Obesity can lead to various forms of brain damage and cognitive impairments. The neuropathological mechanism may involve brain iron deposition and changes in cerebral blood flow perfusion. This study aims to use Quantitative Susceptibility Mapping (QSM) and Arterial Spin Labeling (ASL) to quantitatively assess brain iron deposition and Cerebral Blood Flow (CBF) in patients with obesity, and to explore their patterns of alteration and association with cognitive impairment. 37 patients with obesity and 45 controls underwent 3.0 T MRI and cognitive assessment. We compared susceptibility and cerebral blood flow values within automatically segmented regions of the interest and analyzed associations with cognition using partial correlations. Patients displayed increased iron in the left nucleus accumbens and bilateral red nuclei (p = 0.001, p = 0.001, p < 0.001) and abnormal perfusion in the right cerebellum, right middle frontal gyrus, left putamen, and right anterior cingulate gyrus (p < 0.001). Furthermore, iron deposition correlated with cognitive impairment. This study suggests that obese patients may exhibit iron deposition and perfusion abnormalities in certain areas of the brain. Bilateral red nuclei iron deposition is closely related to cognitive impairment. The multimodal combined application of QSM and ASL provides imaging evidence for revealing the impact of obesity on brain structure and function, and also provides potential biomarkers for targeted interventions in the future.

Sorafenib nanoparticles coated with Eudragit RL for ocular drug delivery: a potential treatment for diabetic retinopathy

Dynamic Cardiac SPECT and Flow Measurements for Evaluating Classical and Endogenous Myocardial Perfusion Abnormalities

Enhancing Hand Vascular Assessment: The Role of Hyperspectral Imaging in Perfusion Monitoring.

This study aims to investigate the impact of intravascular ultrasound (IVUS)-detected attenuated plaque (AP) on coronary microvascular dysfunction (CMVD) in patients with unstable angina undergoing percutaneous coronary intervention (PCI). The primary endpoints were the incidence of the no-reflow phenomenon, peri-procedural myocardial injury (PMI), post-procedural Thrombolysis in Myocardial Infarction (TIMI) myocardial perfusion frame count (TMPFC), and myocardial perfusion assessed by single-photon emission computed tomography (SPECT). This single-center, observational study, conducted in accordance with the STROBE guidelines, enrolled patients with unstable angina who underwent PCI with IVUS guidance. Based on IVUS findings, patients were retrospectively categorized into an AP group and a non-AP group. We compared the incidence of intraprocedural no-reflow, post-PCI cardiac biomarkers (cTnI and CK-MB), post-PCI TMPFC, and SPECT findings at baseline and 3 days post-PCI. Multivariable logistic regression analysis was performed to identify independent predictors of no-reflow, adjusting for confounders such as plaque burden. Secondary outcomes included major adverse cardiovascular and cerebrovascular events (MACCE) at 6-month follow-up. A total of 563 patients were included (229 in the AP group, 334 in the non-AP group). Baseline clinical and lesion characteristics were largely comparable, except for higher total cholesterol in the AP group (5.11 ± 0.37 vs. 4.98 ± 0.86 mmol/L, P = 0.031) and a significantly higher plaque burden in the AP group (76.8 ± 9.4% vs. 68.5 ± 10.2%, P < 0.001). The incidence of no-reflow was significantly higher in the AP group compared to the non-AP group (37.1% vs. 12.8%, P < 0.001). Post-PCI levels of cTnI (0.42 ± 0.28 vs. 0.15 ± 0.09 ng/mL) and CK-MB were significantly elevated in the AP group (P < 0.001), indicating greater peri-procedural myocardial injury. Post-PCI TMPFC was prolonged in the AP group (107.55 ± 24.19 vs. 89.86 ± 18.91 frames, P < 0.001), indicating impaired myocardial perfusion. While pre-procedural SPECT results were similar, at 3 days post-PCI, the AP group exhibited significantly greater stress ischemic segment counts, higher resting and stress perfusion total scores, and larger abnormal perfusion areas compared to the non-AP group (all P < 0.05). Multivariable analysis confirmed that the presence of AP was an independent predictor of no-reflow (OR 3.12, 95% CI 1.85-5.26, P < 0.001), independent of plaque burden. At 6-month follow-up, the incidence of MACCE was not statistically different between the two groups (8.2% vs. 6.2%, P = 0.357). In patients with unstable angina undergoing PCI, the presence of IVUS-detected attenuated plaque is strongly associated with an increased incidence of intraprocedural no-reflow, peri-procedural myocardial injury, and objective evidence of post-procedural coronary microvascular dysfunction. Although this did not translate to a significant difference in 6-month clinical outcomes in this cohort, AP serves as a critical independent imaging marker for identifying patients at higher risk for periprocedural microvascular injury.

In individuals with type 2 diabetes mellitus (T2DM), both myocardial ischemia and myocardial infarction (MI) are associated with adverse cardiovascular outcomes. The incremental prognosis of both risks is unknown. We aimed to investigate whether abnormal myocardial perfusion reserve (MPR), as a surrogate marker for ischemia and presence of MI offers incremental prognostic value in predicting major adverse cardiovascular and cerebrovascular events (MACCE) in patients with T2DM. A retrospective multicentre cohort of 572 individuals with T2DM and healthy controls underwent quantitative stress myocardial perfusion cardiovascular magnetic resonance (CMR) to determine MPR and late gadolinium enhancement (LGE) to identify MI. Patients were divided into three groups: MI- and normal MPR, MI+ or abnormal MPR and MI+ and abnormal MPR. Cox proportional hazard models quantified associations between MPR and MI with MACCE (composite of all-cause death, MI, stroke, heart failure hospitalization, and late coronary revascularization>90 days after the CMR scan). Over a median of 28 months (IQR 25-31 months), 81 participants (14%) accrued at least one MACCE, including 25 (4%) deaths. Presence of either abnormal MPR or MI was associated with increased MACCE (MI- and normal MPR: 8% MACCE; MI+ or abnormal MPR: 15% MACCE (adjusted HR compared with normal 1.86 (95% CI 1.06-3.25, P = 0.03)); presence of both MI and abnormal MPR had the highest event rate: 30% MACCE (adjusted HR compared with normal 3.24 (95% CI 1.75-6.01, P < 0.001)). In T2DM, abnormal MPR or MI are associated with MACCE, and the presence of both offers incremental prognostic value.

Radiomics-based mapping of glioblastoma infiltration beyond contrast enhancement: diffusion-perfusion correlations and survival analysis in large public cohorts.

Whether treatment with balanced crystalloid fluid leads to better outcomes than 0.9% saline in children treated for septic shock is debated. In this pragmatic clinical trial conducted at 47 emergency departments in five countries, patients (2 months to <18 years of age) with suspected septic shock and abnormal perfusion were randomly assigned to receive fluid resuscitation with either balanced fluid or 0.9% saline for up to 48 hours. The primary outcome was a major adverse kidney event (a composite of death, new renal-replacement therapy, or persistent kidney dysfunction) at 30 days after enrollment or hospital discharge, whichever occurred first. Of 9041 enrolled patients, 277 (6.1%) in the balanced-fluid group and 282 (6.2%) in the 0.9%-saline group withdrew from the trial, leaving 4235 and 4247 patients, respectively, for analysis. A primary-outcome event occurred in 137 patients (3.4%) in the balanced-fluid group and in 124 (3.0%) in the 0.9%-saline group (difference, 0.4 percentage points; 95% confidence interval [CI], -0.5 to 1.3; risk ratio, 1.10; 95% CI, 0.88 to 1.40; P = 0.85). The median number of hospital-free days during 28 days after enrollment was 23 (interquartile range, 19 to 25) in both groups. Hyperchloremia occurred in 868 patients (31.4%) in the balanced-fluid group and in 1383 (49.0%) in the 0.9%-saline group; hypernatremia in 52 (1.8%) and 89 (3.1%), respectively; and hyperlactatemia in 260 (19.8%) and 228 (16.7%). No differences in other safety outcomes or adverse events were seen. Among children treated for septic shock, no significant difference was seen in the incidence of death, new renal-replacement therapy, or persistent kidney dysfunction when fluid resuscitation was administered with balanced fluid as compared with 0.9% saline. (Funded by Eunice Kennedy Shriver National Institute of Child Health and Human Development and others; PRoMPT BOLUS ClinicalTrials.gov number, NCT04102371.).

Abstract Radiation-induced heart disease is a well-recognized late complication of thoracic radiotherapy and comprises a broad spectrum of cardiac disorders. Because myocardial metabolic impairment may precede overt structural or perfusion abnormalities, early or subclinical myocardial injury is often challenging to detect using conventional cardiac imaging modalities. We report a case of late-onset radiation-induced myocardial metabolic impairment identified by dual myocardial scintigraphy many years after thoracic radiotherapy for thymoma. The patient, a man diagnosed with malignant thymoma at 42 years of age, underwent two courses of thoracic radiotherapy during the course of his illness. The first course was confined to the mediastinum without cardiac exposure, whereas the second course, delivered at 52 years of age for recurrent disease with pericardial and myocardial invasion, resulted in direct cardiac irradiation. After a prolonged asymptomatic period, at 67 years of age (approximately 15 years after the second course of radiotherapy), the patient developed symptoms consistent with heart failure. Coronary angiography revealed no significant coronary artery stenosis. Dual myocardial scintigraphy demonstrated a characteristic metabolic–perfusion mismatch: reduced uptake of ¹²³I-β-methyl-p-iodophenyl-pentadecanoic acid (BMIPP) in the anterior to lateral wall of the left ventricle, precisely corresponding to the irradiated cardiac region, while myocardial perfusion assessed by ⁹⁹ᵐTc-methoxyisobutylisonitrile (MIBI) was preserved. Retrospective dosimetric analysis demonstrated a mean heart dose of 12.8 Gy during the second course of radiotherapy, supporting a radiation-induced mechanism of myocardial impairment. This case highlights the clinical value of combined ¹²³I-BMIPP and ⁹⁹ᵐTc-MIBI myocardial scintigraphy for the noninvasive detection of late-onset radiation-induced myocardial impairment in long-term cancer survivors, even in the absence of obstructive coronary artery disease.

Background/Objectives: Early neurological deterioration (END) is a frequent and clinically relevant complication in patients with a single small subcortical infarction (SSI), including lacunar infarction and branch atheromatous disease (BAD). Despite initially mild symptoms, END occurs in approximately 20–25% of cases and is strongly associated with poor functional outcomes. However, definitions, mechanisms, predictors, and therapeutic strategies remain heterogeneous. This review aims to synthesize current evidence regarding the incidence, pathophysiology, predictors, and management of END in SSI. Methods: We performed a narrative review of published studies addressing END in patients with lacunar stroke or SSI. We analyzed data on END definitions and incidence, imaging and clinical predictors, proposed pathophysiological mechanisms, and preventive and rescue therapeutic strategies. Results: END definitions vary across studies, most commonly defined as a ≥2-point increase in the National Institutes of Health Stroke Scale within 48–72 h. Hemodynamic compromise due to proximal perforator pathology, particularly in BAD, appears central to END development. Advanced imaging studies demonstrate perfusion abnormalities beyond the infarct core, supporting the concept of a “lacunar penumbra.” Lesion topology, proximal infarct patterns, parent artery plaques, larger infarct size, and vertical extension are consistent imaging predictors. Clinical factors such as diabetes mellitus, higher baseline severity, systemic inflammation, and increased arterial stiffness further modulate risk. Preventive strategies, including early dual antiplatelet therapy and intensified antithrombotic regimens, show promising signals, while induced hypertension may benefit selected patients as a rescue therapy. However, evidence remains largely observational or derived from subgroup analyses. Conclusions: END in SSI is a multifactorial and potentially modifiable process driven by interactions between proximal vascular pathology, hemodynamic failure, and tissue vulnerability. Standardized definitions, MRI-based phenotyping, and mechanism-driven trials are needed to optimize risk stratification and develop targeted preventive and rescue strategies.

Background/Objectives: Sepsis-associated acute kidney injury (SA-AKI) involves complex disturbances in renal microcirculation that may precede overt biochemical evidence of renal dysfunction. This study aimed to characterize early renal perfusion patterns during the emergency department (ED) phase of sepsis, as assessed by the renal resistive index (RRI) and the semiquantitative power Doppler ultrasonography score (SPDUS), and to explore their relationship with subsequent SA-AKI trajectories. Methods: In this prospective observational study, adult ED patients who met the Sepsis-3 criteria were enrolled. Renal perfusion was evaluated using the RRI and SPDUS at ED admission and repeated at the fourth hour. SA-AKI was classified as transient or non-transient based on renal recovery patterns. Trajectory comparisons were performed to identify early physiological differences. Receiver operating characteristic (ROC) analyses were conducted for descriptive and exploratory assessment of perfusion pattern separation between injury trajectories. Results: Fifty-four patients were included, with 35 classified as transient and 19 as non-transient SA-AKI. Patients with non-transient injury exhibited lower baseline SPDUS0 grades and higher RRI0 values compared with those with transient injury. These differences were evident at ED presentation, prior to the initiation of advanced organ support, and persisted at the fourth hour, with the non-transient group continuing to show lower SPDUS4 and higher RRI4 values than the transient group. These findings reflect distinct early renal microcirculatory perfusion patterns across SA-AKI trajectories. Sensitivity, specificity, and cut-off values are reported for descriptive and exploratory purposes only and should not be interpreted as validated clinical thresholds. Conclusions: Early alterations in renal microcirculatory perfusion are detectable during the ED phase of sepsis and differ between transient and non-transient SA-AKI trajectories. Baseline RRI and SPDUS values provide physiological insight into early renal perfusion abnormalities and evolving microcirculatory dysfunction in sepsis, but should not be interpreted as predictive tools.

We compared lung perfusion abnormalities using non-contrast X-ray pulsatility index (XPI) to pulmonary angiography in patients with suspected CTEPH. Volunteers suspected of CTEPH between April 2023 and May 2024 were enrolled and provided consent for the IRB-approved prospective study, resulting in 13 patients (6 male; 7 female) and 18 independent lungs. Fluoroscopic acquisition (70kV, 30 frames/s) was acquired over an 8-second breath-hold. The temporal signal from each pixel was decomposed into individual frequency components using spectral analysis. Signal oscillating at the heart rate was isolated using a band-pass filter and the amplitude (XPI) mapped to form an image. Immediately after each fluoroscopic acquisition for XPI, digital subtraction pulmonary angiography was performed using catheter-injected contrast in the same projection for comparison. Both XPI and DSA perfusion maps were segmented using a semi-automated technique. Segmentation maps were compared using the Dice similarity score, a statistical measurement of overlap. Non-contrast fluoroscopy and contrast DSA images were obtained in 18 lungs. All patients were able to perform satisfactory breath-hold, despite several with moderate to severe CTEPH. Direct comparison of segmentation maps revealed an average Dice score of 0.70, suggesting excellent agreement between XPI and pulmonary angiography in depicting regions of blood flow and perfusion defects. XPI is a non-contrast method to evaluate and monitor pulmonary perfusion, producing maps with excellent agreement to pulmonary angiography, which is confirmatory for CTEPH. This technique could improve clinical efficiency as a screening or diagnostic test to augment clinical pulmonary function assessment.

Early neurodevelopmental brain perfusion abnormalities and functional connectivity findings in infants with Prader-Willi syndrome.

BackgroundCerebellar lesions commonly induce executive dysfunction; however, the underlying neuroplastic mechanisms remain unclear. The fronto-cerebellar diaschisis model, where focal cerebellar damage disrupts widespread frontal networks, offers a compelling hypothesis. Given the pre-supplementary motor area (pre-SMA)'s established role in executive functions, we investigated its specific contribution to post-stroke impairment and its potential function as a dynamic compensatory node during recovery.MethodsWe employed a multimodal approach: resting-state SPECT imaging assessed brain perfusion, and f-NIRS quantified pre-SMA oxygenated hemoglobin ([oxy-Hb]) during a phonemic verbal fluency task (VFT) in 11 patients and 12 age-matched controls. Patients were stratified into Good (N = 6) and Poor (N = 5) recovery subgroups based on VFT performance to isolate the compensatory process. Longitudinal f-NIRS data tracked neural activity changes concurrent with cognitive recovery.ResultsSPECT revealed widespread perfusion abnormalities consistent with diaschisis. Patients exhibited significantly impaired VFT performance. Crucially, the Good Recovery subgroup exhibited a significantly augmented [oxy-Hb] response in the pre-SMA compared to controls, supporting a specific compensatory mechanism. This pre-SMA augmentation was statistically independent of the strong confounding effect of age (F(1,15) = 5.164, P = 0.038). Consistent with a transient compensatory effort, longitudinal data demonstrated a reduction in pre-SMA activity concurrent with subsequent cognitive recovery, suggesting increased neural efficiency.ConclusionsThis study provides preliminary evidence that verbal fluency deficits post-cerebellar stroke are linked to fronto-cerebellar diaschisis. Our findings suggests that the pre-SMA serve as a pivotal compensatory node supporting functional recovery. These results provide a hypothesis-generating basis for future targeted rehabilitation strategies and neuromodulatory interventions.

Diagnostic accuracy of superior vena cava variability by transthoracic echocardiography as a fluid responsiveness predictor in critically ill patients.

Risk stratification in patients with chronic thromboembolic pulmonary hypertension (CTEPH) relies mainly on functional testing and imaging-based structural assessment. The aim of this study was to investigate the prognostic significance of automated regional attenuation analysis on computed tomography pulmonary angiography (CTPA) as a surrogate of perfusion abnormalities. We analyzed 52 consecutive patients diagnosed with CTEPH. Patients underwent either surgical [pulmonary endarterectomy (PEA), n=21] or non-surgical treatments [balloon pulmonary angioplasty (BPA) and/or pharmacotherapy, n=31]. Parameters derived from CTPA, including automated lung attenuation analysis and clinical metrics, were correlated with survival outcomes over a median follow-up of 5.0 years. During follow-up, 19 patients (36.5%) died. In the non-surgical group, predictors of survival derived from CTPA included diameter of the ascending aorta [hazard ratio (HR) =1.37, P=0.013] and right atrial area (HR =1.17, P=0.007). Automated attenuation analysis demonstrated that a higher proportion of hyperemic parenchyma in the middle and peripheral regions of the right middle and both lower lobes was associated with increased mortality (HR from 1.38 to 1.69 and P from 0.002 to 0.027). Oligemic parenchyma in similar regions was protective (HR from 0.72 to 0.74 and P from 0.010 to 0.015). In the surgical group, no significant predictors were identified. Automated, region-specific attenuation analysis of CTPA provides quantitative prognostic information in non-surgically treated CTEPH patients. Increased peripheral hyperperfusion in the right middle and lower lobes was associated with decreased survival. We hypothesize that hyperperfusion in these regions may reflect neovascularization and the development of peripheral collaterals.

Lymphatic Complications in Congenital Heart Disease.

Acute ischemic stroke requires quick identification of infarct core and salvageable tissue for proper management. MRI techniques, including diffusion-weighted imaging (DWI), apparent diffusion coefficient (ADC) mapping and MR perfusion, provide essential early physiologic information. A study conducted at Santosh Medical College Hospital involved 60 patients presenting within 24 hours of neurological symptoms. The results showed DWI and ADC reliably detected restricted diffusion, while MR perfusion highlighted perfusion abnormalities. The findings enhance stroke evaluation by demonstrating the importance of combining diffusion and perfusion imaging to better understand stroke pathophysiology, potentially improving patient outcomes.

Difficulty identifying neonates at highest risk of early-onset bloodstream infection (EO-BSI) leads to high empiric antibiotic use. This retrospective case-control study analysed maternal and neonatal factors, pathogen profile, and outcomes of culture-confirmed EO-BSI (<72 hr of life) at a large neonatal unit in Cape Town, South Africa (1 January 2019–31 December 2021). Cases (neonates with culture-confirmed BSI) were matched 1:3 with randomly selected controls (‘at risk’ neonates with negative blood cultures, C-reactive protein < 10 mg/l and ≤4 days of antibiotics). Factors associated with EO-BSI were identified using multivariable logistic regression. Among 248 neonates included, 62 were cases and 186 were controls. Six factors independently predicted EO-BSI in ‘at risk’ neonates: ≥32 maternal risk factors; birth weight > 2500 g; hypo/hyperglycaemia; abnormal perfusion; seizures and invasive respiratory support. Group B streptococcus and Escherichia coli predominated on birth blood cultures (25/44; 56.8%), whereas Klebsiella. pneumoniae was dominant from 24 to 72 hr of life (13/20; 65%). Ampicillin plus gentamicin was the most frequently prescribed empiric regimen (82% in cases, 100% in controls), followed by regimens targeting healthcare-associated pathogens ≥ 24 hr of life. Cases were nearly 6 times more likely to demise than controls (RR 5.8, 95% CI = 2.7–12.5; case fatality rate 32.5%). Mortality was strongly associated with gram-negative pathogens, discordant antibiotic treatment and gestational age < 32 weeks. A clinical score to evaluate EO-BSI risk may reduce early-life antibiotic exposure. Beyond 24 hr of life, empiric antibiotics should provide coverage of healthcare-associated pathogens.

Acute respiratory distress syndrome (ARDS) is a heterogeneous clinical syndrome rather than a single disease. Patients who meet the same diagnostic criteria may differ in lung morphology, mechanical properties, biological injury, and clinical course. Current classifications rely largely on the severity of hypoxemia and do not capture this variability, limiting prognostic stratification and individualized treatment. This heterogeneity has clinical consequences. Supportive interventions such as positive end-expiratory pressure (PEEP), prone positioning, and recruitment maneuvers are broadly applied, yet their effects vary substantially among patients. Increasing evidence indicates that these differences are partly explained by variation in lung structure, regional aeration, recruitability, and perfusion. Recent international guidelines have identified phenotyping as a priority in ARDS and have highlighted lung morphology as a relevant source of prognostic enrichment and treatment effect heterogeneity. Computed tomography (CT) provides regional, three-dimensional information on lung injury that is not accessible through bedside physiological measurements. It allows evaluation of aeration loss, lung density, lung weight, and perfusion abnormalities. CT has been used to describe key aspects of lung injury in ARDS and to identify imaging patterns associated with lung mechanics, gas exchange, and response to ventilatory settings. Quantitative and dual-energy CT, together with computational methods, allow a more detailed description of these patterns. This review examines the role of CT in characterizing heterogeneity in ARDS, summarizes qualitative, semi-quantitative, and quantitative approaches, and discusses their clinical relevance and limitations, as well as future directions.