Patients with cancer usually report limitations of their functional capacity, which may range from subclinical impairment of cardiopulmonary exercise reserve to poor quality of life with physical, cognitive, or psychosocial consequences. Exercise training is a potent multi-targeted approach to control pre-existing and new risk factors. Preliminary evidence shows that it is associated with a lower risk of cancer therapy-related cardiotoxicity and increased self-reported well-being in patients with cancer. Current evidence demonstrates that supervised exercise therapy, including high-intensity interval training, is safe and well-tolerated and reduces risk in subjects with cancer in the pre-, active-, and post-treatment settings. The present consensus document will discuss the role of exercise training in cardio-oncology, focusing on patients with cardiovascular diseases induced by cancer treatment and on those who received cardiotoxic therapies.

Orthostatic hypotension (OH) is defined as a decline in systolic blood pressure of at least 20 mmHg or a reduction in diastolic blood pressure of at least 10 mmHg, within the first 3 min of standing.

To evaluate the prevalence of OH and to identify the characteristics of patients with OH in hypertensive patients hospitalized in medical inpatient departments.

A multicenter, observational, prospective study (FADOI-HYP-OP) included 1000 hypertensive inpatients from 29 Departments throughout Italy. Demographic, clinical data, blood pressure and the presence of comorbidities were recorded at baseline. Factors associated with OH were assessed in multiple logistic regression analysis.

The prevalence of OH was 25.1%. Factors independently associated with OH included disturbances of consciousness (RR 1.56, 95%CI 1.10-2.20; p = 0.01), Parkinson's disease (RR 2.30, 95%CI 1.47-3.59; p = 0.0002), type-1 diabetes (RR 1.72, 95%CI 1.05-2.80; p = 0.03), respiratory comorbidities/diseases (RR 1.32, 95%CI 1.02-1.70; p = 0.04), ischemic heart disease (IHD) (RR 1.20, 95%CI 1.01-1.43; p = 0.04) and α1-adrenergic receptor blockers use (RR 1.32, 95%CI 1.03-1.69; p = 0.03).

These real-world data indicate considerable prevalence of OH in hypertensive inpatients and confirm the association between OH and several common comorbidities as well as with use of α1-adrenergic receptor blockers.

NCT05247060.

Iron deficiency (ID) is a highly prevalent and clinically significant comorbidity in heart failure with preserved ejection fraction (HFpEF), affecting 40-60% of patients. Independent of anemia, ID is associated with reduced exercise capacity, diminished quality of life (QoL), and increased healthcare utilization. Although intravenous (IV) iron therapy has demonstrated consistent benefits in HF with reduced ejection fraction (HFrEF), including improvements in symptoms, QoL, functional status, and reductions in hospitalizations, its role in HFpEF remains incompletely defined. This review synthesizes the epidemiology, pathophysiologic mechanisms, and diagnostic challenges of ID in HFpEF, with particular attention to emerging data for IV iron supplementation in this clinical setting. It summarizes recent and ongoing clinical trials, highlights limitations of current diagnostic criteria, and outlines innovative strategies, including pragmatic trial designs, patient-reported outcomes, and wearable technologies, to evaluate therapeutic response in this heterogeneous population. Together, these insights provide a roadmap for improving the diagnosis and management of ID in HFpEF and addressing a significant unmet clinical need in this growing patient population.

Obesity is an alarmingly growing global epidemic strongly associated with type 2 diabetes, cardiovascular disease, metabolic syndrome, and chronic kidney disease. Metabolic dysfunction-associated steatotic liver disease (MASLD) is considered an important contributor within this interconnected spectrum, representing a new component of the broader cardio-kidney-metabolic (CKM) syndrome, now more aptly labelled as the cardio-kidney-liver-metabolic (CKLM) syndrome. This narrative review synthesizes evidence from epidemiological studies, clinical trials, and ongoing scientific research to explore the multifaceted associations, complex interplay and shared pathophysiological mechanisms among these disorders. The clinical implications of this interplay are substantial, underscoring the need for a holistic approach encompassing early detection, comprehensive risk assessment, and multi-targeted interventions. Therapeutic strategies discussed include lifestyle modification, anti-diabetic, anti-obesity, lipid-lowering agents, and bariatric surgery. Given MASLD's potential role in the CKLM spectrum, future research should deepen the understanding of shared mechanisms and develop integrated clinical management strategies to improve outcomes and reduce their global burden.

Acute heart failure (AHF) is a major cause of hospitalisation worldwide and remains associated with substantial early rehospitalisation and short-term mortality. Accurate assessment of congestion remains challenging because symptoms, physical signs, body weight, and conventional biomarkers may not fully capture the severity, distribution, or persistence of haemodynamic congestion. This limitation contributes to incomplete decongestion and may partly explain recurrent decompensation after discharge. In this review, we examine the complementary roles of three point-of-care ultrasound modalities in residual congestion assessment: lung ultrasound for pulmonary congestion, venous Doppler/VExUS for systemic venous and end-organ congestion, and focused transthoracic echocardiography for cardiac and haemodynamic profiling. We propose the ICON (Integrated Congestion-Oriented Navigation) framework as a pragmatic bedside model that translates these modalities into a three-phase acute heart failure workflow: initial assessment, inpatient monitoring, and predischarge reassessment. Within this workflow, ICON supports phenotype-based interpretation of residual congestion, including pulmonary-dominant, systemic venous/RV-dominant, mixed, cold-wet/low-output, and near-decongested profiles. Current evidence supports the prognostic value of residual congestion and suggests that ultrasound-guided strategies may improve congestion assessment, but the evidence remains heterogeneous. The ICON framework should therefore be viewed as a proposed physiology-based model requiring prospective validation before adoption as a standard-of-care pathway.

The performance of nanozyme-based biosensing platforms is highly dependent on the composition and microenvironment of the active sites. Inspired by natural coordination environments, a biomimetic nanozyme was developed by incorporating L-glutamic acid (L-Glu) into a copper-imidazole framework (Cu-2MI). The amino acid modulates the copper active centers via coordination interactions, optimizing the local electronic structure and significantly enhancing peroxidase-like activity for efficient signal amplification. Based on this enhanced catalytic performance, an electrochemical aptasensor was constructed for ultrasensitive detection of cardiac troponin I (cTnI). The sensing interface was further engineered by in situ electrodeposition of gold nanoparticles (AuNPs) onto the Cu-2MI@L-Glu-modified electrode, followed by the immobilization of a cTnI-specific aptamer via Au-S bonds. The AuNPs layer significantly enhances interfacial conductivity and biocompatibility, ensuring efficient electron transfer and specific biorecognition. The captured cTnI forms a spatial obstruction that prevents H₂O₂ from accessing the active sites, thereby inhibiting the catalytic reaction. The constructed sensor demonstrates outstanding analytical performance: a wide linear range from 0.5 pg/mL to 300 ng/mL, a low detection limit of 0.16 pg/mL, and operational stability (> 85% response retention after 7 days). Its potential utility was assessed using spiked human serum samples, with satisfactory recovery rates (93% - 106%). By integrating biomimetic catalytic microenvironment design with rational interface engineering, this study provides a strategy for developing highly sensitive biosensing platforms and demonstrates significant potential for early diagnosis of cardiovascular diseases.

To evaluate the neuroprotective potential of YJ-2, a novel peptidylarginine deiminase 4 (PAD4) inhibitor, against ischemia/reperfusion brain injury by targeting neutrophil extracellular trap (NET) formation.

In vitro, a NETs-induced injury model was established using SH-SY5Y and bEnd.3 cells. YJ-2's effects on viability, apoptosis, oxidative stress, and barrier permeability were assessed via CCK-8, flow cytometry, and FITC-dextran assays. In vivo, a rat middle cerebral artery occlusion/reperfusion (MCAO/R) model received YJ-2 (10 μmol/kg) intravenously. Outcomes included infarct volume (TTC staining), neurological score, neuronal apoptosis (TUNEL), and oxidative markers (ELISA). PAD4 activity and histone H3 citrullination (H3cit) were examined by western blot and immunofluorescence.

YJ-2 reduced NET-mediated neuronal death and oxidative stress in vitro, and improved endothelial barrier integrity. In MCAO/R rats, YJ-2 significantly lowered infarct volume (44.2% → 30.6%), improved neurological function, and suppressed apoptosis. It also decreased PAD4 and H3cit expression in ischemic brain tissue, confirming target engagement.

YJ-2, by preserving blood-brain barrier (BBB) integrity and reducing neuronal apoptosis, highlights its therapeutic potential for ischemic stroke.

The 2026 American College of Cardiology/American Heart Association/multisociety dyslipidemia guideline incorporates the PREVENT atherosclerotic cardiovascular disease (ASCVD) equations for estimation of 10-year ASCVD risk, replacing the Pooled Cohort Equations used in previous prevention guidelines. Coronary artery calcium (CAC) has historically been used to refine risk assessment when treatment decisions are uncertain.

In this study, the authors sought to evaluate cardiovascular event rates across CAC strata within statin eligibility groups and 10-year PREVENT risk categories.

Individuals from the MESA (Multi-Ethnic Study of Atherosclerosis) were included. Three groups were created based on statin eligibility: statin recommended, considered, and not recommended. In addition, participants with a low-density lipoprotein cholesterol 70 to 189 mg/dL without diabetes were grouped by 10-year PREVENT-ASCVD risk categories: <3% (low risk), 3% to <5% (borderline risk), 5% to <10% (intermediate risk), and ≥10% (high risk). Incidence rates per 1,000 person-years were calculated across CAC strata within statin eligibility groups and PREVENT-ASCVD risk categories.

Among the 5,698 participants included in this analysis, the mean age was 61.5 ± 10.3 years and 52.8% were female. Statin therapy was not recommended in 1,924 participants (33.8%), considered in 897 participants (15.7%), and recommended in 2,877 participants (50.5%). The event rates per 1,000 person-years in those without CAC in the not recommended, considered, and recommended statin groups were 1.2, 2.7, and 5.8, respectively. In those with CAC >0, the event rates were 4.5, 5.2, and 16.6, respectively. The event rates per 1,000 person-years in participants with CAC 0 vs CAC >0 were, respectively, 1.1 and 3.0 for 10-year PREVENT-ASCVD risk <3%, 2.7 and 5.2 for 10-year PREVENT-ASCVD risk 3% to <5%, 5.9 and 11.3 for 10-year PREVENT-ASCVD risk 5% to <10%, and 6.2 and 20.9 for 10-year PREVENT-ASCVD risk ≥10%.

In this large multiethnic cohort, CAC provided its greatest clinical value when statin treatment decisions were uncertain, particularly among individuals with borderline predicted risk. Among participants who already met guideline-based treatment thresholds, observed ASCVD event rates remained elevated even when CAC was absent, suggesting that CAC 0 should not generally be used to withhold statin therapy in these individuals. These findings support a guideline-centered role for CAC in the PREVENT era: refining risk near treatment thresholds, contextualizing absolute risk, and informing the intensity of preventive efforts.

In China, the associations between long-term fine particulate matter with aerodynamic diameter ≤2.5 μm (PM_2.5) exposure and coronary heart disease appear to differ from those reported in high-income countries, thus potentially reflecting differences in PM_2.5 composition. However, constituent-specific evidence from national cohort studies remains limited.

This study aimed to investigate the associations of long-term exposure to PM_2.5 constituents with the incidence and mortality risks of coronary heart disease and its subtype, acute myocardial infarction (AMI).

This nationwide prospective cohort study was conducted in 101,906 adults from the China-PAR (Prediction for Atherosclerotic Cardiovascular Disease Risk in China) Project who were free of cardiovascular disease at baseline. Participants were followed up from 2003 to 2019. Annual residential exposures to PM_2.5 constituents, including elemental carbon (EC), organic carbon (OC), nitrate, and sulfate, were estimated using validated satellite-based machine learning models. Cox proportional hazards models with time-varying exposures were used to estimate HRs and 95% CIs per IQR increase, adjusted for major demographic, behavioral, and clinical covariates.

During a median follow-up of 11.08 years (1,230,732 person-years), 3,500 incident cases of coronary heart disease, including 1,771 AMI events, and 1,321 coronary heart disease deaths, including 808 AMI deaths, were recorded. Per IQR increase in EC, OC, nitrate, and sulfate exposure, HRs for coronary heart disease incidence were 1.10 (95% CI: 1.01-1.19), 1.60 (95% CI: 1.31-1.95), 1.43 (95% CI: 1.06-1.95), and 0.93 (95% CI: 0.82-1.06), respectively. Similar positive associations for EC, OC, and nitrate were observed for coronary heart disease mortality and AMI outcomes, whereas the health impacts of sulfate were weaker and less consistent across outcomes. Concentration-response curves indicated an overall increasing coronary heart disease risk for OC, EC, and nitrate exposure with a plateau or slight attenuation in the higher exposure range of EC and OC, whereas sulfate exposure showed nonlinear associations without a sustained increase in risk.

Long-term exposure to specific PM_2.5 constituents was associated with increased risks of coronary heart disease and AMI, thus highlighting the need for constituent-specific air pollution control beyond PM_2.5 mass.

Tricuspid regurgitation (TR) rarely exists as an isolated condition and is most frequently secondary due to heart failure (HF), or atrial fibrillation, with prevalent extracardiac comorbidities. Morphological assessment of the anatomy and severity of TR, together with evaluation of symptoms, currently drives interventional approaches, yet a more holistic integration of causal and contributing comorbid conditions might further improve outcomes. The present review explores such a pathophysiology-driven holistic approach to interpret functional changes and symptomatic burden in patients with TR. It focuses on acknowledging the dynamic nature of TR, but most importantly the bidirectional crosstalk between TR and HF, as well as other organ systems that might drive symptoms and prognosis, but also TR progression. Assessment of TR is ideally performed after optimizing the treatment of interfering comorbidities and correcting volume overload to isolate the true effects of the TR itself. Invasive hemodynamic assessment, portal vein Doppler, and liver stiffness measurements may offer useful information in clinical decision-making. When TR is identified as the primary driver of disease, or if it is strongly interacting with concomitant diseases, more aggressive therapeutic approaches may be pursued. In contrast, when it is more a consequence of the underlying HF, the right expectations in terms of symptomatic improvement and prognosis should be set. This framework may help to identify patients who are the most likely to benefit from TR interventions, while acknowledging the complexity of their clinical picture in the context of HF.