Atherosclerosis, the fundamental pathological basis of most cardiovascular diseases which remain the leading cause of global mortality, is driven by both lipid accumulation and dynamic cellular reprogramming within the vessel wall. Central to this process is the remarkable phenotypic plasticity of vascular smooth muscle cells (VSMCs). Far from being terminally differentiated, VSMCs undergo profound transitions from a contractile state to diverse states, including synthetic, macrophage-like, foam cell-like, and fibroblast-like states, which critically influence plaque formation, stability, and rupture. This review synthesizes the multilayered molecular mechanisms governing VSMC plasticity, encompassing transcriptional networks, epigenetic reprogramming, and microenvironmental cues. Moreover, this review highlights recent breakthroughs enabled by single-cell omics and lineage tracing, that have revealed unprecedented heterogeneity and clonal expansion of VSMCs within atherosclerotic lesions. Furthermore, we explore the translational potential of targeting VSMC plasticity, and discuss emerging strategies, including phenotype-specific modulation, immunotherapy, nanomedicine, and senotherapeutics. Finally, we outline future directions focused on dynamic regulatory networks, spatial pathophysiology, and the integration of aging biology to advance precision medicine in atherosclerosis. In summary, VSMC phenotypic plasticity is a core mechanism underlying the initiation and progression of atherosclerosis. Precise modulation of this process holds promise for overcoming current therapeutic limitations and driving a paradigm shift toward mechanism-guided personalized therapy for cardiovascular diseases.
Heart failure (HF) is a clinical syndrome resulting from structural or functional cardiac abnormalities and represents a growing global public health challenge. Common etiologies include myocardial infarction, cardiomyopathy, and myocarditis. Mitochondrial dysfunction is now recognized as a central event in the initiation and progression of HF, making this pathogenesis a key focus of recent research. Recent studies have confirmed that HF with reduced ejection fraction (HFrEF) is driven by defects in excitation-contraction coupling, leading to mechano-energetic uncoupling. In contrast, HF with preserved ejection fraction (HFpEF) is characterized by an imbalance between cardiac workload and mitochondrial energy supply. Mitochondrial dysfunction is evident in both forms of HF, with metabolic disturbances serving as both biomarkers and drivers of disease progression. However, key knowledge gaps remain, including uncertainty regarding the regulation of mitochondrial networks and the limited clinical translation of targeted therapies. Thus, the precise modulation of mitochondrial quality control and the correction of metabolic and oxidative imbalances may offer a promising approach for overcoming current therapeutic limitations. This review analyzes the current literature to summarize the pathological mechanisms and therapeutic strategies targeting mitochondrial dysfunction in HF, as a deeper understanding of these mechanisms may support the development of individualized treatment strategies for HF.
Atherosclerotic cardiovascular disease (ASCVD) remains a leading cause of death worldwide. Accumulating evidence has established ASCVD as a lipid-driven chronic inflammatory disease in which the functional heterogeneity of immune cell subsets plays a pivotal role in plaque development and stability. This review systematically summarizes the dynamic immune microenvironment in atherosclerosis, moving beyond static cell categorization to explicitly link immune heterogeneity to the major stages of disease progression: lesion initiation, necrotic core expansion, fibrous cap weakening, and thrombotic complications. We further describe the continuous phenotypic shifts of key immune populations, particularly the transition of macrophages into specialized lipid-handling states and the context-dependent roles of distinct T-cell, B-cell, and innate immune cell subsets. By integrating recent advances in single-cell transcriptomics, we highlight how local molecular networks, cellular crosstalk, and impaired clearance of apoptotic cells govern plaque vulnerability. Furthermore, we critically evaluate spatiotemporal variations across vascular territories and the complex clinical implications of immune checkpoint regulation. Finally, this review discusses current barriers to clinical translation and explores the therapeutic potential of precision immunomodulatory strategies, aiming to bridge the gap between basic immunological mechanisms and targeted cardiovascular therapies.
Infective endocarditis (IE) remains a life-threatening condition, particularly in complex cases with destruction of the aorto-mitral curtain (AMC), also known as the intervalvular fibrous body (IVFB). Multiple factors have contributed to an increased incidence of IE and more extensive destruction of the valvular apparatus, necessitating more aggressive surgical intervention. Thus, this study aimed to evaluate the role and outcomes of the Commando procedure in managing IE involving the AMC. A narrative literature review was conducted to provide a comprehensive overview of the Commando procedure in IE involving the AMC, focusing on recent trends, indications, operative strategies, and outcomes. The keywords "infective endocarditis", "Commando procedure", "aorto-mitral curtain", "intervalvular fibrous body", and "double-valve replacement" were searched in PubMed, Web of Science, and Google Scholar. Only English language studies were included. Inclusion criteria comprised studies involving IE patients who underwent the Commando procedure or any associated modified version; studies reporting conventional double-valve replacement (DVR) performed for IE without AMC involvement were also included for comparison. Exclusion criteria included patients who underwent the Commando procedure for non-infection indications, such as small annuli or calcification. Commando surgery was associated with a 30-day mortality of 9-32%, with 1-, 5-, and 10-year survival rates of 55.4-92.9%, 37.7-68%, and 37-48%, respectively. High-risk factors included infection by specific microorganisms and the need for emergency surgery. The Hemi-Commando procedure demonstrated lower early mortality (8-13.6%), higher 1-year survival (77.5-91%), and 92.3% freedom from reoperation at 1-3 years. Compared with DVR, the Commando procedure had higher operative mortality but similar long-term survival after risk adjustment. Despite the associated high perioperative risks, the Commando surgical procedure remains critical for managing complex IE with AMC destruction. Modified techniques may balance infection control and functional preservation, potentially improving survival in selected patients. Future research should focus on standardized surgical protocols, long-term durability, and multidisciplinary collaboration to optimize outcomes.
Scar-related ventricular tachycardia (VT) is increasingly recognized as a three-dimensional (3D) arrhythmia sustained by complex reentrant circuits that frequently involve intramural components. Advances in high-density and high-resolution electroanatomical mapping have shifted the paradigm of substrate characterization from purely voltage-based structural definitions toward functional assessment of conduction delay and wavefront discontinuity. Recent studies have described techniques that target critical conduction abnormalities associated with VT circuits, including deceleration zones, lines of conduction block, and rotational activation patterns. A central concept underlying these approaches is that VT substrates are volumetric structures constrained by lateral and depth-oriented boundaries rather than planar pathways. Within this 3D framework, targeted ablation strategies that interrupt functionally relevant conduction abnormalities, rather than empirically modifying scar, have demonstrated clinical outcomes comparable to those of extensive homogenization approaches while potentially reducing procedural burden. Intramural reentry remains a major challenge because surface-based mapping incompletely captures mid-myocardial conduction, and current techniques for real-time intraprocedural assessment of intramural abnormalities remain limited. Adjunctive strategies, including differential pacing, refined annotation methods, and peak frequency analysis, may improve identification of critical substrate components, although no single parameter reliably defines the optimal ablation target. Accordingly, procedural endpoints should evolve beyond empirical surrogates such as VT termination or noninducibility toward confirmation of effective disruption of the 3D arrhythmogenic substrate. Continued integration of advanced mapping technologies, imaging, and lesion-delivery innovations will be essential to refine both ablation strategies and procedural endpoints in scar-related VT.
Mesenchymal stromal cell (MSC) therapy has been investigated for more than two decades as a regenerative approach in cardiovascular disease. Preclinical studies have shown reproducible biological activity; however, clinical translation has been less convincing. Trials in acute myocardial infarction (AMI) and heart failure (HF) have established feasibility and an acceptable safety profile; however, effects on functional and imaging parameters remain modest, and a consistent impact on mortality, hospitalization, and other hard clinical outcomes has not been demonstrated.
Takotsubo syndrome (TS) is an acute cardiac condition that clinically resembles acute coronary syndrome; however, TS is not caused by acute coronary obstruction. Moreover, TS is characterized by a distinctive regional, often circumferential, and typically reversible left ventricular wall motion abnormality, which can also involve the right ventricle. In addition to the takotsubo sign, the disease has several other characteristic features, including a history of an emotional or physical trigger, repolarization changes on electrocardiography, moderate elevations of biomarkers of myocardial cell necrosis, and histopathological myocardial changes in the form of contraction band necrosis (coagulative myocytolysis) with characteristic time-related evolutionary changes. Several pathophysiologic mechanisms underlying the disease process remain under debate. However, there is evidence of sympathetic nervous system involvement, including local cardiac sympathetic hyperactivation and disruption at cardiac sympathetic nerve terminals, with excessive norepinephrine release and spillover. Hence, the pathogenetic term autonomic neurocardiogenic syndrome (ANCA), with or without a takotsubo phenotype, has been introduced. For decades, the histopathological cardiac lesions of focal or multifocal coagulative myocytolysis and focal or multifocal "myocarditis" in TS/ANCA syndrome have been described as diagnostic terms in the medical literature. However, the circumferential and multifocal nature of this disease, along with the characteristic time-related histopathological changes and its presence within normal myocardium, provide further evidence that TS/ANCA syndrome is a disorder of the cardiac sympathetic nerve terminals. Therefore, this review presents evidence supporting the previously unquestioned pathogenetic mechanism, with a focus on the specific role of cardiac sympathetic nerve terminals in this syndrome.
Atherosclerosis remains the leading cause of global mortality, most commonly manifesting as ischemic heart disease, stroke, and peripheral arterial disease. Although age-adjusted cardiovascular mortality has declined in many developed nations, the global burden of atherosclerotic disease continues to rise due to population aging and growth. This narrative review examines the evolving understanding of atherosclerosis, which has shifted from a predominantly lipid-centric model to a chronic inflammatory disease. Atherosclerosis is initiated by the retention and modification of apolipoprotein B-containing lipoproteins within the arterial wall and propagated by innate and adaptive immune responses, alongside the development of new treatment strategies. Central to this process is activation of the NLRP3 inflammasome and downstream IL-1β-IL-6 signaling and pyroptotic cell death, which amplify vascular inflammation and promote plaque progression and instability. Clinical evidence demonstrates that targeting inflammation, independent of lipid lowering, reduces cardiovascular events, as exemplified by agents such as canakinumab and colchicine. Consequently, the therapeutic landscape is rapidly evolving, with ongoing efforts to refine cytokine-targeted approaches (e.g., IL-6 inhibition), develop selective NLRP3 inhibitors, and advance innovative modalities including cell-based interventions. These strategies aim to provide more durable, precise, and potentially disease-modifying or even curative approaches. However, challenges related to safety, the high cost of biologic agents, and optimal patient selection have limited widespread implementation. A major barrier remains the lack of sensitive and specific biomarkers to identify patients with active vascular inflammation, complicating trial design and therapeutic targeting. In addition to circulating markers such as high-sensitivity C-reactive protein (hsCRP) and IL-6, emerging insights highlight the liver as a central hub linking inflammation and thrombosis through complement and coagulation pathways, offering potential avenues for developing novel biomarkers. Despite promising advances, clinical translation faces persistent challenges, including increased infection risk, inadequate biomarkers for patient selection, cost constraints, and regulatory and payer requirements for hard clinical endpoints. Precision medicine approaches, drug repurposing, and innovative delivery systems may help accelerate development. Ultimately, the management of atherosclerosis is shifting toward a multifaceted approach that integrates lipid-lowering, inflammation resolution, and genetic correction to achieve durable cardiovascular protection.
Background:This study aimed to identify search for clinical indicators of ischemia with no obstructive coronary arteries (INOCA) and to develop a preliminary diagnostic and predictive model to identify high-risk patients in clinical practice. Method:(1) We retrospectively reviewed patients admitted to the hospital for chest pain or related symptoms who were clinically suspected of having angina pectoris. Patients who received complete nuclear coronary flow reserve (CFR) measurements obtained by positron emission tomography/computed tomography (PET/CT) quantitative coronary artery assessment, had undergone coronary angiography, and had no obstructive coronary lesions were selected as study subjects. Based on the CFR results, patients with a minimum CFR <2.0 were classified as the INOCA group (diagnosed group), and those with a minimum CFR ≥2.5 were classified as the non-INOCA group (control group). Clinical indicators were compared between the two groups. A multiple logistic regression analysis was performed to identify high-risk factors and to establish an INOCA diagnostic model. Additionally, a random forest INOCA diagnostic model based on decision trees was constructed using machine learning methods. (2) An independent cohort of patients meeting the same inclusion criteria as in Method (1) was used for external validation and evaluation of the previously established multiple logistic regression and random forest models. Results:(1) During the model development phase, the results of the multiple logistic regression analysis indicated that smoking history, standard deviation of normal R-R interval (SDNN), low-density lipoprotein-cholesterol (LDL-C), hematocrit (HCT), and monocyte absolute value (MONO#) may be associated with the risk of INOCA. The preliminary logistic regression model, with internal validation and receiver operating characteristic (ROC) curve analysis, demonstrated moderate discrimination (area under the curve (AUC) = 0.70; 95% confidence interval (CI): 0.66-0.74; sensitivity = 79.80%; specificity = 54.12%). Calibration curve and decision curve analysis (DCA) suggested good predictive accuracy and clinical net benefit. (2) Using machine learning, a random forest model was constructed based on four features (SDNN, LDL-C, age, MONO#). Internal validation with ROC analysis showed excellent discrimination (AUC = 0.92; 95% CI: 0.89-0.95; sensitivity = 84.0%; specificity = 82.3%). (3) During the external validation phase, the logistic regression model showed limited performance (AUC = 0.59; 95% CI: 0.50-0.68; sensitivity = 58.92%; specificity = 58.24%), and the calibration curve and DCA curve showed only average model performance. In contrast, external validation of the random forest model yielded better discrimination (AUC = 0.71; 95% CI: 0.63-0.79; sensitivity = 84.5%; specificity = 53.0%). Conclusion:(1) Decreases in resting and stress left ventricular ejection fraction (LVEF) in patients with INOCA are more readily detected by PET/CT examination. (2) The risk of INOCA is closely associated with smoking history, SDNN, LDL-C, MONO#, and HCT. (3) Compared with multiple logistic regression analysis, the random forest prediction model shows more accuracy in predicting INOCA.
Although left atrial (LA) function is of major clinical importance in cardiovascular diseases, traditional indicators such as LA volume struggle to promptly reflect functional changes. In recent years, the emerging technique of left atrial strain (LAS) has garnered widespread attention. As a quantitative metric based on speckle tracking echocardiography, LAS can detect subtle functional abnormalities in the LA myocardium at an early stage and independently assess atrial reservoir, conduit, and contraction functions beyond volume changes. Numerous recent studies have demonstrated the significant clinical utility of LAS across multiple cardiovascular conditions, including heart failure, atrial fibrillation, hypertension, valvular heart disease, and coronary artery disease. Furthermore, LAS exhibits prognostic value in cardiomyopathies and cancer therapy-related cardiotoxicity. This review summarizes recent advances in LAS across various cardiovascular diseases, objectively evaluates its clinical application prospects and limitations, and outlines future research directions.
Cardiovascular diseases (CVDs) are the leading cause of death and disability worldwide, and atherosclerosis (AS) is a major underlying pathology. This review systematically examines the interplay between inflammation and immunity in AS. Disease initiation involves endothelial injury, formation of oxidized low-density lipoprotein (ox-LDL), and innate immune responses, including monocyte and macrophage infiltration and dendritic cell (DC) activation. Macrophages polarize to a proinflammatory M1 phenotype, phagocytose lipids to form foam cells, and release inflammatory mediators such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), thereby exacerbating plaque inflammation. DCs serve as a crucial link between innate and adaptive immunity by presenting antigens to CD4+ T cells. T helper 1 (Th1) cells facilitate inflammation through interferon-γ (IFN-γ), whereas regulatory T cells (Tregs) exert protective, anti-inflammatory effects. B cells have dual functions: B1 cells secrete immunoglobulin M (IgM) and provide protection, while B2 cells typically contribute to disease progression. In advanced lesions, immune cells cluster within the arterial wall to form arterial tertiary lymphoid organs (ATLOs), and the identification of neuro-immune-cardiovascular interfaces (NICIs) underscores the involvement of the nervous system. Chronic inflammation results in the thinning of the fibrous cap, thereby heightening the risk of plaque rupture and acute clinical events. Current therapies primarily target inflammatory pathways, including statins, colchicine, and proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i), whereas future strategies may focus on directly targeting immune cells.
Background:Eccentric pericardial effusions are non-circumferential fluid collections that may complicate conventional pericardiocentesis, yet the associated clinical characteristics remain poorly defined. Methods:This single-center retrospective comparative cohort study included adult patients with symptomatic pericardial effusion of undetermined etiology who underwent percutaneous pericardiocentesis under transthoracic echocardiographic or fluoroscopic guidance or a surgical pericardial window procedure. Based on preprocedural multi-view transthoracic echocardiography (TTE), effusions were classified as eccentric or circumferential. Baseline characteristics, imaging features, procedural outcomes, pericardial fluid analyses, etiologies, and short-term outcomes were compared. Univariable and multivariable logistic regression analyses were performed to identify factors associated with eccentric distribution. Results:Among 156 patients, 47 (30.1%) had eccentric pericardial effusions. In multivariable analysis, a chronic course (odds ratio (OR) 6.31, 95% confidence interval (CI) 2.68-14.85; p < 0.001) and higher body temperature (per 1 °C increase: OR 2.52, 95% CI 1.13-5.63; p = 0.024) were independently associated with eccentric effusion. Compared with circumferential effusions, eccentric effusions showed a different distribution of dominant maximal-depth sites (overall p = 0.026), with a higher proportion of maximal depth located along the left ventricular lateral wall (57.45% vs. 33.03%). Eccentric effusions also had a shallower anterior echo-free space (5 [3-7] vs. 11 [7-15.9] mm, p < 0.001), and showed fewer classic tamponade signs, including right ventricular diastolic collapse (12.77% vs. 39.45%, p < 0.001). Procedurally, eccentric effusions more frequently required fluoroscopic guidance (44.68% vs. 10.09%, p < 0.001), had lower drainage volumes (600 mL vs. 914 mL, p = 0.005), and showed a higher incidence of poor drainage (44.68% vs. 8.26%, p < 0.001). The etiologic spectrum of eccentric effusions was more heterogeneous and less likely to be malignant (31.91% vs. 55.96%). In-hospital and 90-day outcomes were comparable between groups. Conclusions:In this symptomatic drainage cohort, eccentric pericardial effusions were associated with a chronic course and higher body temperature and were characterized by left ventricular lateral predominance, fewer classic echocardiographic signs of tamponade, and greater reliance on fluoroscopic guidance for drainage. The etiologic spectrum of eccentric effusions was more heterogeneous and less likely to be malignant.
Atherosclerotic cardiovascular disease (ASCVD) is associated with increased morbidity and mortality rates. Numerous studies have shown that lowering low-density lipoprotein cholesterol (LDL-C) levels can reduce the occurrence of cardiovascular disease (CVD). Current data indicate that 80% of patients with ASCVD do not achieve the LDL-C targets recommended by clinical guidelines. Nearly 15% of patients with hypercholesterolemia exhibit statin intolerance, with some experiencing severe adverse reactions such as liver function abnormalities and rhabdomyolysis. Statins require daily administration, and proprotein convertase subtilisin/kexin type 9 (PCSK9) monoclonal antibodies should be injected 12 to 26 times annually. Frequent dosing reduces patient adherence. This review comprehensively discusses inclisiran, the first lipid-lowering small interfering RNA (siRNA) drug, focusing on the associated mechanism of action, pharmacology, clinical trial data, efficacy, safety, use in special populations, and adverse effects. The objective is to provide evidence to guide the appropriate clinical use of inclisiran, a novel option for lipid-lowering therapy. Inclisiran may represent another milestone in the treatment of dyslipidemia.
Background:Clinically, coronary microvascular dysfunction (CMD) remains a significant diagnostic challenge because the associated symptoms frequently overlap with obstructive coronary artery disease (CAD). This condition may contribute to cardiac ischemic events regardless of the presence of obstructive epicardial lesions. While inflammatory pathways, particularly those involving epicardial adipose tissue (EAT) accumulation, play a central role in the development of CMD, the specific influence of EAT quality, as reflected in the associated density-based composition, remains poorly understood. Methods:This retrospective study (n = 155) analyzed a single primary vessel per patient to ensure independence of data. Based on invasive physiological assessment, patients were stratified into an isolated CMD group (n = 81), defined as fractional flow reserve (FFR) ≥0.75 with coronary flow reserve (CFR) <2.5 and/or index of microcirculatory resistance (IMR) ≥25 and a non-CMD control group (n = 74), which included patients with obstructive CAD (FFR <0.75, stenosis >50%) and those with normal physiology. Quantitative assessment using coronary computed tomography angiography (CCTA) applied a range of -190 to -15 Hounsfield units (HU). Perivascular inflammation was evaluated by measuring the low-attenuation adipose volume (LAAV) (<-75 HU) as a percentage of total EAT (LAAV%). Independent determinants of CMD were identified using multivariable logistic regression models. Results:Multivariable analysis identified standardized LAAV% as the primary independent predictor of CMD. Specifically, each one-standard deviation (SD) increase in LAAV% was associated with a 147.1% increase in odds of CMD (odds ratios (OR) = 2.471, 95% confidence interval (CI): 1.577-4.128, p < 0.001). The predictive framework demonstrated robust performance (area under the receiver operating characteristic curve (AUC) = 0.810). Additional significant risk factors included body mass index (BMI) (OR = 1.380) and smoking history (OR = 4.005, p = 0.023). Conclusions:Low-attenuation areas of EAT, particularly as quantified by standardized LAAV%, are strong independent predictors of CMD. The integration of LAAV% into non-invasive risk assessments may improve diagnostic accuracy and help inform targeted interventions for CMD.
Aortic root abscess (ARA) is a life-threatening complication of infective endocarditis (IE) associated with high mortality despite advances in diagnosis and treatment. We conducted a focused review of the clinical characteristics, diagnosis, imaging modalities, causative pathogens, treatment strategies, and outcomes of ARA. This review summarizes results from studies evaluating different surgical approaches for ARA and discusses emerging diagnostic and therapeutic innovations. The mortality rate of ARA complicating IE ranges from 12.2% to 30%. Early diagnosis remains challenging, and multiple surgical approaches are available. The choice of surgical approach depends primarily on the extent and anatomical distribution of the abscess. This review underscores the need for improved diagnostic strategies and optimized surgical strategies to enhance outcomes and long-term prognosis in patients with ARA.
The application of cardiopulmonary bypass (CPB) has significantly advanced cardiovascular surgery. However, CPB-associated brain injury remains a critical complication that affects patient prognosis and quality of life. Overt stroke occurs in approximately 1-5% of cases, while postoperative delirium affects 20-50% of patients, and perioperative neurocognitive disorders are reported in 10-40%, depending on the diagnostic criteria used. This narrative review provides a comprehensive summary of recent research progress on CPB-associated brain injury in cardiac surgery, along with a critical appraisal of the supporting evidence. While the main focus is on adult patients, various pediatric conditions are also discussed. We review the evolution of CPB technology; the classification and clinical burden of brain injury; detailed pathophysiological mechanisms, including hemodynamic injury, microembolism, systemic inflammatory response, and blood-brain barrier disruption; current cerebral protection strategies advances in personalized cerebral perfusion. Furthermore, special consideration is given to genetic susceptibility (such as apolipoprotein E (APOE) polymorphisms), and pediatric cardiac surgery. A systematic screening of high-quality literature from the past five years highlights the challenges that continue to impede clinical translation, despite progress in neuromonitoring and minimally invasive CPB technologies. Future research directions include the application of artificial intelligence and real-time cerebral autoregulation monitoring to support the transition from empirical medicine to precision, individualized cerebral protection.
Coronary no-reflow (NF) and slow-flow (SF) are serious complications following percutaneous coronary intervention (PCI) and are associated with adverse prognoses, with microvascular obstruction (MVO) as the central underlying mechanism. Intravascular imaging techniques, including intravascular ultrasound (IVUS), optical coherence tomography (OCT), and near-infrared spectroscopy (NIRS), enable high-resolution, multidimensional (structural, compositional, and functional) assessment of coronary lesions, thereby facilitating prediction of coronary NF and SF. IVUS, with a penetration depth of 4-8 mm, can identify predictive features such as plaque rupture, attenuated plaque, positive remodeling, and large necrotic cores. OCT, with a spatial resolution of 10-20 μm and a penetration depth of 1-2 mm, is capable of detecting thin-cap fibroatheromas, cholesterol crystals, and intraplaque vasa vasorum. NIRS quantifies lipid content using the parameter maximum 4 mm lipid core burden index (maxLCBI4mm), which demonstrates favorable predictive performance for NF and SF phenomena. When the OCT-derived fibrous cap thickness is <55 µm, the area under the curve (AUC) for predicting NF is 0.985 (95% confidence interval (CI): 0.968-1.000); meanwhile, the corresponding sensitivity and specificity for predicting SF are 93.5% and 96.7%, respectively. When the NIRS-derived maxLCBI4mm is ≥578, the AUC for predicting SF is 0.849.
Cardiogenic shock (CS) is the most serious heart failure manifestation, characterised by a significant risk of morbidity and mortality despite improving diagnosis and treatment: early recognition and accurate hemodynamic phenotypization are crucial to improve its poor prognosis. Recently, point-of-care ultrasound (PoCUS) has evolved as a key method in emergency settings for fast shock assessment. Evidence indicates that PoCUS improves the clinician's diagnostic accuracy by identifying ventricular dysfunction, valvular disease, complications of myocardial infarction, loading conditions, and systemic congestion. Multiorgan protocols that combine cardiac, pulmonary, and vascular assessments enable differentiation among cardiogenic, obstructive, hypovolemic, and distributive shock. Echocardiographic parameters-including ventricular function, volume indices, and dynamic measures such as stroke volume and cardiac output-can guide fluid management, vasoactive therapy, and circulatory support. Limitations include operator dependence and potential imaging challenges due to patient factors. When combined with clinical and laboratory data, PoCUS is a fundamental tool for early CS assessment. With this paper, we aimed to describe the role of PoCUS in the differential diagnosis of undifferentiated shock, confirming or ruling out CS, assessing CS prognosis, guiding appropriate treatment and enabling hemodynamic monitoring. Integrating PoCUS elements with validated classifications, such as the Society for Cardiovascular Angiography and Interventions (SCAI) CS stages, can be useful for improving CS management. This review highlights validated PoCUS markers, practical PoCUS applications within the SCAI framework, and areas for further research, emphasising the increasing role of PoCUS in personalised, physiology-guided management of CS in the emergency department.
