Search Results (2,112)

Radial wall strain (RWS) is an angiography-derived biomechanical index that quantifies plaque deformability from routine coronary angiography, offering a novel approach to assess plaque vulnerability beyond conventional anatomical and physiological parameters. This narrative review synthesizes current evidence on the pathophysiological basis, clinical applications, and prognostic implications of RWS in coronary artery disease. Recent studies have demonstrated that elevated RWS values are associated with established markers of plaque vulnerability, including thin-cap fibroatheromas and large lipid cores, as well as increased risk of major adverse cardiovascular events. Furthermore, RWS has emerged as a promising tool for identifying vulnerable plaques in non-flow-limiting lesions and predicting in-stent restenosis, demonstrating incremental prognostic value when combined with angiography-derived physiological indices such as the quantitative flow ratio. By integrating biomechanical assessment with conventional physiological and morphological characterization, RWS may enhance risk stratification and guide clinical decision-making in percutaneous coronary intervention. While current evidence is encouraging, prospective randomized trials are needed to validate RWS-guided management strategies and establish optimal cutoff values for clinical implementation. Full article

Introduction: Hypertension (HTN) management is essential to improving cardiovascular and cerebrovascular morbidity and mortality in the older adult, yet optimal blood pressure (BP) targets remain uncertain. We aim to compare the incidence of major adverse cardiovascular events (MACE) among older adults presenting to the emergency department (ED) with systolic blood pressure (SBP) 140–159 mmHg and diastolic blood pressure (DBP) 90–99 mmHg versus those with SBP ≥ 160 mmHg and DBP ≥ 100 mmHg. Methods: Retrospective analysis was conducted using the Global Collaborative Network including adults aged ≥ 65 years presenting to the ED with essential HTN without end-stage renal disease. Cohort 1 (SBP ≥ 160 mmHg and DBP ≥ 100 mmHg) included older adults with more severely elevated BP, while Cohort 2 (SBP 140–159 mmHg and DBP 90–99 mmHg) included those with moderately elevated BP. The primary outcome was all-cause mortality over 5 years. Secondary outcomes included AKI, CHF, AMI, ischemic stroke, and hemorrhagic stroke. Propensity score matching was used to balance baseline characteristics. Results: After propensity score matching, 191,829 patients remained in each cohort. The mean age was 72.6 (±5.9) years; 51.8% were female, 10.5% had diabetes mellitus, and 5.65% were obese. Cohort 2 (SBP 140–159 mmHg) had lower risks across all primary and secondary outcomes compared with Cohort 1 (SBP ≥ 160 mmHg). The largest risk difference (RD) was observed for AKI (RD = 1.28%; 95% CI, 1.09–1.46%; p < 0.0001), followed by ischemic stroke (RD = 1.25%; 95% CI, 1.11–1.39%; p < 0.0001), CHF (RD = 1.11%; 95% CI, 0.93–1.29%; p < 0.0001), AMI (RD = 0.70%; 95% CI, 0.58–0.83%; p < 0.0001), all-cause mortality (RD = 0.33%; 95% CI, 0.15–0.51%; p < 0.0001), and hemorrhagic stroke (RD = 0.29%; 95% CI, 0.22–0.36%; p < 0.0001). All outcomes demonstrated consistently higher absolute risk in Cohort 1 compared with Cohort 2. Conclusion: Cohort 2 (SBP 140–159 mmHg) was associated with a statistically significant but small decrease in cardiovascular, cerebrovascular, and mortality outcomes, with all absolute RDs uniformly small (<1%) and minimal survival benefit over time. These small gains must be weighed against overtreatment risks, such as medication costs, hypotension, and falls, underscoring the need for individualized, risk-based HTN management in older adults. Full article

Background/Objectives: Chronic kidney disease (CKD) and cardiovascular disease (CVD) confer a substantial, interrelated health burden. CKD markedly increases cardiovascular risk and premature mortality, while CVD accelerates kidney disease progression. Despite the availability of simple diagnostic tests and validated CVD risk tools, CKD screening remains inconsistent, kidney measures are under-integrated into CVD risk stratification, and guideline-recommended screening is variably adopted due to system-, clinician-, and patient-level barriers. This initiative aimed to develop a consensus-based, practical algorithm to integrate CKD screening into CVD risk management. Methods: A structured Delphi process was used to develop an evidence-informed, consensus-based screening algorithm. In Phase 1, a multidisciplinary expert panel completed iterative surveys to identify and prioritize key screening components and achieve preliminary consensus. Participants received a landscape assessment summarizing current practices, evidence, and implementation gaps. A roundtable discussion reviewed clinical guidelines, published evidence, and survey findings, informing the development of an initial algorithm draft. In Phase 2, a follow-up roundtable refined the algorithm, assessed feasibility within real-world clinical workflows, and confirmed consensus on priority elements. Agreement was finalized through structured group discussion and survey-based validation. Results: Panel discussions identified optimal CKD screening triggers, key gaps in current practice, and opportunities to promote earlier identification of at-risk patients. Refinement during the second roundtable resulted in consensus on algorithm structure, content, and applicability across settings. The final algorithm reflects a streamlined, implementation-focused approach to support consistent and earlier identification of at-risk patients. Conclusions: The algorithm, labeled the Primary Care Cardio-Kidney Risk Navigator, provides a practical, flexible framework that integrates and operationalizes existing guideline recommendations into a unified, workflow-oriented approach for primary care that supports consistent real-world implementation. It supports earlier identification, referral, and prevention strategies for at-risk populations and can be implemented within electronic health records or as a standalone clinical decision support tool. Full article

Very prevalent respiratory and cardiovascular diseases result in chronic hypoxia, promoting metabolic, kidney, heart, and other malignant diseases. Hypoxia research employs animal models based on chronically breathing hypoxic air (O₂ < 21%), usually by injecting N₂ into the animal’s chamber. However, continuous high-flow N₂ supply is available only in limited facilities, reducing the capability for hypoxia research to be widely conducted. Here, we describe an optimized setting for subjecting rodents to chronic normobaric hypoxia by requiring minimal N₂ supply. The primary aim of this study was the technical development and optimization of a system for chronic normobaric hypoxia exposure rather than testing a specific biological hypothesis The setting is based on providing the O₂ consumed by the animals and eliminating the exhaled CO₂ and water vapor. O₂, CO₂, temperature, and humidity in the hypoxic chamber are controlled by an Arduino-based unit activating a pump that introduces room air to restore the metabolized O₂. Another pump continuously recirculates the chamber air through a Peltier-based dryer and CO₂-absorbing soda lime. To correct any deviation in the actual value of hypoxia within the chamber, the control unit allows the injection of N₂ into the chamber from a gas source. The setting performance was successfully tested in vivo when subjecting mice to 11%–O₂ chronic hypoxia. This device, requiring a low N₂ supply, may facilitate in vivo experimental research on hypoxia-related diseases. Full article

Background/Objectives: Suboptimal dietary patterns are among the leading modifiable contributors to global morbidity and mortality, particularly in cardiovascular disease, type 2 diabetes mellitus (T2DM), obesity, metabolic syndrome, and hypertension. Digital nutrition platforms have emerged to improve adherence to evidence-based dietary strategies; however, many systems lack structured optimization, processing-aware nutrient profiling, and explainable artificial intelligence (AI) mechanisms. The integration of large language models (LLMs) into digital health introduces conversational personalization but also risks hallucination and unsafe outputs without constraint enforcement. This study aimed to describe the system development, architecture, database infrastructure, optimization algorithms, explainability enforcement, and digital health implications of NutriSteppe-AI, a chatbot-first LLM-driven system for personalized health menu generation constrained by deterministic nutrient logic and processing-aware scoring. Methods: NutriSteppe-AI integrates: (1) a multi-source structured nutrient database of 20,000 food products with up to 130 tracked nutrients; (2) energy requirement estimation using the revised Harris-Benedict equation; (3) linear programming-based multi-objective optimization; (4) a Healthy Food Index (HFI; 0.5–5.0 scale) incorporating NOVA processing classification penalties; (5) traffic-light nutrient gating; and (6) a constrained LLM orchestration layer governed by structured API contracts. Algorithmic validation was performed using 10,000 simulated user profiles spanning diverse age, anthropometric, activity, dietary exclusion, and budget parameters. Results: The system achieved 96.8% full constraint satisfaction with macronutrient mean absolute errors of 11.60% (energy), 18.86% (protein), 16.26% (fat), and 20.91% (carbohydrates). Incorporating NOVA processing penalties reduced ultra-processed food HFI scores by 0.73 points (p < 0.001). Median optimized menu HFI improved from 3.6 to 4.3. Median system latency was 1.8 s. Explainability validation confirmed 100% deterministic alignment with zero hallucinated numeric claims. Conclusions: NutriSteppe-AI demonstrates that LLM-driven nutrition chatbots can achieve deterministic, explainable, and clinically aligned performance when governed by structured optimization, processing-aware scoring, and explainability enforcement. This architecture provides scalable digital health infrastructure for cardiometabolic disease prevention in diverse populations. Full article

Incretin-based therapies, including glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and dipeptidyl peptidase-4 (DPP-4) inhibitors, have revolutionized the management of type 2 diabetes and obesity. Recent evidence suggests these agents may influence athletic performance through effects on body composition, energy metabolism, and cardiovascular function. This narrative review critically evaluates whether incretin therapies could constitute doping under World Anti-Doping Agency (WADA) criteria. We narratively reviewed the literature on incretin pharmacology, metabolic effects relevant to athletic performance, and anti-doping regulations, searching PubMed, Scopus, and Web of Science using terms including “GLP-1 receptor agonists”, “DPP-4 inhibitors”, “doping”, “athletic performance”, “WADA”, and “sports pharmacology”, without date restrictions. GLP-1 RAs (semaglutide, liraglutide, tirzepatide, exenatide) induce substantial weight loss (predominantly fat mass) but also reduce lean mass by 20–30% of total weight loss. Preclinical studies demonstrate enhanced exercise endurance, mitochondrial biogenesis, and glucose uptake via GLP-1R/AMPK signaling. However, clinical trials show no consistent improvement in physical performance in humans. Currently, incretin therapies are not listed on the WADA Prohibited List. While incretin therapies offer theoretical performance-enhancing potential through weight management and metabolic optimization, current evidence does not support classification as doping agents. Continued surveillance is warranted as misuse patterns emerge. Full article

Measuring platelet function is important for patient stratification to judge bleeding vs. thrombotic risk and for research into antiplatelet drugs to prevent cardiovascular disease. Variability in platelet function is not fully understood, and large studies of inter-individual variation are making gradual progress using laboratory measurements, but rapid and high-performance hematological tests are also needed. We present here a novel microfluidic technology for platelet function analysis that images light scatter by platelets, using a low-cost, open-source, high-throughput and customizable darkfield imaging system called Dark-Pi. The hardware consists of a camera and a simple LED light source controlled by a Raspberry Pi, with 3D-printed parts. Using the Dark-Pi, platelet aggregation was imaged within adenosine 5′-diphosphate-loaded microcapillaries, revealing clearly visible patterns. This darkfield cellular light scatter approach was previously developed for bacterial cells, and here we adapted and optimized it for directly monitoring platelet aggregation. Capturing high-quality time-resolved images of platelets undergoing activation within microcapillaries allowed us to measure changes in light scattering in platelet-rich plasma that correspond with aggregation measured using conventional laboratory methods. This novel prototype system shows that this approach may have potential for use in large-scale studies of platelet function, combining simplicity with low-cost components and using a disposable dip-and-test microfluidic format. Full article

Background and Clinical Significance: Lues remains a global health concern despite the well-known nature of its symptoms, the availability of diagnostic methods, and the existence of effective therapy. The recent increase in maternal syphilis has been accompanied by a rise in congenital infections, which are associated with stillbirth, prematurity, neonatal mortality, and severe multisystemic disorder. In newborns, it may present with highly variable clinical manifestations, making timely diagnosis and treatment essential. We report a case of severe early congenital syphilis in a premature newborn with extensive multiorgan involvement; Case Presentation: We present a case of a male infant born at 31 + 6 weeks of gestation to a 26-year-old mother with inadequate antenatal care and no documented screening or treatment for syphilis during pregnancy. Prenatal ultrasound revealed fetal ascites. At birth, the infant presented with severe respiratory failure requiring immediate resuscitation, endotracheal intubation, and intensive care support. Clinical findings included hepatosplenomegaly, generalized edema, ascites, petechial rash, palmoplantar desquamation, severe thrombocytopenia, anemia, coagulopathy, liver dysfunction, and hemorrhagic syndrome. Maternal and neonatal serologic testing confirmed syphilis infection. The clinical course was complicated by pneumonia with prolonged mechanical ventilation, cardiovascular involvement impairing cardiac function, and heart failure. Treatment consisted of intravenous penicillin G, broad-spectrum antimicrobial therapy, antifungal medication, respiratory support, transfusion therapy, cardiovascular management, and intensive multidisciplinary care; Conclusions: This report presents consequences of untreated maternal syphilis and underscores the importance of timely diagnosis, early initiation of penicillin therapy, and close multidisciplinary follow-up to optimize outcomes in neonates. Full article

Lipoprotein(a) [Lp(a)] has emerged as a major genetically determined cardiovascular risk factor that extends beyond the traditional low-density lipoprotein cholesterol (LDL-C)-centred model of atherosclerotic disease. Despite optimal LDL-C lowering, a substantial proportion of patients continue to experience cardiovascular events, highlighting the clinical relevance of residual cardiovascular risk. This review summarizes current evidence regarding the epidemiology, genetics, pathophysiology and therapeutic implications of Lp(a) in cardiovascular disease. Epidemiological, genetic, and Mendelian randomization studies consistently demonstrate an independent and likely causal association between elevated Lp(a) and atherosclerotic cardiovascular disease, ischemic stroke, calcific aortic valve stenosis, heart failure, and recurrent cardiovascular events, even in patients with well-controlled LDL-C levels. Lp(a) promotes atherosclerosis through proatherogenic, proinflammatory, and prothrombotic mechanisms, largely mediated by oxidized phospholipids and the structural homology of apolipoprotein(a) with plasminogen. Current guidelines increasingly recognize Lp(a) as a risk-enhancing factor capable of refining cardiovascular risk stratification beyond traditional algorithms, thus recommending measuring Lp(a) at least once in a lifetime in all adults. Accurate measurement and standardization of Lp(a) remain essential in clinical practice due to apo(a) isoform size variability; reporting in molar concentrations (nmol/L) is preferred as it better reflects particle number being less affected by isoform size variations and improves the reliability of cardiovascular risk stratification. Collectively, these findings support the integration of Lp(a) into precision-based cardiovascular prevention strategies and suggest a paradigm shift from an exclusively LDL-centric approach toward genetically informed risk assessment and treatment. Full article

Introduction and objectives: Acute heart failure (AHF) is the leading cardiovascular cause of hospitalization and remains associated with high mortality and rehospitalization rates. Contemporary real-world data from cardiology departments are scarce. We aimed to identify admission characteristics associated with one-year outcomes in patients hospitalized with AHF. Methods: RECYLICA is a prospective, multicentre, regional registry including consecutive patients admitted with AHF to cardiology departments across 10 hospitals over a one-year period. Patients were followed for 12 months. The primary endpoint was the composite of all-cause mortality or heart failure (HF) rehospitalization. Results: A total of 602 patients were included (37.0% women; mean age 72.6 ± 12.0 years), of whom 47.4% had heart failure with reduced left ventricular ejection fraction (HFrEF). During follow-up, 83 patients (13.8%) died and 105 (17.4%) were rehospitalized because of HF. Independent predictors of the primary endpoint were elevated admission N-terminal pro-B-type natriuretic peptide (NT-proBNP), atrial fibrillation (AF), chronic kidney disease (CKD), chronic obstructive pulmonary disease (COPD), previous HF, prior implantable cardioverter-defibrillator (ICD) implantation, and higher left ventricular ejection fraction (LVEF). Among patients with HFrEF, less comprehensive implementation of guideline-directed medical therapy (GDMT) at discharge was associated with significantly worse outcomes. Conclusions: In patients hospitalized with AHF, prognosis is primarily determined by comorbidity burden, admission NT-proBNP levels, previous HF, and LVEF. Among patients with HFrEF, more comprehensive implementation of GDMT at discharge was associated with improved clinical outcomes, supporting early optimization of evidence-based therapy during hospitalization. Full article

Titanium and its alloys are cornerstone biomaterials due to their high strength-to-weight ratio, excellent fatigue and corrosion resistance, biocompatibility, and ability to osseointegrate with bone. Their relatively low elastic modulus compared to stainless steels and Co–Cr alloys further enhances their suitability for biomedical applications. Performance is continually improved through alloy design (tailoring α and β phases), advanced manufacturing methods such as CNC machining and additive manufacturing, and surface engineering approaches. In particular, the formation of a stable TiO₂ layer promotes corrosion resistance and cell attachment, while coatings and nanotexturing enhance osseointegration and provide antibacterial functionality. These attributes enable widespread use in orthopedic, dental, and cardiovascular implants. Emerging developments include smart implants with embedded sensors, multifunctional surfaces, and data-driven alloy design, aiming to further optimize mechanical performance, biological response, and long-term reliability. This review summarizes the processing techniques, properties, applications, and recent advances in titanium-based biomaterials. Full article

Background/Objectives: Type 2 diabetes mellitus (T2DM) and menopause are associated with low levels of vitamin D (25[OH]D). Primary trials reported the effects of cholecalciferol supplementation on glycemia and T2DM incidence with conflicting results. This uncontrolled longitudinal prospective study aimed to evaluate changes in metabolic and cardiovascular parameters in postmenopausal women with T2DM during sequential cholecalciferol supplementation. Methods: Thirty-four postmenopausal women (mean of 63.8 ± 7.5 years) with T2DM received 1000 IU/day of cholecalciferol for 12 months, followed by 2000 IU/day for another 12 months. Fasting blood tests, anthropometric assessments, and physical examinations were performed at baseline, 12 months, and 24 months after the intervention. The levels of 25(OH)D, fasting glycemia, glycated hemoglobin, fasting insulin, homeostasis model assessment (HOMA) of insulin resistance, HOMA of β-cell function (HOMA-β), total cholesterol, high-density lipoprotein cholesterol (HDL-c), triglycerides, and C-reactive protein were evaluated. Systolic blood pressure (SBP), diastolic blood pressure, waist circumference (WC), waist-to-hip ratio, and body mass index were also assessed. Results: Serum 25(OH)D and HDL-c levels increased over time during the follow-up period. Lower WC and SBP values were observed across follow-up assessments. Although fasting blood glucose values showed a median of 120 mg/dL at baseline and 110 mg/dL after cholecalciferol supplementation, and HOMA-β values were approximately 35% higher at the end of follow-up, these differences were not statistically significant (p = 0.059 and p = 0.158, respectively). Conclusions: The long-term 25(OH)D dosing regimen had modest beneficial effects on glucose homeostasis, lipid profiles, and blood pressure in postmenopausal women with T2DM. This study contributes to the search for an optimal daily 25(OH)D dose in postmenopausal women with diabetes. Full article

Hypogonadism is increasingly recognized as an independent cardiovascular risk factor, with testosterone deficiency associated with endothelial dysfunction, increased thrombotic risk, and adverse cardiovascular outcomes. Circulating biomarkers provide valuable insights into the vascular health status of hypogonadal men and the cardiovascular effects of testosterone replacement therapy (TRT). This comprehensive review examines the molecular basis of testosterone action on the cardiovascular system and synthesizes evidence on circulating cardiovascular biomarkers in hypogonadism, including endothelial progenitor cells (EPCs), endothelial microparticles (EMPs), platelet markers, endothelial activators, adhesion molecules, and inflammatory/oxidative stress markers. We also compare the cardiovascular safety profiles of transdermal versus intramuscular testosterone formulations. Hypogonadal men exhibit reduced circulating EPCs, elevated EMPs, increased platelet reactivity, higher levels of endothelial activators (ICAM-1, VCAM-1, E-selectin, von Willebrand factor, endothelin-1, ADMA), and increased inflammatory markers (hsCRP, IL-6, TNF-α). TRT improves most of these biomarkers through androgen receptor (AR)-dependent and AR-independent mechanisms involving PI3K/Akt/eNOS signaling, VEGF upregulation, CXCL12/CXCR4 axis modulation, and NF-κB pathway suppression. Current evidence suggests that transdermal testosterone formulations may offer advantages regarding hematological safety and more stable testosterone exposure; however, definitive evidence demonstrating superior cardiovascular outcomes compared with intramuscular formulations remains limited. Circulating cardiovascular biomarkers are significantly altered in hypogonadism and improve with TRT. Available data suggest that transdermal testosterone formulations may offer a more favorable cardiovascular safety profile than intramuscular preparations, particularly with respect to erythrocytosis and pharmacokinetic stability, although head-to-head randomized trials with hard cardiovascular endpoints are still needed. Understanding the molecular mechanisms underlying these changes is essential for optimizing TRT in hypogonadal men with cardiovascular risk factors. The cardiovascular safety advantage of transdermal formulations is currently supported primarily by pharmacokinetic and hematological evidence; direct comparative evidence from randomized trials with hard cardiovascular endpoints remains unavailable. Full article

Background: Despite evidence-based guidelines for cardiovascular risk management, many patients fail to achieve therapeutic targets. The relative contribution of medication non-adherence versus suboptimal treatment optimization to poor cardiovascular outcomes remains unclear in real-world primary care settings. The aim of this study was to describe changes in cardiovascular risk factor control following protocolized adherence reinforcement combined with physician-driven treatment optimization in high-risk patients. Methods: This multicenter, real-world longitudinal study included 789 participants with high or very high cardiovascular risk enrolled from primary care settings across 9 Spanish regions between 2023 and 2025. All participants received a protocolized intervention combining adherence reinforcement and physician-driven treatment optimization. This was a single-arm, pre–post study without a concurrent control group; observed changes therefore cannot be attributed to the intervention alone. Of 789 participants screened, all completed the baseline assessment, and 628 (79.6%) completed the 90-day follow-up. A total of 161 participants (20.4%) were lost to follow-up. Primary outcomes included changes in systolic and diastolic blood pressure, lipid parameters (total cholesterol [TC], low-density lipoprotein cholesterol [LDL-c], high-density lipoprotein cholesterol [HDL-c], triglycerides [TG]), glucose, glycated hemoglobin (HbA1c), and body mass index (BMI) from baseline to 90-day follow-up. Changes were assessed using linear mixed models. Results: Among participants with complete paired data (n = 453–615 depending on the outcome), significant improvements were observed in most cardiovascular risk factors (HDL-c and HbA1c did not change significantly). Mean changes (95% confidence interval [CI]) were: systolic blood pressure, −9.24 mmHg (−10.41 to −8.06; p < 0.001); diastolic blood pressure, −4.75 mmHg (−5.49 to −4.01; p < 0.001); LDL-c, −22.29 mg/dL (−25.59 to −19.00; p < 0.001); TC, −23.24 mg/dL (−26.73 to −19.74; p < 0.001); TG, −16.75 mg/dL (−23.03 to −10.46; p < 0.001); fasting plasma glucose, −10.03 mg/dL (−12.61 to −7.46; p < 0.001); and BMI, −0.46 kg/m² (−0.58 to −0.35; p < 0.001). Linear mixed models including all available data (n = 628 at 90-day follow-up) confirmed these findings. No significant interactions were observed between assessment timepoint and sex, age, or overweight/obesity status for most outcomes, except for age-related differences in lipid responses. Conclusions: Protocolized adherence reinforcement combined with physician-driven treatment optimization was associated with clinically meaningful improvements in multiple cardiovascular risk factors in high-risk primary care patients. Given the single-arm pre–post design, the observed improvements are associative and cannot establish causality. Residual uncontrolled risk, particularly in lipid management and among older adults, persisted despite active treatment optimization (treatment was modified in 82.0% of participants), consistent with residual suboptimal treatment intensification even after adherence had been reinforced. These findings suggest that achieving optimal cardiovascular risk factor control requires addressing both medication adherence and treatment intensification, particularly in patients with multimorbidity. Full article

Atrial fibrillation (AF) and heart failure (HF) frequently coexist and mutually worsen prognosis, creating a complex clinical scenario in which treatment decisions are increasingly imaging driven. Catheter ablation has emerged as a pivotal rhythm control strategy in selected patients with HF, but careful phenotyping of the atrial and ventricular substrate is essential to balance potential benefits against procedural risk and the likelihood of durable sinus rhythm. In this narrative review, we summarize the role of multimodality imaging across the entire AF care pathway in patients with HF, from candidate selection to intraprocedural guidance and post-ablation follow-up. Ultrasound imaging remains the cornerstone of pre-procedural assessment. Cardiac computed tomography (CCT) refines anatomical characterization of the left atrium, pulmonary veins, and left atrial appendage. Cardiovascular magnetic resonance (CMR) offers comprehensive tissue characterization of atrial and ventricular fibrosis, allowing distinction between atrial primary and atrial secondary AF phenotypes and informing expectations of reverse remodelling. During ablation, intracardiac echocardiography and transesophageal echocardiography optimize transseptal access, catheter navigation, and complication monitoring, and they are particularly relevant with contemporary Pulsed Field Ablation systems. In follow-up, echocardiography, CCT, and CMR are pivotal for quantifying structural reverse remodelling and detecting rare but life-threatening complications such as atrio esophageal fistula and pulmonary vein stenosis. An integrated, multimodality, substrate-based imaging strategy is therefore crucial to personalize rhythm versus rate control decisions and to guide safe, effective ablation in patients with AF and HF. Full article