or older, hospitalized for acute dyspnoea in an acute geriatric unit of a university hospital and testing positive for a SARS‐Cov2 infection. We collected demographic characteristics, medical history, biological screening, clinical symptoms, CUS findings (n = 16) and chest CT‐scan conclusions (n = 14). Mean age was 89 years (77–97). All patients presented asthenia and dyspnoea, 56% complained of coughing and diarrhoea, and 50% had fever. Acute heart failure was clinically suspected in seven patients. At CUS, evidence of heart failure was confirmed in three patients (including one without clinical suspicion); interstitial syndrome was confirmed in 12 patients on CUS vs. 9 patients with CT. Conclusions In older patients with COVID‐19 and acute dyspnoea, the use of point‐of‐care CUS allowed the clinician to quickly rule out heart failure in nearly half of suspected cases while easily identifying virus‐related interstitial syndrome. The use of CUS appears to be suitable for the rapid bedside investigation of dyspnoea in older patients, particularly in the context of the COVID‐19 pandemic.

ObjectivesThis cross-sectional study aims to investigate health-related behaviors including tobacco consumption among patients with cardiovascular diseases (CVD), during the first COVID-19-related lockdown.MethodsAfter 5 weeks of COVID-19 lockdown, 220 patients with chronic coronary syndromes (CCS) and 124 with congestive heart failure (CHF) answered a phone questionnaire.ResultsAmong these 344 patients, 43 (12.5%) were current smokers, and none had quit during the lockdown. When compared with non-smokers, smokers were 15 years younger, more often diabetic, more likely to live in an urban than a rural lockdown location, and more often in the CCS cohort (p = 0.011). Smokers described greater psychological impairment, but their rates of decrease in physical activity and of increase in screen time were similar to non-smokers. More than one-third (13/43) increased their tobacco consumption, which was mainly related to stress or boredom, but not driven by media messages on a protective effect of nicotine.ConclusionsDuring the first COVID-19 lockdown, we found a decrease in favorable lifestyle behaviors among patients with CVD. Strikingly, one-third of smokers with CCS or CHF increased their tobacco consumption. Given the major impact of persistent smoking in patients with CVD, this highlights the need for targeted prevention strategies, in particular during such periods.

This study proposes machine learning-based models to automatically evaluate the severity of myocardial infarction (MI) from physiological, clinical, and paraclinical features. Two types of machine learning models are investigated for the MI assessment: the classification models classify the presence of the infarct and the persistent microvascular obstruction (PMO), and the regression models quantify the Percentage of Infarcted Myocardium (PIM) of patients suspected of having an acute MI during their reception in the emergency department. The ground truth labels for these supervised models are derived from the corresponding Delayed Enhancement MRI (DE-MRI) exams and manual annotations of the myocardium and scar tissues. Experiments were conducted on 150 cases and evaluated with cross-validation. Results showed that for the MI (PMO inclusive) and the PMO (infarct exclusive), the best models obtained respectively a mean error of 0.056 and 0.012 for the quantification, and 88.67 and 77.33% for the classification accuracy of the state of the myocardium. The study of the features' importance also revealed that the troponin value had the strongest correlation to the severity of the MI among the 12 selected features. For the proposal's translational perspective, in cardiac emergencies, qualitative and quantitative analysis can be obtained prior to the achievement of MRI by relying only on conventional tests and patient features, thus, providing an objective reference for further treatment by physicians.

Background Data in the literature on acute coronary syndrome in sub‐Saharan Africa are scarce. Methods and Results We conducted a systematic review of the MEDLINE (PubMed) database of observational studies of acute coronary syndrome in sub‐Saharan Africa from January 1, 2010 to June 30, 2020. Acute coronary syndrome was defined according to current definitions. Abstracts and then the full texts of the selected articles were independently screened by 2 blinded investigators. This systematic review was conducted in accordance with Preferred Reporting Items for Systematic Reviews and Meta‐Analyses standards. We identified 784 articles with our research strategy, and 27 were taken into account for the final analysis. Ten studies report a prevalence of acute coronary syndrome among patients admitted for cardiovascular disease ranging from 0.21% to 22.3%. Patients were younger, with a minimum age of 52 years in South Africa and Djibouti. There was a significant male predominance. Hypertension was the main risk factor (50%–55% of cases). Time to admission tended to be long, with the longest times in Tanzania (6.6 days) and Burkina Faso (4.3 days). Very few patients were admitted by medicalized transport, particularly in Côte d'Ivoire (only 34% including 8% by emergency medical service). The clinical presentation is dominated by ST–elevation sudden cardiac arrest. Percutaneous coronary intervention is not widely available but was performed in South Africa, Kenya, Côte d'Ivoire, Sudan, and Mauritania. Fibrinolysis was the most accessible means of revascularization, with streptokinase as the molecule of choice. Hospital mortality was highly variable between 1.2% and 24.5% depending on the study populations and the revascularization procedures performed. Mortality at follow‐up varied from 7.8% to 43.3%. Some studies identified factors predictive of mortality. Conclusions The significant disparities in our results underscore the need for a multicenter registry for acute coronary syndrome in sub‐Saharan Africa in order to develop consensus‐based strategies, propose and evaluate tailored interventions, and identify prognostic factors.

Regulated cell death (RCD) has a significant impact on development, tissue homeostasis, and the occurrence of various diseases. Among different forms of RCD, ferroptosis is considered as a type of reactive oxygen species (ROS)-dependent regulated necrosis. ROS can react with polyunsaturated fatty acids (PUFAs) of the lipid (L) membrane via the formation of a lipid radical L• and induce lipid peroxidation to form L-ROS. Ferroptosis is triggered by an imbalance between lipid hydroperoxide (LOOH) detoxification and iron-dependent L-ROS accumulation. Intracellular iron accumulation and lipid peroxidation are two central biochemical events leading to ferroptosis. Organelles, including mitochondria and lysosomes are involved in the regulation of iron metabolism and redox imbalance in ferroptosis. In this review, we will provide an overview of lipid peroxidation, as well as key components involved in the ferroptotic cascade. The main mechanism that reduces ROS is the redox ability of glutathione (GSH). GSH, a tripeptide that includes glutamic acid, cysteine, and glycine, acts as an antioxidant and is the substrate of glutathione peroxidase 4 (GPX4), which is then converted into oxidized glutathione (GSSG). Increasing the expression of GSH can inhibit ferroptosis. We highlight the role of the xc- GSH-GPX4 pathway as the main pathway to regulate ferroptosis. The system xc-, composed of subunit solute carrier family members (SLC7A11 and SLC3A2), mediates the exchange of cystine and glutamate across the plasma membrane to synthesize GSH. Accumulating evidence indicates that ferroptosis requires the autophagy machinery for its execution. Ferritinophagy is used to describe the removal of the major iron storage protein ferritin by the autophagy machinery. Nuclear receptor coactivator 4 (NCOA4) is a cytosolic autophagy receptor used to bind ferritin for subsequent degradation by ferritinophagy. During ferritinophagy, stored iron released becomes available for biosynthetic pathways. The dysfunctional ferroptotic response is implicated in a variety of pathological conditions. Ferroptosis inducers or inhibitors targeting redox- or iron metabolism-related proteins and signal transduction have been developed. The simultaneous detection of intracellular and extracellular markers may help diagnose and treat diseases related to ferroptotic damage.

The COVID-19 pandemic modified the management of myocardial infarction (MI) and stroke. We aimed to evaluate the effect of the COVID-19 pandemic on the volume and spatial distribution of hospitalizations for MI and stroke, before, during and after the first nationwide lockdown in France in 2020, compared with 2019. Hospitalization data were extracted from the French National Discharge database. Patient’s characteristics were compared according to COVID-19 status. Changes in hospitalization rates over time were measured using interrupted time series analysis. Possible spatial patterns of over or under-hospitalization rates were investigated using Moran’s indices. We observed a rapid and significant drop in hospitalizations just before the beginning of the lockdown with a nadir at 36.5% for MI and 31.2% for stroke. Hospitalization volumes returned to those seen in 2019 four weeks after the end of the lockdown, except for MI, which rebounded excessively. Older age, male sex, elevated rate of hypertension, diabetes, obesity and mortality characterized COVID-19 patients. There was no evidence of a change in the spatial pattern of over- or under-hospitalization clusters over the three periods. After a steep drop, only MI showed a significant rebound after the first lockdown with no change in the spatial distribution of hospitalizations.

Abstract Iodinated contrast agent (ICA)-induced acute kidney injury (AKI) following acute coronary syndrome (ACS) is a frequent complication, which may lead to chronic kidney disease and increased mortality. Optical coherence tomography angiography (OCT-A) of the retina is new tool delivering a rapid and noninvasive assessment of systemic microvascularization, which is potentially involved in the occurrence of ICA-induced AKI. Between October 2016 and March 2017, 452 ACS patients were admitted to our cardiac intensive care unit. OCT-A was performed within 48 h after the ICA injection. Patients with a history of retinal disease were excluded. The patients included were divided into two groups depending on whether or not AKI occurred after injection of ICA, according to KDIGO criteria. Of the 216 patients included, 21 (10%) presented AKI. AKI was significantly associated with age, Mehran score, GRACE score, and NT-proBNP. AKI patients had significantly lower retinal vascular density (RVD)) and had more frequent low RVD (81% vs 45%, P = 0.002). Adding low RVD to the Mehran score and the NT-proBNP, or to the GRACE score and the NT-proBNP, significantly improved their predictive values, suggesting that systemic microvascular involvement remains incompletely addressed by either standard risk scores or factors known to be associated with ICA-induced AKI.

Calprotectin (CLP) belonging to the S-100 protein family is a heterodimeric complex (S100A8/S100A9) formed by two binding proteins. Upon cell activation, CLP stored in neutrophils is released extracellularly in response to inflammatory stimuli and acts as damage-associated molecular patterns (DAMPs). S100A8 and S100A9 possess both anti-inflammatory and anti-bacterial properties. The complex is a ligand of the toll-like receptor 4 (TLR4) and receptor for advanced glycation end (RAGE). At sites of infection and inflammation, CLP is a target for oxidation due to its co-localization with neutrophil-derived oxidants. In the heart, oxidative stress (OS) responses and S100 proteins are closely related and intimately linked through pathophysiological processes. Our review summarizes the roles of S100A8, S100A9 and CLP in the inflammation in relationship with vascular OS, and we examine the importance of CLP for the mechanisms driving in the protection of myocardium. Recent evidence interpreting CLP as a critical modulator during the inflammatory response has identified this alarmin as an interesting drug target.

Objective: To describe the spatial distribution of acute myocardial infarction (AMI) mortality in France in association with the socio-economic characteristics of the patient’s place of residence. Methods: In this population-based study, we included patients hospitalized for AMI identified according to ICD-10 codes, using data from the national health insurance database from January 1, 2013 to December 31, 2014. In- and out-of-hospital deaths were identified over a period of 1 year following the first hospital stay for AMI.An exploratory analysis was performed to classify area profiles. The spatial analysis of AMI mortality was performed using a principal component analysis followed by an ascending hierarchical classification taking into account socio-economic data, access-time by road to coronary angiography, standardized in-hospital prevalence, and 1 year mortality. Results: Over the 2 years, 115,418 patients were hospitalized with a diagnosis of AMI. Patients were a mean of 68 ​± ​15 years and most were men (68.5%). The overall mortality rate was 12.2% after 1 year. More than half of patients (65.5%) underwent an early revascularization procedure. The map of standardized 1 year mortality showed a geographic area of high mortality extending diagonally from north-east to south-west France. We identified 6 different area profiles with standardized mortality varying from 15.9 to 54.4 per 100,000 inhabitants. The spatial distribution of higher mortality was associated with lower socioeconomic levels. These findings were not associated with a lower access to coronary angiography. Conclusion: There are considerable geographical differences in the prevalence of AMI and 1 year mortality. The spatial distribution of lower healthcare indicators follows the distribution of social inequalities. This study highlights the importance of focusing national policies on universally accessible prevention programs such as the promotion cardiac rehabilitation and healthy lifestyles.

Introduction: Cerebral microbleeds (CMB) are associated with intracerebral haemorrhage. Therefore they may represent a concern if anticoagulant and/or antiplatelet therapy is needed. The aim of this study was to determine the prevalence of CMB in patients with acute myocardial infarction (AMI), and to follow their progression at 3 months under dual antiplatelet therapy (DAPT). Methods: This prospective study included patients aged over 60 hospitalized in intensive cardiac care unit in our city for AMI. These patients underwent a first brain Magnetic resonance imaging (MRI) within 72 h of admission, that was repeated 3 months. Results: 108 patients were included between November 2016 and December 2018. The prevalence of CMB was 21.3%, with a female predominance of 65.2% vs 32.1% (p = 0.004). Diabetes is significantly associated with the presence of CMB, 45.5% vs 21.2% (p = 0.021). Patients with at least one acute CMB had higher haemorrhagic risk as evaluated with CRUSADE score (40.5 ± 13.6 vs 31.2 ± 14.8 (p = 0.004).Multivariate analysis showed that only female sex was associated with the presence of a CMB on the initial MRI. On repeated MRI, an increase in CMB was observed in 6% of patients.Our results suggest that discharge treatment with anticoagulant in combination with antiplatelet therapy may be an independent predictor of early progression of CMB. Conclusion: Our study confirms the high prevalence of CMB in patients over 60 years with AMI. The association of anticoagulant with DAPT, 3 months after stenting, may be an independent factor of CMB progression.

Background Optimal blood pressure in elderly patients after acute myocardial infarction is still a matter of debate. In a prospective observational study, we aimed to identify optimal systolic blood pressure during the 48 first hours after admission for acute myocardial infarction and its prognostic value for cardiovascular mortality. Methods and Results From the Observatoire des Infarctus de Côte d'Or survey, all consecutive patients aged >75 years admitted for an acute myocardial infarction in a coronary care unit from 2012 to 2015 and discharged alive were included (n=814). Exclusion criteria were in‐hospital death, cardiogenic shock, and end‐stage renal disease. Average systolic blood pressure (aSBP) values over the first 48 hours after admission were recorded, and the population was dichotomized into 2 groups: low aSBP group (

Background: Our purpose was to describe the care pathway of patients hospitalized for acute heart failure (AHF) and investigate whether a management involving a cardiology department had an impact on in-hospital mortality. Methods: Between June 2014 and October 2018, we included patients hospitalized for AHF in 24 French hospitals. Characteristics of the episode, patient’s care pathway and outcomes were recorded on a specific assessment tool. The primary outcome was the association between patient care pathway and in-hospital mortality. The independent association between admission to a cardiology ward and in-hospital mortality was assessed through a multivariate regression model and propensity score matching. Results: A total of 3677 patients, mean age of 78, were included. The in-hospital mortality rate was 8% (n = 287) and was associated on multivariate regression with advanced age, presence of sepsis, of cardiogenic shock, high New York Heart Association (NYHA) score and increased plasma creatinine level on admission. High blood pressure and admission to a cardiology department appeared as protective factors. After propensity score matching, hospitalization in a cardiology department remained a protective factor of in-hospital mortality (OR = 0.61 [0.44–0.84], p = 0.002). Conclusion: A hospital course of care involving a cardiology department was associated with an increase in hospital survival in AHF patients. These finding may highlight the importance of collaboration between cardiologists and other in-hospitals specialties, such as emergency physicians, in order to find the best in-hospital pathway for patients with AHF.Clinical Trial NCT03903198. Keywords: Acute heart failure, Acute cardiac care, Outcome

Growth and differentiation factor 15 (GDF15) belongs to the transforming growth factor-β (TGF-β) superfamily of proteins. Glial-derived neurotrophic factor (GDNF) family receptor α-like (GFRAL) is an endogenous receptor for GDF15 detected selectively in the brain. GDF15 is not normally expressed in the tissue but is prominently induced by “injury”. Serum levels of GDF15 are also increased by aging and in response to cellular stress and mitochondrial dysfunction. It acts as an inflammatory marker and plays a role in the pathogenesis of cardiovascular diseases, metabolic disorders, and neurodegenerative processes. Identified as a new heart-derived endocrine hormone that regulates body growth, GDF15 has a local cardioprotective role, presumably due to its autocrine/paracrine properties: antioxidative, anti-inflammatory, antiapoptotic. GDF15 expression is highly induced in cardiomyocytes after ischemia/reperfusion and in the heart within hours after myocardial infarction (MI). Recent studies show associations between GDF15, inflammation, and cardiac fibrosis during heart failure and MI. However, the reason for this increase in GDF15 production has not been clearly identified. Experimental and clinical studies support the potential use of GDF15 as a novel therapeutic target (1) by modulating metabolic activity and (2) promoting an adaptive angiogenesis and cardiac regenerative process during cardiovascular diseases. In this review, we comment on new aspects of the biology of GDF15 as a cardiac hormone and show that GDF15 may be a predictive biomarker of adverse cardiac events.

Stroke is a serious complication after acute myocardial infarction (AMI) and is associated with an increased risk of death. Though the pathophysiological mechanisms are not exactly known, increased inflammation and platelet reactivity could play an important role in the occurrence of stroke during AMI. We aimed to investigate the relationship between both mean platelet volume (MPV), a parameter of platelet function, and C-reactive protein (CRP) and the occurrence of in-hospital ischemic stroke (IHS) after AMI. Data were obtained from a French regional survey for AMI that included 5976 patients admitted to an intensive care unit (ICU) between 2001 and 2010. Patients were divided into two groups according to the occurrence of IHS. MPV, platelet count (PC), and CRP were routinely measured at admission to the ICU; 99 (1.6%) IHSs were recorded during hospitalization after admission for AMI. In multivariate analysis, IHS was independently associated with a history of stroke (OR: 1.99%, CI: 1.1–3.49, p = 0.01), impaired left ventricular ejection fraction 10 mg/l (OR: 2.19, 95% CI: 1.44–3.33, p < 0.001), and MPV/PC ratio (OR: 1.04, 95% CI: 1.01–1.08, p = 0.023). Compared with the first to fourth quintiles, the last quintile of the MPV/PC ratio was associated with higher rates of IHS on survival curve analysis (p = 0.014). At hospital admission, a high MPV/PC ratio and a high level of CRP might help to identify patients at increased risk of IHS. Moreover, these results provide new insights into the potential role played by increased inflammation and platelet reactivity in the occurrence of stroke after AMI.

The potential use of stem cell-based therapies for the repair and regeneration of various tissues and organs is a major goal in repair medicine. Stem cells are classified by their potential to differentiate into functional cells. Compared with other sources, adipose-derived stem cells (ADSCs) have the advantage of being abundant and easy to obtain. ADSCs are considered to be tools for replacing, repairing, and regenerating dead or damaged cells. The capacity of ADSCs to maintain their properties depends on the balance of complex signals in their microenvironment. Their properties and the associated outcomes are in part regulated by reactive oxygen species, which mediate the oxidation-reduction state of cells as a secondary messenger. ADSC therapy has demonstrated beneficial effects, suggesting that secreted factors may provide protection. There is evidence that ADSCs secrete a number of cytokines, growth factors, and antioxidant factors into their microenvironment, thus regulating intracellular signaling pathways in neighboring cells. In this review, we introduce the roles of ADSCs in the protection of cells by modulating inflammation and immunity, and we develop their potential therapeutic properties.

One crucial parameter to evaluate the state of the heart after myocardial infarction (MI) is the viability of the myocardial segment, i.e., if the segment recovers its functionality upon revascularization. MRI performed several minutes after the injection of a contrast agent (delayed enhancement-MRI or DE-MRI) is a method of choice to evaluate the extent of MI, and by extension, to assess viable tissues after an injury. The Emidec dataset is composed of a series of exams with DE-MR images in short axis orientation covering the left ventricle from normal cases or patients with myocardial infarction, with the contouring of the myocardium and diseased areas (if present) from experts in the domains. Moreover, classical available clinical parameters when the patient is managed by an emergency department are provided for each case. To the best of our knowledge, the Emidec dataset is the first one where annotated DE-MRI are combined with clinical characteristics of the patient, allowing the development of methodologies for exam classification as for exam quantification.

The transfer of metabolites through the mitochondrial membranes is a vital process that is highly controlled and regulated by the inner membrane. A variety of metabolites, nucleotides, and cofactors are transported across the inner mitochondrial membrane (IMM) by a superfamily of membrane transporters which are known as the mitochondrial carrier family (MCF) or the solute carrier family 25 (SLC25 protein family). In humans, the MCF has 53 members encoded by nuclear genes. Members of the SLC25 family of transporters, which is the largest group of solute carriers, are also known as mitochondrial carriers (MCs). Because MCs are nuclear-coded proteins, they must be imported into the IMM. When compared with normal cells, the mitochondria of cancer cells exhibit significantly increased transmembrane potentials and a number of their transporters are altered. SLC25 members were identified as potential biomarkers for various cancers. The objective of this review is to summarize what is currently known about the involvement of mitochondrial SLC25 carriers in associated diseases. This review suggests that the SLC25 family could be used for the development of novel points of attack for targeted cancer therapy.

Human skin is composed of three layers: the epidermis, the dermis, and the hypodermis. The epidermis has four major cell layers made up of keratinocytes in varying stages of progressive differentiation. Skin aging is a multi-factorial process that affects every phase of its biology and function. The expression profiles of inflammation-related genes analyzed in resident immune cells demonstrated that these cells have a strong ability to regenerate adult skin stem cells and to produce endogenous substances such as growth differentiation factor 11 (GDF11). GDF11 appears to be the key to progenitor proliferation and/or differentiation. The preservation of youthful phenotypes has been tied to the presence of GDF11 in different human tissues, and, in the skin, this factor inhibits inflammatory responses. The protective role of GDF11 depends on a multi-factorial process implicating various types of skin cells such as keratinocytes, fibroblasts and inflammatory cells. GDF11 should be further studied for the purpose of developing novel therapies for the treatment of skin diseases.

To better understand the role of myeloperoxidases (MPO) in microvascular obstruction (MO) phenomenon and infarct size (IS) using cardiac magnetic resonance (CMR) data in patients with acute myocardial infarction (AMI).40 consecutive patients classified according to the median level of MPO in the culprit artery. A CMR study was performed during the week following AMI and at 6 months, with late gadolinium enhancement sequences.Persistent MO was observed in the same proportion (50 vs. 65%, p = 0.728) between the low vs. high MPO group levels. However, the extent of the microvascular obstruction was significantly greater in the high-MPO group (6 (0-9) vs.16.5 (0-31), p = 0.027), together with a greater infarct size, and a trend towards a lower left ventricular ejection fraction (LVEF) (p = 0.054) at one week. CMR data at 6 months showed that reverse systolic remodeling was two fold more present in the low-MPO group (p = 0.058). Interestingly, the extent of MO (8.5 (6.5-31) vs. 4.1 (3-11.55), p = 0.042) and IS remained significantly greater (24.5 (9.75-35) vs. 7.5 (2.5-18.75), p = 0.022) in the high-MPO group. Moreover, MPO in the culprit artery appeared to correlate positively with MPO in non-culprit arteries and serum, and with troponin levels and peak CK.This patient-based study revealed in patients after AMI that high MPO levels in the culprit artery were associated with more severe microvascular obstruction and greater IS. These findings may provide new insights pathophysiology explanation for the adverse prognostic impact of MO.

We aimed to investigate whether SDMA- symmetric dimethylarginine -the symmetrical stereoisomer of ADMA- might be a marker of left ventricular function in AMI.Asymmetric dimethylarginine (ADMA) has been implicated in the prognosis after acute myocardial infarction (AMI) and heart failure (HF).Cross sectional prospective study from 487 consecutive patients hospitalized 2, and death.Patients were analysed based on SDMA tertiles. Sex, diabetes, dyslipidemia, and prior MI were similar for all tertiles. In contrast, age and hypertension increased across the tertiles (p

The superfamily of tumor necrosis factor (TNF) receptors includes osteoprotegerin (OPG) and its ligands, which are receptor activators of nuclear factor kappa-B ligand (RANKL) and TNF-related apoptosis-inducing ligand (TRAIL). The OPG/RANKL/RANK system plays an active role in pathological angiogenesis and inflammation as well as cell survival. It has been demonstrated that there is crosstalk between endothelial cells and osteoblasts during osteogenesis, thus establishing a connection between angiogenesis and osteogenesis. This OPG/RANKL/RANK/TRAIL system acts on specific cell surface receptors, which are then able to transmit their signals to other intracellular components and modify gene expression. Cytokine production and activation of their receptors induce mechanisms to recruit monocytes and neutrophils as well as endothelial cells. Data support the role of an increased OPG/RANKL ratio as a possible marker of progression of endothelial dysfunction in metabolic disorders in relationship with inflammatory marker levels. We review the role of the OPG/RANKL/RANK triad in vascular function as well as molecular mechanisms related to the etiology of vascular diseases. The potential therapeutic strategies may be very promising in the future.

Aging is a complicated pathophysiological process accompanied by a wide array of biological adaptations. The physiological deterioration correlates with the reduced regenerative capacity of tissues. The rejuvenation of tissue regeneration in aging organisms has also been observed after heterochronic parabiosis. With this model, it has been shown that exposure to young blood can rejuvenate the regenerative capacity of peripheral tissues and brain in aged animals. An endogenous compound called growth differentiation factor 11 (GDF11) is a circulating negative regulator of cardiac hypertrophy, suggesting that raising GDF11 levels could potentially treat or prevent cardiac diseases. The protein GDF11 is found in humans as well as animals. The existence of endogenous regulators of regenerative capacity, such as GDF11, in peripheral tissues and brain has now been demonstrated. It will be important to investigate the mechanisms with therapeutic promise that induce the regenerative effects of GDF11 for a variety of age-related diseases.

Atrial fibrillation (AF), whether silent or symptomatic, is a frequent and severe complication of acute myocardial infarction (AMI). Asymmetric dimethylarginine (ADMA), an endogenous eNOS inhibitor, is a risk factor for endothelial dysfunction. We addressed the relationship between ADMA plasma levels and AF occurrence in AMI.273 patients hospitalized for AMI were included. Continuous electrocardiographic monitoring (CEM) ≥48 hours was recorded and ADMA was measured by High Performance Liquid Chromatography on admission blood sample.The incidence of silent and symptomatic AF was 39(14%) and 29 (11%), respectively. AF patients were markedly older than patients without AF (≈ 20 y). There was a trend towards higher ADMA levels in patients with symptomatic AF than in patients with silent AF or no AF (0.53 vs 0.49 and 0.49 μmol/L, respectively, p = 0.18,). After matching on age, we found that patients with symptomatic AF had a higher heart rate on admission and a higher rate of patients with LV dysfunction (28% vs. 3%, p = 0.025). Patients who developed symptomatic AF had a higher ADMA level than patients without AF (0.53 vs. 0.43 μmol/L; p = 0.001). Multivariate logistic regression analysis to estimate symptomatic AF occurrence showed that ADMA was independently associated with symptomatic AF (OR: 2.46 [1.21-5.00], p = 0.013) beyond history of AF, LVEF

Low levels of high-density lipoprotein (HDL) cholesterol are associated with an increased risk of acute myocardial infarction possibly through impaired endothelial atheroprotection and decreased nitric oxide (NO) bioavailability. Asymmetric dimethylarginine (ADMA) mediates endothelial function by inhibiting nitric oxide synthase activity. In patients with acute myocardial infarction, we investigated the relationship between serum levels of HDL and ADMA.Blood samples from 612 consecutive patients hospitalized for acute MI

AIM: We investigated the relationships between the autonomic nervous system, as assessed by heart rate variability (HRV) and levels of N-terminal Pro-B-type Natriuretic Peptide (Nt-proBNP) in patients with acute myocardial infarction (MI). METHODS AND RESULTS: The mean of standard deviation of RR intervals (SDNN), the percentage of RR intervals with >50 ms variation (pNN50), square root of mean squared differences of successive RR intervals (rMSSD), and frequency domain parameters (total power (TP), high frequency and low frequency power ratio (LF/HF)) were assessed by 24 h Holter ECG monitoring. 1018 consecutive patients admitted

BACKGROUND: The presence of pre-infarction angina (PIA) has been shown to confer cardioprotection after ST-segment elevation myocardial infarction (STEMI). However, the clinical impact of PIA in non-ST-segment elevation myocardial infarction (NSTEMI) remains to be determined. METHODS AND RESULTS: From the obseRvatoire des Infarctus de Côte d'Or (RICO) survey, 1541 consecutive patients admitted in intensive care unit with a first NSTEMI were included. Patients who experienced chest pain