搜索结果：Circulation. Cardiovascular imaging

Artificial intelligence (AI) is increasingly embedded across cardiovascular care, serving as a powerful adjunct for symptom assessment, bedside examination, electrocardiography, and multimodality imaging interpretation. We aim to thoroughly review current evidence for AI applications across the cardiovascular diagnostic pathway and to highlight key considerations for clinical integration. We performed a narrative review of clinical trials and observational studies retrieved from MEDLINE/PubMed, Embase, and Google Scholar (January 1st 2000-July 10th 2025), limited to publications in English, using AI- and cardiovascular diagnostic specific search terms. Regulatory resources [e.g., U.S. Food and Drug Administration (FDA) clearance databases and publicly available summaries] were also reviewed to identify cardiovascular AI software with regulatory authorization. Across diagnostic domains, AI has demonstrated potential to improve diagnostic performance and workflow efficiency. Large language models and other AI systems can support structured history-taking, triage, and automated clinical documentation. Digital stethoscope and phonocardiography algorithms enable scalable screening for murmurs and valvular disease with a higher sensitivity for murmur detection compared with conventional auscultation. Electrocardiography-based AI models have been reported for rapid detection of arrhythmias, ischemia, and heart failure with reduced ejection fraction (EF). In echocardiography, AI enables automated view classification, chamber quantification, EF estimation, and valve assessment, while substantially reducing acquisition and processing time. Advanced imaging tools support coronary computed tomography (CT) angiography plaque characterization, calcium scoring, and CT-derived fractional flow reserve (FFR), as well as cardiac magnetic resonance segmentation and scar/late gadolinium enhancement (LGE) quantification. However, much of the evidence remains retrospective with heterogeneous endpoints, and outcome-improving, prospective, real-world integration studies remain limited. Future work should prioritize multicenter prospective validation and implementation studies that address model generalizability, quality control, bias, data drift, and governance. Multimodal, workflow-embedded AI systems that fuse clinical and imaging signals may ultimately enable individualized risk prediction and improve access and cardiovascular outcomes.

Neurological injury remains a major complication of pediatric cardiac surgery and is closely related to alterations in cerebral blood flow during extracorporeal circulation (ECC). However, the real-time assessment of cerebral perfusion under these conditions has been limited by the lack of magnetic resonance (MR)-compatible perfusion systems. The aim of this pilot feasibility study was to establish a porcine model enabling simultaneous cardiopulmonary bypass (CPB) and real-time MR-based assessment of cerebral blood flow during simulated pediatric cardiac surgery. We conducted a pilot study on 11 Duroc pigs (14.6 ± 1.4 kg BW), designed in iterative cycles. The experimental setup included an MR-conditional heart-lung machine and a surgical protocol closely mimicking pediatric cardiac surgery. After the initiation of CPB and hemodynamic stabilization, animals were cooled to target temperatures (20 °C or 28 °C) depending on the perfusion strategy. Structural and functional MRI, including phase-contrast imaging, arterial spin labeling, diffusion-weighted imaging, and MR spectroscopy, were performed during cooling and rewarming. Procedural feasibility, technical challenges, and optimization strategies were systematically documented. The study successfully established a reproducible porcine model enabling MR imaging during extracorporeal circulation. Key technical challenges, including vascular access, cannulation of the ascending aorta, and blood volume management, were identified and addressed through the iterative refinement of the surgical and perfusion protocols. The use of the Seldinger technique significantly improved cannulation safety and reduced blood loss. Stable CPB conditions and target hypothermic temperatures were achieved in successfully cannulated animals. MRI acquisition during CPB was feasible, providing simultaneous structural and functional assessment of cerebral perfusion. Representative imaging data demonstrate the capability of the model to capture cerebral hemodynamics in real time. This pilot study establishes a novel MR-compatible porcine model for the real-time assessment of cerebral blood flow during extracorporeal circulation. The platform provides a robust foundation for future quantitative investigations of cerebral perfusion, mechanisms of brain injury, and neuroprotective strategies in pediatric cardiac surgery.

The cardiovascular system is among the earliest functional systems in fetal development, playing a central role in maintaining circulation and ensuring oxygen and nutrient delivery. The fetal heart undergoes continuous maturation in anatomical configuration, hemodynamics, and biventricular coupling throughout gestation. Recent advances in ultrasound imaging-including Doppler, tissue doppler imaging (TDI), and two- and three-dimensional speckle tracking-have enabled comprehensive assessment of fetal cardiac structure and function. In addition, emerging techniques such as fetal heart quantification and multimodal imaging, along with artificial intelligence-based approaches, may offer new perspectives for evaluating ventricular coupling. This review indicates that pathological changes such as congenital heart disease (CHD) and premature closure of the ductus arteriosus can lead to fetal cardiac structural abnormalities and hemodynamic disturbances. Based on the core mechanism of biventricular decoupling in adults, these changes form the pathophysiological basis for impaired fetal biventricular coupling. Accordingly, further exploration is warranted for the evaluation of fetal biventricular coupling status. Subsequent studies should first establish its normal reference criteria and clarify the correlation between this indicator and perinatal outcomes.

Ischemic cardiovascular and cerebrovascular diseases remain the leading causes of morbidity and mortality worldwide. Reactive oxygen species (ROS) act as central mediators of ischemia-induced injury, connecting mitochondrial dysfunction, calcium overload, inflammatory activation, endothelial damage, and maladaptive tissue remodeling. However, conventional antioxidant therapies have demonstrated limited clinical efficacy due to poor bioavailability, short circulation half-lives, insufficient lesion specificity, and systemic off-target effects. Consequently, ROS-responsive nanosystems have emerged as promising nanotheranostic platforms that exploit oxidative stress as both a diagnostic cue and a therapeutic trigger for lesion-selective intervention. This review summarizes the sources and pathophysiological roles of ROS in ischemic heart and brain injury, and critically examines recent advances in ROS-guided nanodiagnostics and nanotherapeutics across major ischemic cardiovascular and cerebrovascular conditions. Diagnostic progress is discussed in relation to direct redox-activatable probes, ROS-associated surrogate probes, and multimodal or self-reporting platforms across major imaging modalities. Therapeutic applications are reviewed in the context of atherosclerosis, myocardial ischemia-reperfusion injury, heart failure progression, ischemic stroke, and thrombotic disease, with an emphasis on catalytic ROS scavenging, ROS-triggered local drug release, and targeted theranostic nanoplatforms for lesion-selective intervention. Key translational priorities include oxidant specificity, quantitative validation, biosafety, scalable manufacturing, control of in vivo biological identity, and clinically actionable endpoints aligned with disease stage and treatment timing.

Computational models of cardiac mechanics can improve diagnosis, surgical planning, and device design; yet their accuracy is limited by the quality of the underlying imaging data used in routine care. Our team recently reported a free-breathing, four-dimensional cardiac magnetic resonance imaging (MRI) protocol (AutoCMR), which provides 30 volumetric frames per cardiac cycle at 1.6mm isotropic resolution. Here, we investigate whether this high spatiotemporal resolution imaging data, along with cuff systolic and diastolic blood pressures (SBP, DBP), improves non-invasive calibration and internal consistency of patient-specific 0D lumped-parameter and 3D finite element (FE) cardiac models. Five adults were imaged with the AutoCMR protocol. Every frame was segmented to obtain left ventricular (LV) and left atrial (LA) volume-time curves. These curves and SBP/DBP calibrated a closed-loop 0D model of LA, LV, and the systemic circulation. To assess the impact on key metrics, the LV elastance up-stroke exponent was varied, while all other calibrated parameters remained fixed. The resulting pressure-volume metrics included end-systolic elastance, effective arterial elastance, ventriculo-arterial coupling, stroke volume, ejection fraction, and stroke work. The calibrated parameters initialized a subject-specific 3D FE LV model. Simulated chamber volumes closely matched MRI, with LV volume root mean square error (RMSE) of 5.55±1.13mL with R2=0.951 for 0D; and 7.76±1.65mL with R2=0.931 for 3D. Similarly, LA volume RMSE was 3.55±2.61mL with R2=0.976 for 0D and 4.32±2.64mL with R2=0.973 for 3D. Absolute LV peak-to-cuff systolic pressure target differences averaged 2.81±1.91mmHg (0D) and 4.81±1.10mmHg (3D), while absolute arterial diastolic pressure target differences were 1.64±1.33mmHg (0D) and 1.58±1.51mmHg (3D). In baseline-referenced sensitivity analysis, the 30-frame cine constraints kept mid-systolic LV pressure deviations ∼3-4 mmHg, compared to ∼18-25 mmHg when only end-diastolic and end-systolic constraints were used. Thirty-frame 3D cine MRI at 1.6mm isotropic resolution, combined with SBP/DBP, supported non-invasive calibration of 0D lumped parameter and 3D FE models with close in-sample agreement to MRI-derived volumes and cuff-pressure targets. The achieved in-sample agreement indicates that this AutoCMR-based simulation approach has the potential to support patient-specific computational assessments of cardiac function in clinical settings.

The aim of this study was to translate the Attitudes and Beliefs about Cardiovascular Disease (ABCD) Risk Questionnaire into Norwegian and assess its psychometric properties among individuals with a history of myocardial infarction. The study adopted a cross-sectional design. The original questionnaire was translated into Norwegian and adapted for use in the target population. The Norwegian version was pilot tested in a sample of patients and then validated in the target population. Norway, using a web-based solution to collect data. A random sample of Norwegian individuals <85 years old with a history of myocardial infarction and no cardiovascular disease before their first myocardial infarction. Internal consistency was tested using Cronbach's &#x3b1; and test-retest reliability using intraclass correlation coefficient (ICC). Difficulty and discrimination indices were determined for the Knowledge scale. Confirmatory factor analysis (CFA) was used to assess structural validity of the Risk scale. Data for 746 participants (mean age, SD: 66.4, 10.3 years), of which 26.9% females were analysed. The Norwegian version showed satisfactory internal consistency (Cronbach's &#x3b1; 0.73-0.79)&#x2009;but modest test-retest reliability (ICC 0.35-0.64). The Knowledge scale showed moderate difficulty (0.39-0.84)&#x2009;and good discrimination power (0.44-0.60). The one-factor model CFA for each scale achieved acceptable fit, and the four-factor model showed moderate fit (root mean square error of approximation=0.05, standardised root mean squared residual=0.07, Comparative Fit Index=0.91, Tucker-Lewis Index=0.88). The Norwegian translated ABCD Risk Questionnaire demonstrated satisfactory psychometric properties and can be considered a useful instrument for assessing knowledge and risk perception among individuals with a history of myocardial infarction.

The 2021 ESC guidelines on cardiovascular (CV) disease prevention recommend the SMART-REACH lifetime risk model to guide treatment decisions in patients with established atherosclerotic CV disease. The aim was to develop the SMART-REACH2 model for estimating lifetime risk of recurrent CV events and treatment benefits in patients with established atherosclerotic CV disease, with systematic recalibration to the four European and other global risk regions. SMART-REACH2 was derived in 8708 individuals aged 40-90 years with coronary, cerebrovascular, peripheral artery disease and/or abdominal aortic aneurysm from the UCC-SMART cohort. Sex-stratified, cause-specific Cox models for recurrent CV events and non-CV death were fitted using age as timescale and routinely available predictors. Recurrent CV events were defined as a composite of myocardial infarction, stroke, or CV death. Recalibration was based on representative cohorts per risk region. External validation was performed in 2 085 780 patients from 54 countries; model performance was assessed by calibration plots and Harrell's C-statistic. In the derivation cohort, 2057 recurrent CV events occurred over a median follow-up of 8.5 years (25th-75th: 4.3-13.0). In external validation, 307 706 events occurred. The pooled C-statistic was 0.68 (95% confidence interval 0.66-0.69) and ranged from 0.66 (0.64-0.69) for European low-risk region up to 0.72 (0.66-0.78) for Latin America, with adequate calibration across risk regions. Performance was consistent across sexes and CV disease subtypes. Using SMART-REACH2, estimated potential gains in CV disease-free life expectancy for a 50-year-old example patient receiving intensified preventive treatment (15 mmHg systolic blood pressure and 1.0 mmol/L low-density lipoprotein cholesterol reduction) ranged from 2 years in the low-risk region to 4.4 years in the very-high-risk region. The updated SMART-REACH2 model accounts for geographical and sex-specific variations and allows estimation of short-term and lifetime risk of recurrent CV events and treatment benefits, facilitating shared decision-making as recommended by guidelines.

Intravascular imaging (IVI) during percutaneous coronary intervention (PCI) improves outcomes. Pullback pressure gradient characterizes coronary artery disease patterns as focal or diffuse; however, the benefit of IVI across this spectrum remains incompletely understood. We aimed to evaluate clinical outcomes after PCI with or without IVI guidance in patients with focal and diffuse disease defined by pullback pressure gradient. Prospective, multicenter, single-arm study of 811 patients (840 vessels) undergoing PCI. Pullback pressure gradient was calculated from manual fractional flow reserve pullbacks to define focal (pullback pressure gradient &#x2265;0.62) or diffuse coronary artery disease. IVI use was at the operator's discretion. The primary outcome was target vessel failure at 1-year follow-up. IVI-guided PCI was performed in 41% of patients. In the overall cohort, target vessel failure was lower with IVI guidance (adjusted hazard ratio, 0.60 [95% CI, 0.36-0.99]; P=0.044), with a lower incidence of cardiac death (P=0.042). The results were consistent irrespective of the baseline coronary artery disease pattern (Pinteraction=0.128). Among patients with focal disease, IVI-guided PCI was associated with a significantly lower incidence of target vessel failure compared with non-IVI-guided PCI (hazard ratio, 0.41 [95% CI, 0.18-0.91]; P=0.029). There was no statistical difference in target vessel failure with the use of IVI among patients with diffuse disease (hazard ratio, 0.91 [95% CI, 0.48-1.73]; P=0.771). In patients undergoing physiology-guided PCI, the use of IVI reduced clinical events at 1 year. These findings suggest that the benefit of IVI extends across the full spectrum of coronary artery disease.

Coronary microvascular dysfunction often coexists with epicardial coronary artery disease. Data regarding its prevalence and prognosis in patients undergoing invasive coronary angiography are scarce. This study aimed to evaluate the prevalence and prognosis of coronary microvascular dysfunction in patients undergoing clinically indicated invasive coronary angiography in routine practice. In this prospective, multicentre cohort study done in seven tertiary medical hospitals in South Korea, consecutive patients aged 18 years and older who were referred for clinically indicated invasive coronary angiography were systematically screened and evaluated by coronary physiological assessment. Obstructive epicardial coronary artery disease was defined as an intermediate stenosis (40-90% diameter stenosis), with fractional flow reserve of 0&#xb7;80 or less or severe stenosis (>90% of diameter stenosis) treated with revascularisation without fractional flow reserve measurement. Coronary microvascular dysfunction was identified as coronary flow reserve below 2&#xb7;0 and index of microcirculatory resistance of &#x2265;25. The primary endpoint was a composite of all-cause death, myocardial infarction, clinically driven repeat revascularisation, or hospitalisation for heart failure. The Multicenter FLOW-CMD Registry study is registered with ClinicalTrials.gov (NCT05369182). Between April 22, 2022, and Nov 19, 2024, 5764 patients were screened and 1003 patients were enrolled (756 men and 247 women). Among these patients, coronary microvascular dysfunction was observed in 123 (21&#xb7;5%) of 573 patients with obstructive epicardial coronary artery disease and in 40 (9&#xb7;3%) of 430 patients without obstructive epicardial coronary artery disease. At a median follow-up of 1&#xb7;9 years, the primary endpoint occurred in 26 patients (2-year Kaplan-Meier estimate 18&#xb7;8%) with coronary microvascular dysfunction and 70 patients (2-year Kaplan-Meier estimate 10&#xb7;5%) with preserved microvascular function (hazard ratio 1&#xb7;91 [95% CI 1&#xb7;22-2&#xb7;99]; p=0&#xb7;0047). In patients with suspected ischaemic heart disease undergoing invasive coronary angiography, coronary microvascular dysfunction coexisted with epicardial coronary artery disease and was associated with a higher risk of the composite of all-cause death, myocardial infarction, clinically driven repeat revascularisation, or hospitalisation for heart failure. Abbott Vascular and Boston Scientific.

Global Vhl knockout results in vascular defects and early lethality, limiting our knowledge of von Hippel-Lindau/HIF (hypoxia-inducible factor) signaling in coronary vessel formation and homeostasis. The hypoxia pathway has been implicated in cardiovascular diseases characterized by inflammation and vascular remodeling, such as atherosclerosis, but its involvement in Kawasaki disease (KD) remains unknown. Coronary artery dilation and vessel rupture are the most serious complications of KD. However, the molecular mechanisms underlying these cardiac events are not fully understood. We investigated the role of the von Hippel-Lindau/HIF pathway in cardiovascular pathology and its relevance to KD. We generated a novel mouse model with genetic hyperactivation of the hypoxia pathway in progenitors contributing to coronary vessels and cardiac fibroblasts. We characterized the model using echocardiography, magnetic resonance imaging, histology, and molecular profiling. In parallel, we examined cardiac tissues from patients with KD with fatal coronary aneurysms for evidence of HIF signaling and inflammation using immunohistochemistry. Mice with conditional deletion of Vhl in Wt1 (Wilms tumor 1)-expressing cells developed normally but exhibited cardiomegaly, vascular abnormalities, progressive coronary artery dilation, pericardial hemorrhage, and systemic inflammation shortly after birth. Histologic analysis revealed coronary arteritis, elastin breaks, vascular remodeling, smooth muscle cell loss, perivascular fibrosis, and frequent intracoronary thrombus formation. In addition, vascular calcification, severe cardiac inflammation, and interstitial hemorrhages were observed, culminating in sudden death between 15 and 20 weeks of age, likely due to vessel rupture. Cardiac transcriptomic profiling identified dysregulated expression of genes involved in extracellular matrix organization, epithelial-mesenchymal transition, angiogenesis, inflammation, coagulation, and calcification, indicating compromised vascular stability and increased remodeling in Vhl conditional knockout mice. Simultaneous deletion of Hif2a rescued both the cardiovascular abnormalities and transcriptomic profile observed in Vhl conditional knockout mice, implicating Hif2 (hypoxia-inducible factor 2) as a key mediator. Human KD cardiac samples showed expression of HIF2 in coronary lesions and surrounding inflammatory infiltrates, confirming hypoxia pathway activation in severe KD. Our findings establish HIF2 as a central driver of coronary inflammation, vascular remodeling, and thrombotic complications resembling those observed in severe KD. The Vhl/Wt1 conditional knockout mouse model recapitulates key cardiovascular features of KD and offers a valuable platform for mechanistic studies and therapeutic exploration.

Hypertension induces structural and functional damage in multiple organs. Evidence of subclinical damage increases risk of vascular events and death but can be difficult to identify in the clinic. We developed a novel machine learning approach that quantifies current hypertension-associated multiorgan damage, mapping progression from health to advanced disease, in a pseudotemporal manner and predicts organ-specific disease progression trajectories. We analyzed 566 multimodal imaging and nonimaging variables from 27 099 participants in the UK Biobank imaging substudy to develop a semisupervised contrastive trajectory inference (cTI) framework that models multiorgan alterations associated with hypertension exposure, including heart, brain, kidneys, vasculature, lungs, liver, and metabolic information. Model stability was validated through multiple internal validation steps, and external validity was tested on 5507 participants from the Atherosclerosis Risk in Communities study (ARIC). Clinical relevance was evaluated against existing risk scores and through ability to predict survival and incident multiorgan disease for up to 7 years, across both UK Biobank and ARIC. In the UK Biobank (mean age 63.27&#xb1;7.48 years; 53.4% women) our global organ damage score (HyperScore) achieved an area under the curve of 0.964 (0.941-0.987) for identification of individuals with severe end-organ disease and robust stability in cross-validation with a mean root mean square error of 0.104&#xb1;0.084. Survival odds differed significantly across HyperScore stages (P<0.001), whereas stratification by blood pressure was nonsignificant. We further revealed 6 hypertensive disease phenotypes (HyperTrajectory), characterized by predominant cardiac, lipoprotein, atherothrombosis, brain, cardiorenal, and liver features, respectively. External testing in ARIC confirmed stability of the model, with Jensen-Shannon distances as low as 0.10 for HyperScore distributions, without significant deviation in organ damage progression patterns (P>0.05) and consistent end-organ and outcome characteristics between ARIC and UK Biobank across HyperTrajectories. Machine learning-derived global organ damage scores are feasible in hypertension and enable identification of distinct hypertension-associated organ-disease phenotypes. New frameworks for hypertension assessment and monitoring using imaging to derive personalized risk assessment and phenotype-specific intervention may be achievable.

Myocardial flow reserve (MFR) reflects the ability of the coronary circulation to augment blood flow in response to increased demand, integrating both epicardial and microvascular function. Although its prognostic value has been demonstrated with invasive techniques and positron emission tomography (PET), evidence using cadmium-zinc-telluride (CZT) single-photon emission computed tomography (SPECT) remains limited. The aim of this study was to evaluate the prognostic impact of MFR assessed by CZT-SPECT in patients with and without obstructive coronary artery disease (CAD). We retrospectively analyzed 452 consecutive patients who underwent one-day rest/stress &#x2c6;99mTc-sestamibi dynamic CZT-SPECT for MFR quantification. MFR was calculated as the ratio of stress to rest myocardial blood flow, with values <2 considered abnormal. Median follow-up was 792 days. Follow-up was censored at the last documented clinical visit for patients without events. Adverse cardiovascular events included angina, myocardial infarction, stroke, revascularization, hospitalization for angina or heart failure, and death. Major adverse cardiovascular events (MACE) were defined as death, myocardial infarction, revascularization, or stroke. Kaplan-Meier survival curves and Cox proportional hazard models were used, and incremental prognostic value was assessed with the C-index and likelihood ratio tests. Among 452 patients (mean age 63 &#xb1; 12 years, 54% male), 190 (42%) had MFR <2. During follow-up, 190 total events and 63 major events occurred. All deaths (n=7) were observed in the reduced MFR group. MFR <2 was significantly associated with a higher risk of total events (hazard ratio [HR] 3.8, 95% confidence interval [CI] 2.5-5.7; p<0.001) and major events (HR 7.9, 95% CI 3.5-17.6; p<0.001). Incorporating MFR improved predictive performance (C-index from 0.63 to 0.77 for total events and from 0.76 to 0.84 for MACE; both p<0.001). MFR <2 assessed by CZT-SPECT significantly predicted adverse cardiovascular outcomes, including death, and provided incremental prognostic value beyond clinical risk factors and relative perfusion imaging. Routine incorporation of MFR assessment may improve risk stratification and guide personalized management of chronic coronary syndromes.

Immune checkpoint inhibitors (ICIs) have transformed the therapeutic landscape of oncology but are increasingly associated with cardiovascular immune-related adverse events (irAEs), including myocarditis, heart failure, arrhythmias, and vascular complications. Among these, ICI-associated myocarditis represents the most severe manifestation, often characterized by high mortality and challenging early diagnosis. Detecting subclinical myocardial injury before irreversible cardiomyocyte necrosis occurs remains a major unmet need in contemporary cardio-oncology. This narrative expert review critically examines the biological rationale, preclinical evidence, and emerging clinical data supporting the potential role of heart-type fatty acid-binding protein (H-FABP) as an adjunctive biomarker of early immune-mediated myocardial injury during ICI therapy. H-FABP is a small cytosolic lipid chaperone abundantly expressed in cardiomyocytes and rapidly released into the circulation following subtle membrane destabilization and metabolic stress, frequently preceding detectable troponin elevation in other forms of myocardial injury. Experimental studies support a mechanistic association between H-FABP release, inflammasome activation, cytokine amplification, mitochondrial dysfunction, and immune-metabolic cardiomyocyte stress. Preliminary clinical observations further suggest that H-FABP elevations may occur during ICI treatment even in the absence of overt myocarditis or concomitant increases in high-sensitivity cardiac troponins (hs-cTns). Although H-FABP cannot replace hs-cTn, which remains the cornerstone biomarker for the diagnosis of clinically significant ICI-associated myocarditis, its rapid kinetics and sensitivity to early metabolic membrane injury support its potential role as an investigational adjunctive biomarker for early surveillance and risk stratification. This approach may be particularly relevant in patients receiving high-risk combination ICI regimens or in individuals with pre-existing cardiovascular disease. However, current evidence remains limited, and large prospective multicenter studies integrating H-FABP with hs-cTns, natriuretic peptides, cardiac magnetic resonance imaging, and clinical outcomes are required before routine clinical implementation can be considered.

Cerebral air embolism (CAE) is a rare but potentially fatal complication, characterized by the entry of air bubbles into the arterial circulation, subsequently obstructing cerebral blood flow and causing ischemic injury. While CAE is a recognized risk in cardiovascular surgery, barotrauma, trauma of the chest or head, it remains an extremely rare complication of pleural procedures, which is even more exceptional when occurring during chest tube placement. To our knowledge, we report the first case of CAE induced by insertion of a small-bore (12 Fr) chest tube via a safety Verres needle technique in a patient with hydropneumothorax. The patient was admitted with cough, confusion, fever, and dyspnea. Diagnostic imaging, including a chest x-ray (CXR) and chest Computed Tomography (CT), detected a rightsided hydropneumothorax, which was also identified by thoracic ultrasound. During the 12 Fr chest tube insertion with the patient in the supine position, a sudden loss of consciousness and convulsions occurred. The patient was administered the Trendelenburg position and high-flow oxygen therapy, recovering consciousness within minutes, with residual neurologic deficits. A subsequent head CT scan revealed CAE. This case highlights an exceptionally rare but potentially devastating complication of pleural drainage insertion, underscoring the need for heightened clinical vigilance during all pleural procedures, regardless of procedural complexity or drainage size. Although thoracic ultrasound is fundamental for guiding chest tube placement, a thickened pleura is associated with increased procedural risk due to increased resistance. Clinicians should promptly recognize acute neurological deterioration during chest tube placement as a possible manifestation of CAE, performing an early neuroimaging and immediate management.

Carotid artery disease represents a significant clinical challenge in patients undergoing ophthalmic surgery due to its direct impact on cerebral and ocular perfusion. Its prevalence increases with age and is strongly associated with cardiovascular risk factors such as hypertension, diabetes mellitus, dyslipidemia, and smoking. These patients often present with impaired cerebral autoregulation, making cerebral blood flow highly dependent on systemic blood pressure. Consequently, even minor hemodynamic fluctuations during the perioperative period may precipitate ischemic complications. The pathophysiology involves both hypoperfusion and embolic mechanisms. Reduced cerebral blood flow, compounded by limited collateral circulation through the Circle of Willis, increases the risk of neurological injury. Simultaneously, embolization of atherosclerotic plaques may lead to acute cerebral or ocular events, including retinal artery occlusion and ischemic optic neuropathy. These risks highlight the importance of maintaining stable systemic and ocular perfusion throughout the surgical process. Preoperative evaluation requires a comprehensive neurological, cardiovascular, and imaging assessment to stratify risk and guide management. Intraoperatively, the primary objective is to preserve cerebral perfusion by maintaining stable mean arterial pressure and avoiding both hypotension and excessive hypertension. This is achieved through careful titration of anesthetic agents, appropriate fluid therapy, and the use of vasopressors when necessary. The choice of anesthetic technique should prioritize hemodynamic stability, with regional anesthesia and monitored sedation often preferred. Pharmacological management, including the selective continuation or withholding of medications, further contributes to optimizing outcomes. Overall, a tailored, multidisciplinary approach is essential to minimize perioperative complications and ensure patient safety.

Based on the Chapel Hill consensus criteria, the primary forms of vasculitis are classified by the predominant size of the affected blood vessels into large, medium, or small vessels. The two main forms of large vessel vasculitis (LVV) are giant cell arteritis and Takayasu arteritis, both of which are more prevalent in women while showing distinct geographic patterns of prevalence. The pathogenesis of LVV is complex and multifactorial, involving a combination of genetic predisposition, environmental and geographic triggers, immune dysregulation, and aging or (premature) senescence of the immune system and blood vessels. Diagnosis based on clinical presentation alone can be challenging because of the wide variety and often nonspecific symptoms that are associated with LVV. This has prompted the development of novel diagnostic tools to aid patient management, in particular advanced vascular imaging approaches. New therapies targeting specific immune pathways are now becoming available to improve outcomes while limiting the side effects associated with traditional glucocorticoid treatment. Advances in molecular imaging techniques may also enhance our ability to objectively monitor disease and treatment response in patients with LVV. Ongoing research aims to better understand the underlying mechanisms and to develop better targeted therapies for LVV, and to improve patient assessment and life time management. This narrative review will provide an in-depth update on current challenges and future trends in LVV, enhancing our understanding of its pathogenesis, diagnostic features, and management strategies, including disease- and treatment-related cardiovascular complications.

This study aimed to investigate the relationship between cerebral collateral status and MRI-derived oxygen metabolism in acute ischemic stroke (AIS) patients undergoing mechanical thrombectomy METHODS: The HIBISCUS-STROKE cohort (CoHort of Patients to Identify Biological an Imaging markerS of CardiovascUlar Outcomes in Stroke; NCT: 03149705), a single-center observational study, enrolled AIS patients for thrombectomy following MRI triage due to anterior circulation large vessel occlusion treated with mechanical thrombectomy. Dynamic-Susceptibility Contrast perfusion (DSC perfusion), Diffusion-Weighted Imaging (DWI) and penumbral volume (Tmax &#x2265; 6 secs) were post-processed to generate oxygen extraction fraction (OEF) and cerebral metabolic rate of oxygen (CMRO2) maps within DWI and penumbral anomalies, compared to contralateral areas. Collateral status, assessed via pretreatment digital subtraction angiography, was categorized as poor (0-2) or good (3-4) based on ASITN/SIR collateral grading system score from Higashida. A total of 137 patients were included (mean age 71 years; 56.2% male). The median National Institutes of Health Stroke Scale (NIHSS) score was 15 (interquartile range [IQR]: 8.0-18.0), and the median time from symptom onset to admission was 96.0 min ([IQR]: 78.0-137.0). 78 patients (57.00%) had good collaterals, while 59 patients (43.10%) had poor collaterals. Good collaterals were independently associated with a smaller baseline infarct core volume and less decrease in CMRO2 within the ischemic penumbra (respectively OR = 0.94; 95% CI: [0.92; 0.96]; (P < 0.0001), and (OR = 1.30; 95% CI: [1.06; 1.82]; P = 0.001). Good collateral circulation was independently associated with less severe impairment of cerebral metabolic rate of CMRO2 in the penumbra.

Primary aldosteronism (PA) carries excess cardiovascular risk not fully explained by hemodynamic load. While aldosterone promotes fibroblast activation experimentally, in vivo evidence linking adrenocortical activity with myocardial remodeling remains limited. This study integrated CXCR4 (C-X-C chemokine receptor type 4)-targeted 68Ga-Pentixafor positron emission tomography (PET)/magnetic resonance and FAP (fibroblast activation protein)-targeted 68Ga-FAPI-04 PET/cardiac magnetic resonance to evaluate the adrenal-cardiac axis in PA. Eighty-two participants (40 with PA [21 aldosterone-producing adenoma (APA), 19 idiopathic hyperaldosteronism], 21 with essential hypertension, and 21 normotensive controls) underwent 68Ga-FAPI-04 PET/cardiac magnetic resonance; 48 concurrently underwent 68Ga-Pentixafor PET/magnetic resonance. Adrenal CXCR4 and myocardial FAPI uptake, as well as integrated volumetric-uptake burdens, were quantified and correlated with clinical and cardiac magnetic resonance indices. Eight patients with APA underwent follow-up imaging postadrenalectomy. Adrenal volume-adjusted CXCR4 signal served as a reliable marker of in vivo aldosterone burden and was significantly associated with adverse left ventricular remodeling, independent of blood pressure levels or hypertension duration. Myocardial 68Ga-FAPI-04 uptake was detected in 55% of patients with PA (APA 71.4%, idiopathic hyperaldosteronism 36.8%), compared with 19% of patients with essential hypertension and 0% of controls (P<0.001), localizing predominantly to the basal septum. Importantly, total adrenal volume-adjusted CXCR4 signal correlated with myocardial FAPI activity (r=0.38-0.64; all P<0.05) and cardiac magnetic resonance markers of remodeling, both of which were positively associated with aldosterone levels. At 5.2&#xb1;1.2 months post-adrenalectomy, myocardial FAPI uptake in 8 patients with APA declined significantly (P<0.01), whereas late gadolinium enhancement and global cardiac function showed no significant change. URL: https://www.clinicaltrials.gov; Unique identifier: NCT06756737. Dual-tracer PET/magnetic resonance provided in vivo molecular evidence of a CXCR4-FAP-mediated adrenal-cardiac axis in PA, revealing cross-talk between adrenocortical function, aldosterone secretion, and myocardial fibroblast activation beyond blood pressure effects. FAPI PET demonstrated more severe myocardial activation in APA, with partial postadrenalectomy reversibility, underscoring the value of early diagnosis and timely surgical intervention.

Pulmonary arterial hypertension (PAH) is characterized by progressive remodeling of the pulmonary vasculature, leading to increased pulmonary vascular resistance and chronic right ventricular (RV) pressure overload. As RV dysfunction develops, ventricular interdependence alters the structural and functional relationship between the right and left ventricles. Although normal left-sided filling pressures define PAH, growing evidence indicates that left ventricular (LV) mechanics may be substantially affected. Leftward septal displacement, pericardial constraint, and reduced pulmonary venous return contribute to chronic underfilling of the left atrium and LV, impairing ventricular geometry and contractile dynamics despite preserved intrinsic myocardial function. However, secondary myocardial remodeling in advanced disease remains debated. These alterations may lead to subclinical or overt LV dysfunction and represent an underrecognized component of PAH pathobiology. Imaging markers such as LV global longitudinal strain, LV outflow tract velocity-time integral, and left atrial strain have emerged as potential indicators of left-sided involvement and may provide additional prognostic information. In this narrative review, we summarize current evidence on the pathobiological mechanisms linking RV dysfunction to left-sided cardiac alterations and discuss the role of ventricular interdependence in the coupling of the pulmonary circulation. Understanding this interaction may help redefine PAH as a progressive biventricular syndrome and may improve risk stratification and clinical assessment.