Background: Heart failure (HF), chronic kidney disease (CKD), and atrial fibrillation (AF) frequently coexist, forming a high-risk triad that amplifies morbidity and mortality through shared pathophysiological mechanisms such as neurohormonal activation, fluid overload, and inflammation. Current risk stratification tools, including CHA₂DS₂-VASc and HAS-BLED, inadequately capture the complexity of these multimorbid patients. This study aims to explore the influence of comorbidities, hypertension severity, anticoagulation strategy, and risk scores on hospitalization outcomes in patients with coexisting HF, CKD, and AF. Materials and Methods: A retrospective case study was conducted on 174 hospitalized patients with HF, CKD, and AF. Clinical data included hypertension grade, HF phenotype (HFpEF vs. HFrEF), NYHA classification, renal function (KDIGO stage), stroke and bleeding risk scores (CHA₂DS₂-VASc: congestive heart failure, hypertension, age ≥ 75, diabetes, and stroke/TIA; HAS-BLED: hypertension, abnormal renal/liver function, stroke, bleeding, labile INR, elderly, and drugs/alcohol), comorbidities (neurological, psychiatric, COPD, and diabetes), anticoagulation type (DOACs vs. VKAs), and length of hospital stay. Statistical analysis included Spearman correlation, independent t-tests, and multivariate regression to evaluate associations between variables and clinical outcomes. Results: Most patients were elderly (mean age 75 ± 12), with advanced CKD (stage 3b) and systolic HF (77% HFrEF). Mean CHA₂DS₂-VASc was 5.67, HAS-BLED was 4.40, and ATRIA was 4.74, indicating high stroke and bleeding risk. Anticoagulation was predominantly via DOACs (69.5%). Hypertension severity did not significantly correlate with NYHA class (ρ = −0.14, p = 0.068). Neurological, psychiatric, and metabolic comorbidities showed no significant associations with HF severity. COPD and diabetes correlated inversely with CHA₂DS₂-VASc scores (ρ = −0.83, p = 0.014). No significant differences were observed in hospital stay between HF phenotypes or prior stroke history. In-hospital mortality was low (2.3%). Conclusions: Traditional risk scores do not fully capture the complexity of multimorbid patients. Metabolic comorbidities showed an inverse correlation with stroke risk scores, and no significant correlation was observed between hypertension severity and HF symptom burden. Hypertension and common comorbidities did not correlate with HF symptom burden, and metabolic diseases may paradoxically associate with lower stroke risk scores. These findings highlight the need for improved multimodal risk assessment strategies that consider the heterogeneity of multimorbid populations. Personalized, integrated approaches are essential to optimize anticoagulation, reduce hospitalization, and improve prognosis.

Cancer medications can cause cardiac issues, which are difficult to treat in oncologic patients because of the risk of complications. In some cases, this may significantly impact their well-being and treatment outcomes. Overall, these complications fall under the term “drug induced cardiotoxicity”, mainly due to chemotherapy drugs being specifically toxic to the heart, causing a decrease in the heart’s capacity to pump blood efficiently and leading to a reduction in the left ventricular ejection fraction (LVEF), and subsequently possibly leading to heart failure. Anthracyclines, alkylating agents, and targeted therapies for cancer hold the potential of causing harmful effects on the heart. The incidence of heart-related issues varies from patient to patient and depends on multiple factors, including the type of medication, dosage, duration of the treatment, and pre-existing heart conditions. The underlying mechanism leading to oncologic-drug-induced cardiovascular harmful effects is quite complex. One particular group of drugs, called anthracyclines, have garnered attention due to their impact on oxidative stress and their ability to cause direct harm to heart muscle cells. Reactive oxygen species (ROS) cause harm by inducing damage and programmed cell death in heart cells. Conventional biomarkers alone can only indicate some degree of damage that has already occurred and, therefore, early detection is key. Novel methods like genetic profiling are being developed to detect individuals at risk, prior to the onset of clinical symptoms. Key management strategies—including early detection, personalized medicine approaches, and the use of novel biomarkers—play a crucial role in mitigating cardiotoxicity and improving patient outcomes. Identification of generated genetic alterations and the association to an increased likelihood of cardiotoxicity will allow treatment in a more personalized approach, aiming at decreasing rates of cardiac events while maintaining high oncological efficacy. Oncology drug-induced cardiotoxicity is managed through a combination of preventive strategies and therapeutic interventions from the union of cardiac and oncological knowledge.

Background: Cardio-renal syndrome (CRS) is a complex condition involving bidirectional dysfunction of the heart and kidneys, in which the failure of one organ exacerbates failure in the other. Traditional pharmacologic treatments are often insufficient to manage the hemodynamic and neurohormonal abnormalities underlying CRS, especially in cases resistant to standard therapies. Device-based therapies have emerged as a promising adjunct or alternative approach, offering targeted intervention to relieve congestion, improve renal perfusion, and modulate hemodynamics. This study aimed to evaluate the efficacy and safety of various device-based therapies in CRS management, utilizing DRI2P2S classification to categorize interventions as dilators, reducers, interstitial modulators, pullers, pushers, and shifters. Methods: A comprehensive analysis of clinical trial data and observational studies involving device-based therapies in patients with CRS was conducted, with a focus on hemodynamic endpoints, renal and cardiac function, symptom relief, and adverse events. Devices included in the analysis were splanchnic denervation systems (dilators), devices for central and pulmonary pressure reduction (reducers), and systems targeting interstitial fluid (fluid shifters), among others. A systematic literature review from 2004 to 2024 was performed using databases including PubMed, Embase, and ClinicalTrials.gov, following PRISMA guidelines for study selection. Data were extracted on patient demographics, device type, trial design, outcomes, and follow-up duration. Results: Device-based therapies demonstrated varying levels of efficacy in CRS, with significant improvements observed in specific parameters. Notable results were a reduction in central venous pressure and improved diuretic responsiveness in acute CRS cases, while also stabilizing or improving renal function. Other relevant endpoints were fewer heart failure hospitalizations and a reduction in renal adverse events, reduced tissue congestion and improved quality of life scores. However, some devices presented challenges, including procedure-related complications and a learning curve for optimal device implantation. Conclusions: Device-based therapies offer a valuable addition to the CRS treatment paradigm, particularly in cases unresponsive to conventional diuretics and other pharmacologic measures. Each of them addresses specific pathophysiological components of CRS and shows promise in improving clinical outcomes. Nevertheless, further large-scale, long-term trials with comprehensive endpoints are needed to establish these therapies’ roles in standard care and to optimize patient selection criteria. Enhanced understanding of device mechanisms and refinement of trial endpoints will be key to maximizing the impact of these therapies on quality of life and clinical outcomes for CRS patients.

Secondary dilated cardiomyopathy (DCM) refers to left ventricular dilation and impaired systolic function arising from identifiable extrinsic causes, such as ischemia, hypertension, toxins, infections, systemic diseases, or metabolic disorders. Unlike primary DCM, which is predominantly genetic, secondary DCM represents a diverse spectrum of pathophysiological mechanisms linked to external insults on myocardial structure and function. The increasing prevalence of conditions such as alcohol use disorder, chemotherapy-induced cardiotoxicity, and viral myocarditis underscores the need for heightened awareness and early recognition of secondary DCM. A comprehensive analysis of clinical trial data and observational studies involving secondary dilative cardiomyopathy was conducted, with a focus on mortality, symptom relief, and major adverse events. A systematic literature review was performed using databases, including PubMed, Embase, and ClinicalTrials.gov, following PRISMA guidelines for study selection. Data were extracted on patient demographics, etiology of dilation, trial design, outcomes, and follow-up duration. Advances in diagnostic modalities have refined the ability to identify underlying causes of secondary DCM. For example, high-sensitivity troponin and cardiac magnetic resonance imaging are pivotal in diagnosing myocarditis and differentiating it from ischemic cardiomyopathy. Novel insights into toxin-induced cardiomyopathies, such as those related to anthracyclines and immune checkpoint inhibitors, have highlighted pathways of mitochondrial dysfunction and oxidative stress. Treatment strategies emphasize the management of the causing condition alongside standard heart failure therapies, including RAAS inhibitors and beta-blockers. Emerging therapies, such as myocardial recovery protocols in peripartum cardiomyopathy and immune-modulating treatments in myocarditis, are promising in reversing myocardial dysfunction. Secondary DCM encompasses a heterogeneous group of disorders that require a precise etiological diagnosis for effective management. Timely identification and treatment of the underlying cause, combined with optimized heart failure therapies, can significantly improve outcomes. Future research focuses on developing targeted therapies and exploring the role of biomarkers and precision medicine in tailoring treatment strategies for secondary DCM.

Introduction: Artificial intelligence (AI) and robot-assisted platforms are increasingly influencing cardiothoracic surgery. AI enhances risk prediction, imaging interpretation, and early complication detection, while robotics improves visualization, dexterity, and minimally invasive access. This systematic review evaluates the current evidence supporting these technologies and their implications for clinical practice. Methods: A systematic literature search was conducted across PubMed, Embase, Scopus, Web of Science, and Google Scholar (January 2000–May 2025) following PRISMA 2020 guidelines. After screening and eligibility assessment, 67 studies met predefined inclusion criteria and were incorporated into the qualitative synthesis. Additional high-impact reviews and consensus documents were consulted for contextual interpretation. Results: Machine learning models demonstrated modest but consistent improvements in predictive performance compared with EuroSCORE II and STS scores, particularly in high-risk cohorts. Robot-assisted mitral and coronary procedures showed reduced postoperative pain, blood loss, ICU stay, and recovery time in experienced centers, though early learning phases were associated with longer operative, cross-clamp, and bypass times. AI-enabled intraoperative tools, such as video analysis, workflow recognition, and real-time anatomical segmentation, emerged as promising adjuncts for surgical precision. Structured robotic training programs, especially simulation-based and dual-console pathways, accelerated proficiency acquisition. Conclusions: AI and robotic systems act as augmentative technologies that enhance rather than replace the surgeon’s role. Their safe and effective adoption requires standardized training, transparent AI decision pathways, and clear ethical and medico-legal governance.

Background/Objectives: The early neonatal respiratory transition involves rapid changes in lung aeration and respiratory mechanics, but serial diaphragm-ultrasound trajectories in term neonates remain incompletely characterized. To describe bilateral diaphragmatic thickness, excursion, and diaphragmatic thickening fraction (DTF) during the first 48 h after birth. Methods: This prospective, single-center observational study analyzed 112 term neonates with complete ultrasound examinations at 1, 24, and 48 h of life. Bilateral thickness, excursion, DTF, and lung ultrasound score (LUS) were assessed during quiet spontaneous breathing. Serial comparisons used the Friedman test. No a priori sample-size calculation was reported. The analysis included all eligible neonates with complete serial data. Results: Right and left excursion increased from 5.65 ± 0.71 and 5.64 ± 0.69 mm at 1 h to 5.91 ± 0.58 and 5.91 ± 0.54 mm at 48 h, respectively (p = 0.024 and p = 0.033; Kendall’s W = 0.033 and 0.031). These effect sizes were small. DTF remained stable, whereas LUS decreased from 7.01 ± 2.64 at 1 h to 0.09 ± 0.35 at 48 h (p < 0.001; Kendall’s W = 0.885). Conclusions: In this single-center cohort, lung aeration changed substantially during the first 48 h, whereas diaphragm-ultrasound changes were small. These preliminary trajectories are descriptive and require standardized, multicenter validation before they can be used as reference values or guide clinical decisions.