Maria Carelli

Heart failure (HF) and atrial fibrillation (AF) are among the most prevalent cardiovascular diseases, often coexisting and sharing common pathophysiological pathways such as systemic inflammation, oxidative stress, mitochondrial dysfunction, and endothelial impairment. Despite substantial progress in pharmacological treatment, including renin–angiotensin–aldosterone system (RAAS) inhibitors, beta‐blockers, sodium–glucose cotransporter 2 (SGLT2) inhibitors, mineralocorticoid receptor antagonists (MRAs), diuretics, and antiarrhythmic drugs, many patients continue to experience residual symptoms and drug‐related adverse effects. Nutraceuticals have emerged as potential adjuncts to conventional therapy due to their ability to modulate key biological processes involved in HF and AF. Polyphenols from Olea europaea , Hibiscus sabdariffa , Camellia sinensis , and Vitis vinifera (resveratrol) exhibit antioxidant, anti‐inflammatory, and vasoprotective effects. Omega‐3 fatty acids and astaxanthin contribute to inflammation control and redox balance, while Orthosiphon stamineus and Taraxacum officinale show mild diuretic activity. Moreover, anthocyanins, ursolic acid, and Rhodiola crenulata may exert antifibrotic and antiarrhythmic properties. This review provides a mechanistic comparison between pharmacological agents and nutraceuticals with overlapping mechanisms of action, highlighting their potential role in integrative cardiovascular care. While nutraceuticals are not substitutes for established therapies, emerging evidence supports their complementary use in improving treatment response, reducing side effects, and enhancing patient outcomes. Future research should focus on large‐scale trials, improved bioavailability, standardized formulations, and the development of personalized therapeutic strategies. Challenges related to dosage consistency, clinical validation, and regulatory oversight are also addressed to guide innovation in integrative cardiology.

Background: Catheter ablation is a validated treatment for ventricular arrhythmias (VA), but conventional radiofrequency (RF) energy may cause collateral injury due to non-selective thermal damage. Pulsed Field Ablation (PFA), a non-thermal modality based on irreversible electroporation, offers myocardial tissue selectivity and enhanced safety. While PFA is widely adopted for atrial arrhythmias’ ablation, its application in the ventricles remains an evolving frontier. Methods: We report a single-center experience using the Centauri PFA system integrated with a focal, contact-force sensing irrigated catheter (Tacticath™ SE, Abbott Laboratories, St. Paul, MN, USA) in four consecutive patients with drug-refractory VA. Two patients presented with frequent premature ventricular complexes (PVC) arising from the right and left ventricular outflow tract, respectively, while two had ischemic cardiomyopathy with recurrent scar-related ventricular tachycardia (VT). All procedures were guided by high-density mapping using the EnSite X system (Abbott Laboratories, St. Paul, MN, USA). Procedural safety, acute efficacy, and early follow-up outcomes were assessed. Results: All ablations achieved acute procedural success without complications. In both PVC cases, PFA led to immediate and complete suppression of ectopy, with a ≥95% reduction in arrhythmic burden at 12- and 9-months follow-up, respectively. In the VT cases, the arrhythmogenic substrate was effectively modified, rendering the clinical VT non-inducible. ICD interrogation during a 9-month follow-up showed complete absence of recurrent sustained VT. No coronary spasm, atrioventricular block, pericardial effusion, or other adverse events occurred. Conclusions: In this initial experience, focal PFA using a contact-force sensing catheter appeared feasible and effective for both focal and scar-related VA. This system provides an intuitive workflow similar to RF ablation. While our data suggest a favourable safety profile, larger studies are required to definitively confirm safety margins near critical structures.

Atrial fibrillation (AF) management has historically relied on thermal ablation modalities—radiofrequency (RF) and cryoballoon—which have established a high benchmark for pulmonary vein isolation (PVI). However, the inherent risk of collateral thermal injury and lesion inconsistency has driven the search for alternative energy sources. The recent clinical adoption of pulsed-field ablation (PFA), based on irreversible electroporation, represents a significant technological evolution. This narrative review provides a critical appraisal of the transition from thermal to pulsed-field technologies. We synthesized data from pivotal trials and recent health-economic analyses to evaluate the biophysical mechanisms, clinical efficacy, and safety profiles of contemporary devices. We conduct a head-to-head comparison of all modalities regarding critical safety endpoints (esophageal, neurological, and vascular), real-world procedural challenges (anesthesia, lesion assessment), and economic sustainability. While PFA offers distinct advantages in procedural speed and tissue selectivity, we highlight that thermal modalities—particularly cryoballoon and very-high-power RF—retain competitive profiles in terms of cost-effectiveness and established long-term durability. This review aims to provide a balanced roadmap for clinicians navigating the complex choice between established thermal efficacy and the promising, yet evolving, landscape of electroporation.

A significant portion of embolic strokes occurs without documented atrial fibrillation (AF), challenging the traditional paradigm of cardioembolism. This review addresses the emerging concept of “atrial cardiopathy” as a distinct clinical entity—an underlying atrial substrate abnormality, characterized by fibrosis and dysfunction, that promotes thromboembolism independent of AF. We posit that AF is often a late-stage manifestation of atrial cardiopathy, not the sole trigger for thrombosis. This paper synthesizes the growing evidence linking biomarkers of atrial cardiopathy to Embolic Stroke of Undetermined Source (ESUS). This new framework has profound clinical implications, suggesting a shift from arrhythmia detection to assessing atrial substrate health for stroke risk stratification. Recognizing atrial cardiopathy is fundamental for developing novel “upstream” therapies, such as targeted anticoagulation, aimed at preventing both AF and its devastating thromboembolic consequences. This review critically evaluates the evidence and translational gaps in the field, synthesizing the emerging role of advanced computational modeling as a key future tool for personalized risk stratification.

The TRIGGER Horizon Europe project aims to enhance evidence-based connections between climate change and health threats and human well-being.As clearly emerging in the EXPOSOME paradigm on which the project is rooted, the interactions among climate, health and ecosystems are multiple and complex, and research aiming at identification, monitoring, and quantification of impacts of climate change on human health requires the application of novel and transdisciplinary approaches. To this aim, TRIGGER has envisaged activities in a wide variety of disciplines developed in different real-world contexts considering the climatic, social, economic, and cultural richness of the European continent.Specifically, TRIGGER has identified a set of five demonstration labs, the Climate Health Connection Labs (CHCLs) in which citizens are part of a codesign mechanism to directly monitor health, weather-climate, environmental and socio-economic data.These labs operate in five strategically selected cities, Augsburg, Bologna, Geneva, Heraklion, and Oulu, chosen to reflect diverse climatic, socio-economic, and cultural contexts.The objectives of the TRIGGER CHCLs are to:• Investigate the complex interplay between climate change and health.• Define a common language to foster collaboration among stakeholders, including medical, professionals, policymakers, climatologists, patient associations, and citizens, addressing local challenges.• Provide a platform for interdisciplinary research and robust stakeholder engagement.To achieve these ambitious aims, the CHCLs implement three interconnected clinical studies—RetroCLAVIS, CrossCLAVIS, and LongCLAVIS, which collectively provide a comprehensive understanding of the climate-health interplay. Each study contributes unique insights while building upon the others to create an integrated, multi-layered approach to identifying risk profiles and actionable interventions.RetroCLAVIS:• Retrospectively analyzes pre-existing lifelong health and environmental data.• Identifies long-term trends and emerging health threats, providing a temporal context to complement acute and longitudinal findings.CrossCLAVIS:• Serves as the foundation by analyzing cardiovascular and respiratory disease patterns in real-time across diverse European settings.• Investigates molecular and microbiological mechanisms, such as the respiratory microbiome and mitochondrial DNA.• Provides baseline data to inform and validate hypotheses in RetroCLAVIS and LongCLAVIS.LongCLAVIS:• Extends CrossCLAVIS findings through a longitudinal study enrolling 300 healthy volunteers.• Use wearable technology and citizen science to capture detailed data on health, personal and environmental exposures over a one-year period.• Explores molecular and microbiological pathways underlying climate-driven disease susceptibility.In this complex scenario, the Bologna CHCL specifically examines how extreme heat and air pollution could trigger cardiovascular and respiratory diseases. This lab combines cross-sectional and longitudinal studies, to analyze environmental exposures and health threats using harmonized datasets.Overall, this work will present how the CHCL approach in the TRIGGER project provides an innovative, user-centered framework that integrates interdisciplinary collaboration and stakeholder engagement. By enabling capacity-building and deepening the understanding of the climate-health connection, the CHCLs deliver critical insights and practical mitigation and adaptation solutions, advancing societal preparedness for the challenges posed by climate change.

The Achromobacter genus comprises 22 species and various genogroups. Some species with higher virulence or antibiotic resistance are more likely to cause chronic infections in people with cystic fibrosis (CF). Current identification methods often fail to accurately distinguish between the species or result in misidentifications due to biochemical similarities. This study aims to develop an accurate qPCR protocol for species-level identification that is applicable in clinical diagnostic laboratories. Whole-genome sequencing of clinical isolates from different Achromobacter species identified species-specific single-nucleotide polymorphisms (SNPs) in two 16S gene regions. Based on these SNPs, two sets of primers and qPCR probes were designed to generate unique identification profiles. Thermal profiles were optimized, and qPCR was performed on serial bacterial DNA dilutions to determine the detection limit (LOD). Four probes successfully identified three species: A. xylosoxidans, A. dolens, and A. insuavis. Two additional probes were designed for novel genotypes unrelated to publicly available sequences. The LOD ranged from 0.005 pg/µL to 1 pg/µL. Combined probes achieved 100% sensitivity, with specificity ranging from 97.95% to 100%. This qPCR protocol enables accurate species identification, overcoming the limitations of current methods, and represents a reliable tool for clinical diagnostics.

Achromobacter spp. lung infection in cystic fibrosis has been associated with inflammation, increased frequency of exacerbations, and decline of respiratory function. We aimed to evaluate in vivo the inflammatory effects of clinical isolates exhibiting different pathogenic characteristics. Eight clinical isolates were selected based on different pathogenic characteristics previously assessed: virulence in Galleria mellonella larvae, cytotoxicity in human bronchial epithelial cells, and biofilm formation. Acute lung infection was established by intratracheal instillation with 10.5 × 10⁸ bacterial cells in wild-type and CFTR-knockout (KO) mice expressing a luciferase gene under control of interleukin-8 promoter. Lung inflammation was monitored by in vivo bioluminescence imaging up to 48 h after infection, and mortality was recorded up to 96 h. Lung bacterial load was evaluated by CFU count. Virulent isolates caused higher lung inflammation and mice mortality, especially in KO animals. Isolates both virulent and cytotoxic showed higher persistence in mice lungs, while biofilm formation was not associated with lung inflammation, mice mortality, or bacterial persistence. A positive correlation between virulence and lung inflammation was observed. These results indicate that Achromobacter spp. pathogenic characteristics such as virulence and cytotoxicity may be associated with clinically relevant effects and highlight the importance of elucidating their mechanisms.