Explore the vast range of titles available.

This review examines the intricate relationship between obesity and venous thromboembolism (VTE), highlighting the underlying pathophysiological mechanisms and clinical implications. Obesity is an established independent risk factor for VTE, which includes deep vein thrombosis (DVT) and pulmonary embolism (PE). The risk of VTE escalates with increasing body mass index (BMI) and is particularly associated with abdominal adiposity. Dysfunctional adipose tissue (AT) in obesity promotes a pro-thrombotic state through chronic low-grade inflammation and impaired fibrinolysis. This inflammation is driven by stress within hypertrophied adipocytes, which leads to localized hypoxia, cellular dysfunction, and ultimately, cell death. This inflammation is driven by adipocyte stress and the infiltration of immune cells. The adipokine leptin exemplifies the complex link between obesity and VTE. While leptin has pro-thrombotic effects, low leptin levels are paradoxically associated with an increased morbidity and mortality in patients with acute PE, a phenomenon termed the “obesity paradox”. Furthermore, metabolic syndrome significantly increases the risk of recurrent VTE, with the risk growing with each additional metabolic component. Ultimately, a deeper understanding of the molecular and cellular links between obesity and VTE is essential for developing targeted strategies to reduce risk and improve outcomes in this vulnerable population.

Over the past few years, artificial intelligence (AI) has significantly improved healthcare. Once the stuff of science fiction, AI is now widely used, even in our daily lives - often without us thinking about it. All healthcare professionals - especially executives and medical doctors - need to understand the capabilities of advanced AI tools and other breakthrough innovations. This understanding will allow them to recognize opportunities and threats emerging technologies can bring to their organizations. We hope to contribute to a meaningful public discussion about the role of this new type of AI and how our approach to healthcare and medicine can best evolve with the rapid development of this technology. Since medicine learns by example, only a few possible uses of AI in medicine are provided, which merely outline the system's capabilities. Among the examples, it is worth highlighting the roles of AI in medical notes, education, preventive programs, consultation, triage and intervention. It is believed by the authors that large language models such as chat generative pre-trained transformer (ChatGPT) are reaching a level of maturity that will soon impact clinical medicine as a whole and improve the delivery of individualized, compassionate, and scalable healthcare. It is unlikely that AI will replace physicians in the near future. The human aspects of care, including empathy, compassion, critical thinking, and complex decision-making, are invaluable in providing holistic patient care beyond diagnosis and treatment decisions. The GPT-4 has many limitations and cannot replace direct contact between an experienced physician and a patient for even the most seemingly simple consultations, not to mention the ethical and legal aspects of responsibility for diagnosis.

Factor XII (FXII) is a central mediator at the intersection of coagulation, fibrinolysis, inflammation, and immunity. It is activated upon contact with negatively charged surfaces, triggering the intrinsic coagulation pathway and driving thrombus formation and stabilization. Beyond clotting, FXII contributes to activation of the kallikrein–kinin system, generation of bradykinin, and modulation of inflammatory and immune responses. Congenital FXII deficiency does not increase bleeding risk, highlighting its unique role and making FXII inhibition an attractive strategy for anticoagulation and immune modulation with a potentially superior safety profile. Preclinical studies provide compelling evidence for this concept. In models of ischemic stroke and traumatic brain injury, FXII blockade significantly reduced infarct volume, improved neurological outcomes, and attenuated neuroinflammation without increasing hemorrhage. Similarly, in extracorporeal circulation and vascular stent implantation, FXII inhibition prevented thrombus formation and reduced fibrin deposition, achieving effects comparable to heparin but with markedly lower bleeding risk. Several classes of FXII inhibitors are currently in development, including antisense oligonucleotides, peptides, recombinant proteins, and monoclonal antibodies. Among them, Ixodes ricinus contact phase inhibitor (Ir-CPI) and recombinant human albumin-fused Infestin-4 (rHA-Infestin-4) have demonstrated strong antithrombotic efficacy in animal models. Most notably, garadacimab, a monoclonal anti-FXIIa antibody, has completed phase 3 trials and received regulatory approval for hereditary angioedema (HAE) prophylaxis, where it markedly reduces attack frequency with a favorable safety profile. This review summarizes current knowledge on FXII biology and evaluates its translational potential as a novel target for anticoagulant and anti-inflammatory therapies.

In recent years, the immune system has emerged as a key player in the development of atherosclerosis, heart failure, venous thromboembolism, and systemic hypertension. Obesity and related cardiovascular diseases (CVDs) remain the leading global cause of death. Adipokines—hormones produced by adipose tissue—exert diverse endocrine and immunomodulatory effects. Among them, chemerin, discovered in the early 20th century, is a chemotactic molecule that recruits dendritic cells, endothelial cells, macrophages, and lymphocytes during early immune responses. It regulates cell migration and vascular homeostasis. Dysregulated adipokine profiles contribute to chronic inflammation, insulin resistance, metabolic syndrome, and impaired blood pressure control. This review explores chemerin’s potential role in CVD pathogenesis, focusing on its immunomodulatory functions, impact on vascular inflammation, and endothelial dysfunction. The presented work also examines recent findings on chemerin’s diagnostic and therapeutic potential in cardiovascular health.

We are currently experiencing a third digital revolution driven by artificial intelligence (AI), and the emergence of new chat generative pre-trained transformer (ChatGPT) represents a significant technological advancement with profound implications for global society, especially in the field of education. The aim of this study was to see how well ChatGPT performed on medical school exams and to highlight how it might change medical education and practice. Recently, OpenAI's ChatGPT (OpenAI, San Francisco; GPT-4 May 24 Version) was put to the test against a significant Polish medical specialization licensing exam (PES), and the results are in. The version of ChatGPT-4 used in this study was the most up-to-date model at the time of publication (GPT-4). ChatGPT answered questions from June 28, 2023, to June 30, 2023. ChatGPT demonstrates notable advancements in natural language processing models on the tasks of medical question answering. In June 2023, the performance of ChatGPT was assessed based on its ability to answer a set of 120 questions, where it achieved a correct response rate of 67.1%, accurately responding to 80 questions. ChatGPT may be used as an assistance tool in medical education. While ChatGPT can serve as a valuable tool in medical education, it cannot fully replace human expertise and knowledge due to its inherent limitations.

Cardiovascular circulation and kidney function are closely interrelated. The impairment of renal function is a well-known hazard of increased mortality and morbidity of patients with heart failure or coronary artery disease. Acute pulmonary embolism (APE) impacts pulmonary and systemic circulation, and can severely impair functions of other organs, including kidneys, as a result of hypoxemia and increased venous pressure. Previous studies indicate that renal dysfunction predicts short- and long-term outcomes and can improve the risk assessment in APE. However, renal function should also be cautiously considered during the diagnostic workup because the contrast-induced nephropathy after computed tomography pulmonary angiography is noticed more frequently in APE. Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare but imminent complication of APE. This condition promotes renal impairment by increasing venous pressure and decreasing glomerular filtration. The renal function improvement and serum creatinine concentration reduction were noted in CTEPH subgroup with glomerular filtration rate ≤ 60 mL/min/1.73 m2 after successful treatment. In this review, we present the essential research results on the kidney function in thromboembolism disease.

According to the literature, cardiovascular diseases (CVDs)—including myocardial infarction, stroke, and venous thromboembolism (VTE)—are among the leading causes of mortality and morbidity worldwide. Evidence suggests that CVDs share common risk factors and pathophysiological mechanisms. Similar to the Mosaic Theory of Hypertension proposed by Irvine Page in 1949, the pathophysiology of VTE is multifactorial, involving multiple interacting processes. The concept of immunothrombosis, introduced by Engelmann and Massberg in 2009, describes the interplay between the immune system and thrombosis. Both thrombosis and hemostasis share core mechanisms, including platelet activation and fibrin formation. Additionally, immune mediators—such as monocytes, neutrophil extracellular traps (NETs), lymphocytes, selectins, and various molecular factors—play a critical role in thrombus formation. This review highlights inflammation as a key risk factor for pulmonary embolism (APE). Immunity is central to the complex interactions among the coagulation cascade, platelets, endothelium, reactive oxygen species (ROS), and genetic factors. Specifically, we examine the roles of the endothelium, immune cells, and microRNAs (miRNAs) in the pathophysiology of APE and explore potential therapeutic targets. This review aims to elucidate the roles of the endothelium, immune cells, and miRNAs in the pathophysiology of APE and explore potential future perspective.

Objectives Closer reading of computed tomography pulmonary angiography (CTPA) scans of patients presenting with acute pulmonary embolism (PE) may identify those at high risk of developing chronic thromboembolic pulmonary hypertension (CTEPH). We aimed to validate the predictive value of six radiological predictors that were previously proposed. Methods Three hundred forty-one patients with acute PE were prospectively followed for development of CTEPH in six European hospitals. Index CTPAs were analysed post hoc by expert chest radiologists blinded to the final diagnosis. The accuracy of the predictors using a predefined threshold for ‘high risk’ (≥ 3 predictors) and the expert overall judgment on the presence of CTEPH were assessed. Results CTEPH was confirmed in nine patients (2.6%) during 2-year follow-up. Any sign of chronic thrombi was already present in 74/341 patients (22%) on the index CTPA, which was associated with CTEPH (OR 7.8, 95%CI 1.9–32); 37 patients (11%) had ≥ 3 of 6 radiological predictors, of whom 4 (11%) were diagnosed with CTEPH (sensitivity 44%, 95%CI 14–79; specificity 90%, 95%CI 86–93). Expert judgment raised suspicion of CTEPH in 27 patients, which was confirmed in 8 (30%; sensitivity 89%, 95%CI 52–100; specificity 94%, 95%CI 91–97). Conclusions The presence of ≥ 3 of 6 predefined radiological predictors was highly specific for a future CTEPH diagnosis, comparable to overall expert judgment, while the latter was associated with higher sensitivity. Dedicated CTPA reading for signs of CTEPH may therefore help in early detection of CTEPH after PE, although in our cohort this strategy would not have detected all cases. Key Points • Three expert chest radiologists re-assessed CTPA scans performed at the moment of acute pulmonary embolism diagnosis and observed a high prevalence of chronic thrombi and signs of pulmonary hypertension. • On these index scans, the presence of  ≥  3 of 6 predefined radiological predictors was highly specific for a future diagnosis of chronic thromboembolic pulmonary hypertension (CTEPH), comparable to overall expert judgment. • Dedicated CTPA reading for signs of CTEPH may help in early detection of CTEPH after acute pulmonary embolism.

Baseline prognostic assessment in patients with pulmonary hypertension (PH) may help in the selection of treatment. High plasma levels of natriuretic peptide type B have been reported in patients with right ventricular (RV) dysfunction and suggest poor prognosis in patients with idiopathic pulmonary arterial hypertension (IPAH). We prospectively assessed the correlation of N-terminal brain natriuretic peptide (NT-proBNP) with echocardiographic and hemodynamic indexes of RV function as well as with baseline functional status and long-term survival of PH patients. Fifty-five consecutive patients with a mean (± SD) age of 41 ± 15 years and severe PH (including 36 patients with IPAH) were followed up for up to 36 months. Serum samples for NT-proBNP were secured, and 6-min walk test (6 MWT), RV catheterization, and echocardiography were all performed on the same day, before the introduction of targeted treatment. The median baseline serum NT-proBNP concentration was 1,674 pg/mL (range, 51 to 10,951 pg/mL). NT-proBNP concentration correlated with 6MWT distance (r = 0.6 p < 0.001), cardiac index, pulmonary vascular resistance, and right atrial pressure (RAP), but not with pulmonary arterial pressure. NT-proBNP levels were also related to the ratio of the diastolic area of the RV and the LV, and to pericardial effusion during echocardiography. Receiver operating characteristic analysis identified ≥ 1,400 pg/mL as the best NT-proBNP threshold predicting fatal outcome for the entire study group as well as for IPAH patients (sensitivity, 88% and 100%, respectively; specificity, 53% and 56%, respectively). In multivariate analysis, NT-proBNP, troponin T, and RAP were identified as independent factors for poor prognosis for the entire study group, while only NT-proBNP and RAP were identified as markers for poor prognosis in the IPAH subgroup. NT-proBNP level is related to the right heart morphology and dysfunction in PH patients. A serum NT-proBNP level of ≥ 1,400 pg/mL was found to be useful in identifying patients with poor long-term prognosis both in the whole studied group and in the IPAH subgroup.