Cardiology and cardiovascular medicine最新文献

Congenital heart defects are the most prevalent congenital anomalies, occurring in approximately 1% of live births and accounting for nearly one-third of all major congenital disorders worldwide. Within this spectrum, critical congenital heart defects (CCHDs) represent the most severe forms, often necessitating surgical or catheter-based intervention within the first year of life. Delayed or missed diagnosis of CCHDs remains a major cause of preventable neonatal morbidity and mortality, underscoring the importance of timely detection. Pulse oximetry screening has emerged as a noninvasive, inexpensive, and highly specific method to identify hypoxemia, particularly in duct-dependent lesions that may otherwise escape early clinical recognition. Since its universal adoption in the United States in 2011, pulse oximetry screening has consistently demonstrated value as a complementary tool to prenatal ultrasound and physical examination, improving detection rates, reducing emergency hospitalizations, and lowering infant mortality. Despite its proven clinical impact, important challenges remain. Screening sensitivity is limited, especially for conditions such as coarctation of the aorta that may not produce early hypoxemia. Variability in protocols, including timing of screening, pre- versus post-ductal measurement, and thresholds for repeat testing, contributes to inconsistent performance across hospitals. Moreover, recent evidence of racial bias in pulse oximetry accuracy, along with persistent disparities in early detection across demographic groups, highlights the need for inclusive device validation and standardized protocols. In low- and middle-income countries, pilot studies from Rwanda, Nigeria, and India demonstrate feasibility and dual benefits for detecting both cardiac and non-cardiac hypoxemic conditions, but widespread implementation is hindered by resource constraints, inadequate referral pathways, and limited access to confirmatory echocardiography. Emerging strategies, including integration with electronic medical records, computerized clinical decision support systems, and mobile health technologies, hold promise for standardizing workflows, improving compliance, and extending reach to resource-limited settings. This article presents a synthesisis of current evidence on the effectiveness, limitations, and global implementation of pulse oximetry screening for the detection of congenital heart defect detection, highlighting both its established role in neonatal care and the urgent need for innovations to address disparities, optimize protocols, and ensure equitable access to screening worldwide.

Deep vein thrombosis (DVT) and pulmonary embolism (PE) are key initiating events in the development of venous thromboembolism (VTE), a condition associated with significant morbidity, mortality, and long-term complications. While traditional therapies have focused on anticoagulation and thrombolysis, current evidence describes the pivotal role of immune pathways in the pathogenesis and progression of thrombosis. This review explores the multifaceted mechanisms underlying DVT and PE, emphasizing the contribution of inflammation, leukocyte activation, and immuno-thrombosis to thrombus formation and embolization. Key immune players such as neutrophil extracellular traps (NETs), inflammasomes, antibodies, and the STING pathway act in concert with coagulation cascades, highlighting potential targets for therapeutic modulation. We critically evaluated and discussed the efficacy and risks associated with thrombolytic agents such as alteplase, reteplase, and tenecteplase, particularly in severe or hemodynamically unstable cases. In addition, we reviewed new and innovative approaches including immune-targeted therapies and nanoparticle-based drug delivery systems, which provide the promise of more precise, safer, and cost-effective interventions. By integrating immunologic insights with evolving thrombolytic strategies, this paper supports a more tailored approach to managing DVT and PE, with the goal of reducing recurrence, minimizing complications, and enhancing long-term patient outcomes.

Retinal artery occlusions, encompassing central retinal artery occlusion and branch retinal artery occlusion, are acute vascular events that can result in significant and often irreversible vision loss. These ocular emergencies are closely associated with systemic vascular risk factors, including hypertension, diabetes mellitus, advanced age, and cardiovascular comorbidities. Atrial fibrillation (AFib), the most common sustained cardiac arrhythmia, has emerged as a notable contributor to the risk of retinal artery occlusions. The prevalence of AFib is rising, particularly among older adults, paralleling the age-dependent increase in retinal artery occlusion incidence. Recent studies indicate a significant association between AFib and retinal artery occlusions, with AFib conferring an elevated risk for both retinal and cerebral ischemic events. Notably, Patients with retinal artery occlusion exhibit a heightened risk of subsequent AFib, stroke, and thromboembolic complications. The pathophysiological interplay involves embolic phenomena originating from cardiac or carotid sources, with AFib facilitating thrombus formation and embolization to the retinal circulation. Diagnostic advances, including prolonged cardiac monitoring and optical coherence tomography, have improved detection of both AFib and retinal ischemic changes. Despite the lack of a universally accepted treatment for retinal artery occlusions, early interventions such as thrombolysis and hyperbaric oxygen therapy may improve visual outcomes if administered promptly. This manuscript underscores the importance of comprehensive cardiovascular evaluation in patients with retinal artery occlusion, particularly for AFib, to optimize risk stratification, guide management, and reduce the likelihood of recurrent vascular events. Enhanced awareness and interdisciplinary collaboration are critical to improving prognosis and preventing further morbidity in this high-risk population.

Arteriovenous fistula (AVF) is created in end-stage renal disease patients for hemodialysis. AVF maturation failure is a common complication due to thrombosis and stenosis of the vessels involved in AVF. Chronic inflammation along with perivascular cuffing plays a critical role in AVF maturation failure. Luminal as well as periluminal factors with the involvement of transcription and epigenetic factors play a critical role in AVF maturation failure. Our previous study reported MYOD1, a factor associated with muscle regeneration and increased with muscle injury, as a significantly increased transcription factor in AVF arteries compared to control. This study aims to characterize the perivascular and vascular AVF tissues for the expression of MYOD1, mediators of inflammation, immune cell markers, and apoptosis markers with the hypothesis that muscle injury mediates the recruitment of immune cells and activation of apoptosis leading to increased apoptosis and vascular thrombosis and fibrosis of perivascular structures. Previously collected tissues from Yucatan miniswine were stained and analyzed, and the results revealed increased expression of mediators of inflammation, immune cell markers, and apoptosis markers in association with increased MYOD1 expression. The findings suggest an interaction between the expression of perivascular factors and luminal factors, but further investigations using in-vitro studies are needed to establish this relationship.

Immune system function is intricately shaped by nutritional status, dietary patterns, and gut microbiota composition. Micronutrients such as vitamins A, C, D, E, B-complex, zinc, selenium, iron, and magnesium are critical for maintaining physical barriers, supporting immune cell proliferation, and regulating inflammation. Macronutrients-including proteins, fats, and carbohydrates-also modulate immune responses through their impact on immune metabolism and the gut-immune axis. Epigenetic mechanisms, including DNA methylation, histone modifications, and microRNA expression, mediate the long-term effects of diet on immune function and tolerance. Diet-induced alterations in gut microbiota further influence immune homeostasis via microbial metabolites like short-chain fatty acids. Imbalanced diets, particularly the Western diet, contribute to immune dysregulation, chronic inflammation, and the development of metabolic disorders such as obesity and type 2 diabetes. While plant-based and Mediterranean dietary patterns have shown anti-inflammatory and immunoregulatory benefits, gaps remain in understanding the long-term epigenetic impacts of these diets. This review integrates current knowledge on how nutrition and the microbiome regulate immunity, highlighting future directions for personalized dietary strategies in preventing chronic immune-related conditions.

Apolipoprotein B (ApoB) has emerged as a central biomarker and mechanistic driver of atherosclerotic cardiovascular disease (ASCVD), outperforming traditional lipid metrics in both risk stratification and therapeutic targeting. In this article a critical evaluation of the information is presented on the molecular biology, metabolic regulation, and clinical relevance of ApoB isoforms, ApoB100 and ApoB48, which play their own distinct, yet complementary roles in hepatic and intestinal lipid transport. The ways in which ApoB particle density is influenced by insulin resistance, nutrient status, hepatic lipid flux, inflammation, and genetic variation, all of which contribute to dyslipoproteinemic phenotypes associated with ASCVD and metabolic syndrome. Importantly, ApoB levels provide a direct measure atherogenic particle number, offering superior predictive value over low-density lipoprotein cholesterol (LDL-C), particularly in cases of lipid discordance and among statin-treated patients with residual cardiovascular risk. Emerging evidence demonstrates therapies targeting ApoB reduction, including statins, PCSK9 inhibitors, and glucose-lowering agents such as GLP-1 receptor agonists, can significantly reduce major adverse cardiovascular events. However, the lipid-modulating effects of agents like SGLT2 inhibitors, metformin, and thiazolidinediones are variable or independent of ApoB changes. The classification of four ApoB-related dyslipoproteinemic phenotypes, normotriglyceridemic hyperApoB, hypertriglyceridemic normoApoB, hypertriglyceridemic hyperApoB, and hyperchylomicronemia, offers a more nuanced approach to cardiovascular risk assessment than LDL-c alone. Collectively, these findings support the integration of ApoB measurement into routine clinical practice as both diagnostic tool and therapeutic target, with the potential to substantially enhance personalized management of cardiometabolic disease.

Atherosclerosis is a chronic inflammatory disease that leads to acute embolism via the formation of atherosclerotic plaques. Plaque formation is first induced by fatty deposition along the arterial intima. Inflammation, bacterial infection, and the released endotoxins can lead to dysfunction and phenotypic changes of vascular smooth muscle cells (VSMCs), advancing the plaque from stable to unstable form and prone to rupture. Stable plaques are characterized by increased VSMCs and less inflammation while vulnerable plaques develop due to chronic inflammation and less VSMCs. Oncostatin M (OSM), an inflammatory cytokine, plays a role in endothelial cells and VSMC proliferation. This effect of OSM could be modulated by p27^KIP1, a cyclin-dependent kinase (CDK) inhibitor. However, the role of OSM in plaque vulnerability has not been investigated. To better understand the role of OSM and its downstream signaling including p27^KIP1 in plaque vulnerability, we characterized the previously collected carotid arteries from hyperlipidemic Yucatan microswine using hematoxylin and eosin stain, Movat Pentachrome stain, and gene and protein expression of OSM and p27^KIP1 using immunostaining and real-time polymerase chain reaction. OSM and p27^KIP1 expression in carotid arteries with angioplasty and treatment with either scrambled peptide or LR12, an inhibitor of triggering receptor expressed on myeloid cell (TREM)-1, were compared between the experimental groups and with contralateral carotid artery. The results of this study elucidated the presence of OSM and p27^KIP1 in carotid arteries with plaque and their association with arterial plaque and vulnerability. The findings suggest that targeting OSM and p27^KIP1 axis regulating VSMC proliferation may have therapeutic significance to stabilize plaque.

Per- and polyfluoroalkyl substances (PFAS) are pervasive environmental pollutants frequently detected in drinking water worldwide. Reports linking PFAS exposure to cardiovascular disease have increased significantly in recent years. Furthermore, women appear to be more susceptible to the adverse effects of PFAS. However, the potential role of ovaries in the increased vulnerability of females to PFAS-related health effects remains unknown. In this study, we investigated the impact of perfluorooctane sulfonate (PFOS), a prominent PFAS, on the cardiovascular function in female rats with intact ovaries and ovariectomized (OVX) females. Bilateral OVX or sham surgeries were performed in 8-week-old female SD rats. Following recovery from surgeries, the rats were given drinking water containing 50 μg/mL of PFOS for 3 weeks. Control groups received PFOS-free water. PFOS exposure significantly reduced body weight but increased blood pressure similarly in both intact and OVX rats. Echocardiography analysis revealed that PFOS exposure decreased cardiac output, end-systolic volume, and end-diastolic volume in intact but not OVX rats. Vascular function studies demonstrated that PFOS equally reduced endothelium-dependent and -independent relaxation responses in intact and OVX rats. The endothelium-independent contractile responses were more pronounced in both intact and OVX rats. eNOS protein levels were similarly decreased in both intact and OVX rats. In conclusion, PFOS affects cardiac function through hormone-dependent mechanisms, while vascular function is impaired independent of ovarian status, indicating an intricate interplay between PFOS exposure, ovarian status, and cardiovascular function.

Importance: Improved pre-operative risk stratification methods are needed for targeted risk mitigation and optimization of care pathways for cardiac patients. This is the first report demonstrating pre-operative, aging-related biomarkers of cellular senescence and immune system function can predict risk of common and serious cardiac surgery-related adverse events.

Design: Multi-center 331-patient cohort study that enrolled patients undergoing coronary artery bypass grafing (CABG) surgery with 30-day follow-up. Included a quaternary care center and two community-based hospitals. Primary outcome was KDIGO-defined acute kidney injury (AKI). Secondary outcomes: decline in eGFR ≥25% at 30d and a composite of major adverse cardiac and kidney events at 30d (MACKE30). Biomarkers were assessed in blood samples collected prior to surgery.

Results: A multivariate regression model of six senescence biomarkers (p16, p14, LAG3, CD244, CD28 and suPAR) identified patients at risk for AKI (NPV 86.6%, accuracy 78.6%), decline in eGFR (NPV 93.5%, accuracy 85.2%), and MACKE30 (NPV 91.4%, accuracy 79.9%). Patients in the top risk tertile had 7.8 (3.3-18.4) higher odds of developing AKI, 4.5 (1.6-12.6) higher odds of developing renal decline at 30d follow-up, and 5.7 (2.1-15.6) higher odds of developing MACKE30 versus patients in the bottom tertile. All models remained significant when adjusted for clinical variables.

Conclusions: A network of senescence biomarkers, a fundamental mechanism of aging, can identify patients at risk for adverse kidney and cardiac events when measured pre-operatively. These findings lay the foundation to improve pre-surgical risk assessment with measures that capture heterogeneity of aging, thereby improving clinical outcomes and resource utilization in cardiac surgery.

Cardiovascular diseases are the leading cause of mortality worldwide, with a disproportionately high burden in low- and middle-income countries. Biomarkers play a crucial role in the early detection, diagnosis, and treatment of cardiovascular diseases by providing valuable insights into the normal and abnormal conditions of the heart and vascular system. The biomarkers derived from the cells and tissues can be identified and quantified in the blood and other body fluids and in tissues. Changes in their expression level under a pathological condition provide clinical information on the underlying pathophysiology that could have predictive, diagnostic, and prognostic value in the treatment of a disease process, and therefore incorporated in clinical guidelines. This enhances the effectiveness of biomarkers in risk stratification and therapeutic decisions in personalized medicine and improvement in patient outcomes. Biomarkers could be protein, carbohydrate, or genome-based and may also be derived from lipids and nucleic acids. Computational biology has emerged as a powerful discipline in biomarker discovery, leveraging computational techniques to identify and validate biological markers for disease diagnosis, prognosis, and drug response prediction. The convergence of advanced technologies, such as artificial intelligence, multi-omics profiling, liquid biopsies, and imaging, has led to a significant shift in the discovery and development of biomarkers, enabling the integration of data from multiple biological scales and providing a more comprehensive understanding of the complex signaling and transcriptional networks underlying disease pathogenesis. In this article, we reviewed the role of computational biology integrated with genomics, proteomics, and metabolomics, together with machine learning techniques and predictive modeling and data integration in the discovery of biomarkers in cardiovascular diseases. We discussed specific biomarkers, including epigenetic, metabolic, and emerging biomarkers, such as extracellular vesicles, miRNAs, and circular RNAs, and their role in the pathophysiology of the heart and vascular diseases.