Dimethyl fumarate (DMF) is an electrophilic compound used clinically for multiple sclerosis and psoriasis. We elaborate here that the pharmacological effects of DMF extend beyond the well-known activation of the NRF2 antioxidative pathway. Indeed, DMF directly modifies reactive cysteine residues on multiple proteins in immune and neural cells, leading to diverse anti-inflammatory, immunomodulatory, and neuroprotective actions. Recent studies revealed that DMF may affect proteins involved in inflammasome activation, glycolysis, and cell signaling pathways, including JAK-STAT and NF-kB. These effects may expand the potential clinical applications of DMF in diverse pathologies, including neurodegenerative, cardiovascular, and pulmonary diseases. We summarize current findings on chemical reactivity, target proteins, and emerging clinical applications of DMF, highlighting new opportunities for DMF repurposing.

Heavy metal exposure is an emerging major environmental risk factor associated with metabolic and cardiometabolic disorders. Arsenic exposure via drinking water leads to cardiotoxicity through lipid metabolism. Exposure to arsenic can cause various heart conditions by activating oxidative stress and inflammatory pathways. Pioglitazone is a thiazolidinedione that activates PPARγ and is an approved clinical drug for the treatment of type 2 diabetes, widely used. Pharmacokinetics results indicate pioglitazone has good oral bioavailability. In this study, we employed a network pharmacology approach and a molecular docking approach to identify the potential mechanism by which pioglitazone may mitigate arsenic-induced cardiotoxicity via lipid metabolism. Key genes that target arsenic-induced cardiotoxicity via lipid metabolism and pioglitazone have been identified using the Swiss Target Prediction, Gene Cards, OMIM, and CTD databases. A protein-protein interaction (PPI) network was generated by analysing frequently intersecting genes with the STRING and Cytoscape tools. Shiny GO was used to conduct pathway enrichment analysis for the KEGG and Gene Ontology databases. Pioglitazone and arsenic-related cardiotoxicity shared 54 common targets. Enrichment analysis pathways involved fluid and shear stress atherosclerosis, NAFLD, lipid, and atherosclerosis. Molecular docking was performed using ten targets. The binding affinity of the ten targets was ALB (6M4R) -8.6 Kcal/mol, BCL2 (2YXJ) -8.0 Kcal/mol, CASP3 (4JJE) -7.1 Kcal/mol, EGFR (2ITO) -7.8 Kcal/mol, HSP90AA1 (6GP8) -7.3 Kcal/mol, PPARα (4UND) -8.4 Kcal/mol, PPARγ (5Y20) -8.6 Kcal/mol, SRC (2SRC) -8.1 Kcal/mol, TNF (5UUI) -6.5 Kcal/mol, and TP53 (4MZI) -5.6 Kcal/mol. And also, we carried out docking with known inhibitors (Asciminib, Emricasan, Navitoclax, Osimertinib, Geldanamycin, GW6471, GW9662, Dastinib, Balinatufnib, and pifithrin), and resveratrol as a positive control. Pioglitazone as a multi-target potential against arsenic-induced cardiotoxicity via lipid metabolism by modulating mitochondrial dysfunction. Overall, this study provides a system-level assumption that indicates lipid metabolism to arsenic-induced cardiotoxicity and identifies key molecular targets that show a way to further experimental validation.

Laminopathies are a diverse group of genetic disorders caused by variants in nuclear lamina proteins, with heart failure being a major cause of morbidity and mortality in patients. By shifting the perspective from distinct clinical phenotypes to a continuous spectrum of metabolic observations in laminopathies, this review aims to elucidate the molecular mechanisms underlying metabolic dysregulation in laminopathies and their impact on cardiac health.

Emerging evidence links A-type lamins to cellular metabolism, with systemic metabolic changes such as lipodystrophy, insulin resistance and hypertriglyceridemia often detected in laminopathy patients before cardiac symptoms onset. At the molecular level, LMNA variants disrupt the regulation of genes involved in fatty acid, oxidation glucose utilization, and mitochondrial function. These disturbances increase cardiomyocyte susceptibility, promoting fibrosis and apoptosis. Metabolic dysregulation is a recurring observation across the laminopathy spectrum. Targeting metabolic pathways shows preclinical promise for improving cardiac outcomes in patients.

Pulmonary arterial hypertension (PAH) is a progressive, often fatal disease characterized by an elevation in pulmonary arterial pressure and pulmonary vascular resistance (PVR). Oral treprostinil is indicated for the treatment of PAH and has been shown to delay disease progression and to improve exercise capacity.

The purpose of this report is to examine and summarize the data on the use of oral treprostinil in patients already on dual therapy with an endothelin receptor antagonist (ERA) and phosphodiesterase type-5 inhibitor (PDE-5i), using data from the FREEDOM-C study, FREEDOM-C2 study, and a retrospective chart review.

In this analysis, background monotherapy versus dual therapy did not have an impact on clinical parameters (6-min walk distance). Additionally, the number of background therapies did not have an impact on the dose of oral treprostinil achieved at week 16 or measures typically used to assess clinical efficacy in patients with PAH (change in 6MWD at week 16 and NT-proBNP).

Oral treprostinil is a safe and efficacious treatment option and has been shown to further improve clinical parameters and risk status in patients with PAH on background dual therapy.

ClinicalTrials.gov identifier, NCT00325442 and NCT00887978.

The subjective experience of stroke in the elderly, as well as the specific support it requires, remains insufficiently explored. While much attention has been given to the psychopathological manifestations frequently observed post-stroke (such as mood disorders, agitation, and aggression), there is a risk that the potential role of the psychological dynamics may be overshadowed by a more direct symptomatic reading of the cerebral lesion. Nevertheless, stroke represents a significant existential disruption, a somatic and psychological experience whose sequelae and resulting psychological suffering profoundly impact quality of life. The aim of this article is to outline certain consequences of stroke on the psychological organization and the ways in which the individual experiences and appropriates this event. It will be shown that, alongside functional and cognitive impairments, there are multiple losses of individual and social supports that further destabilize the subject, thereby heightening vulnerability. With a commitment to supporting the psychological life of these individuals, we have implemented a therapeutic intervention in our clinical practice through drawing mediation, aimed at facilitating communication and fostering new forms of expression. Using a single-case study approach, we present the therapeutic process applied to a brain-injured nursing home resident exhibiting behavioral disorders, and its impact on the emergence of a psychological dynamic conducive to emotional relief.

Atherosclerosis (AS) constitutes the pathological basis of multiple cardiovascular diseases, predisposing to severe clinical complications. Isorhynchophylline (IRN), a principal bioactive alkaloid derived from Uncaria rhynchophylla, exhibits anti-inflammatory properties, yet its therapeutic potential and molecular mechanisms in AS remain unexplored. Scratch wound healing and Transwell migration assays were conducted to evaluate the effects of monomer compounds on cellular migratory and invasive capabilities. The changes in mRNA and protein expression levels of inflammation genes were determined using RT-PCR and western blot analyses, respectively. Molecular docking and drug affinity responsive target stability analyses were performed to assess the binding affinity of IRN and PP2AC. Our findings demonstrate that IRN treatment effectively ameliorates atherosclerotic plaque progression and mitigates endothelial inflammation. The underlying mechanism involves the binding of IRN to PP2AC and the subsequent regulation of YAP activity. This study underscores the therapeutic potential of IRN in alleviating inflammation and its promise as a treatment for AS.

This case report describes the capability of a smartphone-based electrocardiogram (ECG) in detecting multivessel coronary artery disease (CAD), with initial findings suggestive of double-vessel involvement, which was later confirmed as triple-vessel disease (TVD) by coronary angiography.

In this case report, we describe a 51-year-old woman with a known medical history of CAD, hypertension, TVD, and a prior episode of acute coronary syndrome who presented to Swami Rama Himalayan University, Dehradun, with complaints of chest pain. She had previously undergone percutaneous coronary intervention with stent placement. Conventional 12-lead ECG (Philips PageWriter ECG) indicated myocardial ischemia. Follow-up smartphone-based ECG (Spandan Pro) revealed inferolateral ischemia possibly affecting the left anterior descending artery (LAD) and left circumflex artery (LCX), with a possible diagnosis of double-vessel disease (DVD). Coronary angiography later confirmed the diagnosis of TVD with significant stenosis of the LAD, LCX, and right coronary artery, along with additional involvement of the left main coronary artery. Post-angiography, the patient was recommended for coronary artery bypass grafting as the first option and percutaneous transluminal coronary angioplasty as an alternative.

This case illustrates the clinical efficacy of the smartphone-based ECG device in detecting inferolateral ischemia suggestive of DVD in patients with suspected or known CAD and highlights its diagnostic concordance with standard investigations, particularly coronary angiography.

Healthcare systems were reorganised in 2020 to manage the COVID-19 pandemic. Despite their urgent status, hospital admissions for acute heart failure (AHF) were reported to decline from 9% to 66% worldwide between 2020 and 2021, with divergent findings regarding in-hospital mortality. This study aimed to investigate in detail the evolution of AHF hospitalisations and in-hospital mortality in France from 2013 to 2024.

Based on the 2.9 million AHF hospitalisations recorded in France from 2013 to 2024, yearly numbers of hospitalisations and deaths expected in years 2020-2024 were estimated using a Poisson regression model, with 2013-2019 as the reference period. The differences between observed and expected event counts in the years 2020-2024 were used to quantify the disruptions that occurred since the emergence of the pandemic.

A total deficit of -222 913 (-223 908 to -221 926) (mean (95% CI)) AHF hospitalisations was estimated for the years 2020-2024, corresponding to a 16.1% decrease compared with pre-pandemic trends. The yearly reduction in AHF hospitalisations worsened over time, from -39 268 (-39 685 to -38 847) fewer cases in 2020 to -55 521 (-55 984 to -55 051) in 2024. Between 2020 and 2024, 7794 (7557 to 8028) excess in-hospital deaths were estimated, corresponding to an 8.4% excess compared with pre-pandemic trends. From 2021 to 2024, this excess ranged from 9.6% to 16% for females compared with 7.1% to 11.1% for males.

The apparent long-lasting changes in the management of patients with AHF in France observed since the COVID-19 pandemic emergence, particularly among females, suggest further research for better understanding the sustained observed disruptions.

Perivascular adipose tissue (PVAT) has emerged as an active paracrine and metabolic organ that modulates vascular function in both humans and rodents, rather than serving merely as structural support. Vascular inflammation is a central mechanism driving cardiovascular diseases such as atherosclerosis, representing a maladaptive response to vascular injury. Recent evidence indicates that PVAT actively participates in this process through dynamic phenotypic changes, including adipose tissue browning or beiging. Furthermore, advances in imaging have enabled the noninvasive evaluation of vascular inflammation using computed tomography-derived indices that reflect PVAT characteristics. This review summarizes current understanding of the interplay between PVAT and vascular inflammation, highlights the biological and clinical implications of PVAT remodeling, and discusses emerging diagnostic approaches and future research directions.

Post-traumatic stress disorder (PTSD) has emerged as a significant and independent risk factor for cardiovascular disease (CVD), yet its incorporation into routine cardiovascular prevention and care remains limited. This review synthesizes epidemiological evidence showing consistent associations between PTSD and increased incidence of hypertension, coronary artery disease, myocardial infarction, stroke, heart failure, and cardiovascular mortality across diverse populations, including veterans, civilians, women, and disaster-exposed cohorts. The review also highlights the bidirectional relationship between PTSD and CVD, since traumatic cardiovascular events such as myocardial infarction and cardiac arrest can precipitate persistent PTSD symptoms that negatively influence prognosis and recovery. Multiple biological and behavioral mechanisms are described, including autonomic dysregulation, activation of the hypothalamic-pituitary-adrenal (HPA) axis, systemic inflammation, endothelial dysfunction, metabolic disturbances, and maladaptive health behaviors. Clinical implications include gaps in current screening practices, the need for trauma-informed approaches in cardiovascular care, the impact of PTSD on treatment adherence and cardiac rehabilitation, and the potential role of PTSD-targeted interventions in reducing cardiovascular risk. Key limitations in the existing literature are identified, such as heterogeneity in diagnostic criteria, residual confounding from comorbid psychiatric conditions, and the underrepresentation of women and non-veteran populations. The review concludes by outlining future research priorities, with emphasis on mechanistic studies, longitudinal cohorts, clinical intervention trials, and the integration of social determinants of health. A deeper understanding of the complex relationship between PTSD and CVD is essential for advancing both prevention and clinical management in trauma-exposed individuals.