Normal Vessels Research Articles

Vascular cellular senescence in human atherosclerosis: The critical modulating roles of CDKN2A and CDK4/6 signaling pathways.

Vascular cellular senescence in human atherosclerosis: The critical modulating roles of CDKN2A and CDK4/6 signaling pathways.

Shear Stress-Responsive Peptide Cubic Vesicles Assembled from Membranes with Different Curvatures.

Stenotic blood vessels differ from normal blood vessels in that the blood flow shear stress is increased to a higher order of magnitude. Therefore, drug delivery systems (DDSs) capable of responding to changes in the shear stress are highly desirable. To prepare sheer stress-responsive carriers, a peptide cubic vesicle (PCV) is prepared by combining two types of sheet-forming amphiphilic polypeptides: planar sheet-forming GA-(PSar)10-b-(l-Leu-Aib)6-b-(PSar)10-GA (S10L12S10) and curved sheet-forming GA-(PSar)24-b-(l-Leu-Aib)7 (S26L14), which GA, PSar, Leu and Aib mean glycolic acid, polysarcosine, leucine and α-aminoisobutyric acid. The PCV is successfully constructed from a mixture of S10L12S10 and S26L14 in molar ratios of 2:1 and 1:1. In addition, curved S26L14 membrane forms edges and corners, while planar S10L12S10 membrane forms the faces of the PCV. Notably, the PCV deforms under pathological shear stress conditions (10Pa) but retains its original structure under the normal physiological shearing force of 1Pa. Moreover, the PCV releases 84% of its encapsulated cargo in response to simulated pathological flow. Targeting the changing biophysical environment for drug development has the potential to shift the paradigm for treating vascular occlusion-inducing diseases from biochemical to mechanical stimulation, thereby lowering the required dose and side effects of drugs while maximizing their therapeutic efficacy.

Identification and Verification of the Driver Genes for the Formation and Development of Intracranial Aneurysms.

Research on driver genes that can be used to diagnose and control the formation and development of intracranial aneurysms (IAs) is still limited, and bioinformatics and machine learning approaches are implemented in the study in an aim to identify and validate them. By applying datasets from the Gene Expression Omnibus database for human cerebrovascular tissue, 47 cases of ruptured IA, 71 cases of ruptured IA, and 64 cases of normal control intracranial vessels were analyzed. Apply bioinformatics and machine learning methods to screen for the driver genes that contribute to the occurrence and development of IAs. Construct animal models to verify them. STX17 was identified as a key driver gene for the occurrence and development of IAs (AUC: 0.724). The animal model of IA was successfully constructed. Immunohistochemistry: The average optical density values of vascular smooth muscle and STX17 antibodies in the model group were significantly decreased compared with those in the normal group (P < 0.001). reverse transcription - polymerase chain reaction: The mRNA expression level of the STX17 gene in the model group was significantly lower than that in the normal group (P < 0.001). Western blot: The protein expression level of the STX17 gene in the model group was significantly decreased compared with that in the normal group (P < 0.001). STX17-mediated changes in the smooth muscle cell phenotype are new driver genes for IA formation and progression, providing a new approach for the early screening, diagnosis, and treatment of IA.

Effect of gestational diabetes mellitus and its management on the histological and histomorphometric structure of umbilical cord: a comparative study.

The umbilical cord lacks vasavasorum and is prone for hypoxic injuries. Gestational diabetes mellitus (GDM) causes structural changes with in umbilical cord blood vessels. Knowledge of which would be helpful for the gynecologist and obstetricians to assess the prognosis and prevent the complications. The present study was concentrated from December 2016 to December 2019 on 50 normal and 56 GDM umbilical cords. GDM group included 23 GDM mothers managed by diet (GDM-Diet) and 33 GDM mothers managed by drugs (GDM-Drug). Placentas along with the attached umbilical cords were collected and stored in 10% formaline. Tissue processing, slide preparation and stainings were done using standard protocols. A significant reduction was observed in the number of Hoboken nodules of umbilical arteries of GDM-Diet. Reduction of myofibroblasts with an increase in the empty spaces was observed in the Wharton's jelly of both GDM cases. Similarly, smooth muscle disintegration and migration of smooth muscles to intima was significantly higher in GDM umbilical arteries and veins than normal umbilical vessels. The total wall thickness and tunica media was significantly thicker in the umbilical arteries of GDM-Drug group only. The umbilical venous lumen was found significantly wider in GDM groups compared to normal. The elastin fibers were significantly found reduced in the tunics of umbilical arteries and veins in GDM. However, a significant difference in these parameters was not observed between the GDM-Diet and GDM-Drug groups except for total wall and tunica media thickness of umbilical arteries.

BLEscope: A Bluetooth Low Energy (BLE) Microscope for Wireless Multicontrast Functional Imaging.

Recent advances in low-power wireless-capable system-on-chips (SoCs) have accelerated diverse Internet of Things (IoT) applications, encompassing wearables, asset monitoring, and more. Concurrently, the field of neuroimaging has experienced escalating demand for lightweight, untethered, low-power systems capable of imaging in small animals. This article explores the feasibility of using a low-power asset monitoring system as the basis of a new architecture for fluorescence and hemodynamic contrast-based wireless functional imaging. The core system architecture hinges on the fusion of a Bluetooth Low Energy (BLE) 5.2 SoC and a low-power 560×560, 8-bit monochrome CMOS image sensor module. Successful integration of a multicontrast optical front-end consisting of a fluorescence channel (FL) and an intrinsic optical signal (IOS) channel resulted in the creation of a wireless microscope called 'BLEscope'. Next, we developed a wireless (i.e. BLE) protocol to remotely operate the BLEscope via a laptop and acquire in vivo images at 1 frame per second (fps). We then conducted a comprehensive characterization of the BLEscope to assess its optical capabilities and power consumption. We report a new benchmark for continuous wireless imaging of ∼1.5 hours with a 100 mAh battery. Via the FL channel of the BLEscope, we successfully tracked the kinetics of an intravenously injected fluorescent tracer and acquired images of fluorescent brain tumor cells in vivo. Via the IOS channel, we characterized the differential response of normal and tumor-associated blood vessels to a carbogen gas inhalation challenge. When miniaturized, the BLEscope will result in a new class of low-power, implantable or wireless microscopes that could transform preclinical and clinical neuroimaging applications.

A single-cell atlas of normal and KRASG12D-malformed lymphatic vessels.

Somatic activating mutations in KRAS can cause complex lymphatic anomalies (CLAs). However, the specific processes that drive KRAS-mediated CLAs have yet to be fully elucidated. Here, we used single-cell RNA sequencing to construct an atlas of normal and KrasG12D-malformed lymphatic vessels. We identified six subtypes of lymphatic endothelial cells (LECs) in the lungs of adult wild-type mice (Ptx3, capillary, collecting, valve, mixed, and proliferating). To determine when the LEC subtypes were specified during development, we integrated our data with data from four stages of development. We found that proliferating and Ptx3 LECs were prevalent during early lymphatic development and that collecting and valve LECs emerged later in development. Additionally, we discovered that the proportion of Ptx3 LECs decreased as the lymphatic network matured but remained high in KrasG12D mice. We also observed that the proportion of collecting and valve LECs was lower in KrasG12D mice than in wild-type mice. Last, we found that immature lymphatic vessels in young mice were more sensitive to the pathologic effects of KrasG12D than mature lymphatic vessels in older mice. Together, our results expand the current model for the development of the lymphatic system and suggest that KRAS mutations impair the maturation of lymphatic vessels.

Syncope Induced by Dynamic Head and Shoulder Motion in the Setting of Left Subclavian Stenosis.

Dynamic vertebral artery insufficiency is a rare vascular phenomenon characterized by insufficient flow of the posterior cerebral circulation induced by dynamic motion of the head. Prior case reports have been limited to vertebral artery occlusion by cervical osteophytes or other structural impingements. In this case report, we discuss the unusual case of a 61-year-old female with a history of vertigo, diplopia, nystagmus, and left subclavian stenosis admitted to the hospital for syncope elicited by a left head turn and left shoulder raise. Transcranial Doppler (TCD) ultrasound and angiography showed evidence of dynamic vertebrobasilar insufficiency elicited by a left-head turn. Percutaneous stenting of the left subclavian artery led to the resumption of normal vessel flow as assessed by TCD and the resolution of the patient's symptoms. This case highlights an unusual cause of dynamic vertebrobasilar insufficiency induced by head turn and/or left shoulder raise due to subclavian stenosis, diagnosed by TCD and angiography, and successfully treated with subclavian artery stenting.

Deep learning model for automatic detection of different types of microaneurysms in diabetic retinopathy.

This study aims to develop a deep-learning-based software capable of detecting and differentiating microaneurysms (MAs) as hyporeflective or hyperreflective on structural optical coherence tomography (OCT) images in patients with non-proliferative diabetic retinopathy (NPDR). A retrospective cohort of 249 patients (498 eyes) diagnosed with NPDR was analysed. Structural OCT scans were obtained using the Heidelberg Spectralis HRA + OCT device. Manual segmentation of MAs was performed by five masked readers, with an expert grader ensuring consistent labeling. Two deep learning models, YOLO (You Only Look Once) and DETR (DEtection TRansformer), were trained using the annotated OCT images. Detection and classification performance were evaluated using the area under the receiver operating characteristic (ROC) curves. The YOLO model performed poorly with an AUC of 0.35 for overall MA detection, with AUCs of 0.33 and 0.24 for hyperreflective and hyporeflective MAs, respectively. The DETR model had an AUC of 0.86 for overall MA detection, but AUCs of 0.71 and 0.84 for hyperreflective and hyporeflective MAs, respectively. Post-hoc review revealed that discrepancies between automated and manual grading were often due to the automated method's selection of normal retinal vessels. The choice of deep learning model is critical to achieving accuracy in detecting and classifying MAs in structural OCT images. An automated approach may assist clinicians in the early detection and monitoring of diabetic retinopathy, potentially improving patient outcomes.

Endothelial activating transcription factor 3 promotes angiogenesis and vascular repair in the mouse retina.

Ischemia and pathological angiogenesis in retinal vascular diseases cause serious vision-related problems. However, the transcriptional regulators of vascular repair remain unidentified. Thus, the factors and mechanisms involved in angiogenesis must be elucidated to develop approaches for restoring normal blood vessels. Here, we investigated the effects of the stress response activating transcription factor 3 (ATF3) on angiogenesis and vascular regeneration invitro and invivo. ATF3 was expressed specifically in retinal vascular endothelial cells (ECs) during vascular development. Vascular endothelial growth factor stimulation upregulated ATF3 expression in cultured ECs. The downregulated ATF3 expression in ECs caused the deterioration of vascular network formation invitro and invivo. Moreover, ATF3 deletion in a model of oxygen-induced retinopathy inhibited retinal vascular repair but not pathological neovascularization. Transcriptome analysis confirmed that high ATF3 expression upregulated the expression of angiogenesis-related genes in ECs. ATF3 may aid vascular repair therapy in retinal vascular diseases.

The contribution of cerebral small vessel disease in idiopathic normal pressure hydrocephalus: Insights from a prospective cohort study.

Idiopathic normal pressure hydrocephalus (iNPH) and cerebral small vessel disease (CVSD) are age-related diseases, but their prevalence and clinical relationship are unclear. This prospective cohort study enrolled 95 patients with probable iNPH in China and evaluated their CSVD burden using magnetic resonance imaging. Linear regression models were used to analyze the association between CSVD scores and clinical outcomes. The results showed 78% of the patients had at least one CSVD imaging marker, and higher total CSVD scores were significantly associated with declines in attention, executive function, psychomotor speed, and gait performance after multivariate adjustments. However, the preoperative CSVD score did not affect the post-shunt improvement in modified Rankin scale or iNPH grading scale scores. Our findings suggest that CSVD is prevalent in patients with iNPH and is associated with more severe symptoms, but it may not affect shunt outcomes. Future studies are needed to elucidate the underlying mechanisms. We found that 78% of the patients with idiopathic normal pressure hydrocephalus (iNPH) had at least one type of cerebral small vessel disease (CSVD) imaging marker. The CSVD burden aggravates cognitive and gait impairments in patients with iNPH but may not affect shunt outcomes. The effects of different imaging markers of CSVD on cognition and gait are different and worthy of further investigation.

Screening and identification of vascular endothelial cell targeting peptide in gastric cancer through novel integrated in vitro and in vivo strategy

PurposeAntiangiogenesis therapy has become a hot field in cancer research. Given that tumor blood vessels often express specific markers related to angiogenesis, the study of these heterogeneous molecules in different tumor vessels holds promise for advancing anti-angiogenic therapy. Previously using phage display technology, we identified a targeting peptide named GX1 homing to gastric cancer vessels for the first time. However, GX1 also showed some non-specific binding with normal gastric vessels, which can lead to toxic side effects on normal endothelial cells. Therefore, we urgently need to adopt new screening strategies to avoid non-specific binding to normal vessels and obtain gastric cancer vascular targeting peptides with higher specificity.MethodsIn this study, we designed a new strategy which combined “positive screening” in vivo and “negative screening” in vitro for the first time. An in vivo positive screening was conducted using tumor bearing nude mice to identify peptides that were specifically enriched within the vasculature of gastric cancer. Concurrently, an in vitro negative screening process was conducted on normal vasculature endothelial cells, including human umbilical vein endothelial cells (HUVECs) and human microvascular endothelial cells (HMVECs), to eliminate peptides binding to normal vasculature. After four rounds of iterative screening, a targeting peptide specifically targeting gastric cancer vasculature was obtained. In addition, an in vitro co-culture model by culturing HUVEC in tumor conditioned medium (Co-HUVEC) was established to investigate the affinity of these peptides. The targeting peptide was labeled with fluorescein isothiocyanate (FITC) for competitive and inhibitory assays.ResultsBlood vessel density analysis confirmed redundant capillary vessels in the xenografts, indicating that the mouse model was suitable for positive screening. Following four rounds of panning, a significant enrichment for phages specifically binding to gastric cancer vasculature was observed, with minimal binding to normal endothelial cells. The peptide CNTGSPYEC exhibited the highest reproducibility. In vitro immunofluorescence staining confirmed that the peptide CNTGSPYEC could specifically enrich in Co-HUVECs while showing no binding to normal vascular endothelial cells. In vivo immunofluorescence staining revealed that the peptide CNTGSPYEC could only bind to vascular endothelial cells specifically in gastric cancer but show no non-specific binding with normal tissue. Competitive and inhibitory assay also verified the targeting characteristics of the peptide with the fluorescence intensity of 17.13. As the concentration increases, the competitive inhibition rate can be incrementally raised to 93% (p < 0.05). Endothelial tube formation assay indicated that the peptide could suppress neovascularization, with the microvessel count reducing by 40% (p < 0.05). Furthermore, Cell Counting Kit-8 assay (CCK8) showed that the targeting peptide could partly inhibit cell proliferation of Co-HUVEC (61.7%).ConclusionOur novel strategy of the combined in vitro and in vivo screening outperforms previous methods that relied solely on negative/positive screening. In vivo and in vitro test confirmed the high targeting characteristic of the new peptide. Therefore, the peptide CNTGSPYEC may be a potential candidate in diagnosis and anti-angiogenesis therapy of gastric cancer. Our further exploration employs it as a vehicle for mediating drug accumulation in gastric cancer tissue.

Quantitative flow ratio of the donor coronary artery supplying a chronic total occlusion territory.

Coronary physiology to guide multi-vessel coronary intervention is associated with better outcome. In the presence of a coronary chronic total occlusion (CTO), hemodynamic evaluation of intermediate lesions in the donor coronary artery supplying a CTO territory still has limitations. We aim to evaluate implementing quantitative flow ratio (QFR) in assessing angiographically intermediate lesions of the main donor coronary artery supplying a CTO territory. We recruited 219 patients with a single main donor vessel to a CTO territory from a single-center CTO registry between 2017 and 2020. Angiographically intermediate coronary lesions of the donor vessels were evaluated using offline QFR before and at a median of 6 months after successful percutaneous coronary intervention (PCI) of CTO. The mean age of the study population was 66.9 ± 11.3 years, and 77.6% were males. Three-vessel disease was documented in 49.8%. The mean QFR value increased significantly in the donor vessels after successful CTO revascularization (0.93 ± 0.062 vs. 0.95 ± 0.046, p < 0.001) and was more prominent in donor vessels with angiographically intermediate stenosis (0.88 ± 0.063 vs. 0.92 ± 0.053, p < 0.001). While the change in QFR was not significant in angiographically normal donor vessel (0.97 ± 0.025 vs. 0.97 ± 0.026, p = 0.814). Fifteen patients had hemodynamically significant stenosis in the donor coronary artery (QFR ≤ 0.80) before CTO-PCI. Among those patients, 40% (n = 6) were turned to be non-significant with QFR > 0.80 after CTO recanalization, and 30% (n = 5) patients remained significant and were treated with PCI. QFR overestimates the severity of intermediate coronary lesions of a donor vessel supplying a CTO territory like other invasive modalities for physiology assessment.

A novel homozygous missense variant in POC1B causes cone dystrophy in a consanguineous Pakistani family

ABSTRACT Background Cone dystrophy is a heterogeneous hereditary retinal disorder with disease symptoms appearing in the late first or early second decades of life. Methods A consanguineous Pakistani family with three affected individuals underwent detailed clinical and genetic investigation. Results The proband, a 63-years old male, showed severely reduced day vision, a visual acuity of counting fingers (CF), color vision deficiency, high myopia and photophobia. Fundus images showed bilateral peripapillary atrophy, bilateral dull foveal reflex, tilted disc, tessellated fundus, and hyperfluorescence at the peripheral superior temporal arcade and leak at an early stage. OCT macula and angiography findings suggested traction near the disc in the right eye and sub-retinal fluid at the fovea in the left eye. Retinal layers were normal toward the periphery but disorganized near the disc. Full visual field tests showed bilateral central scotoma, while single visual field tests indicated bilateral generalized depression of the visual field. The proband showed normal bilateral intraocular pressure, normal choroidal vessels, and unremarkable anterior segment. Exome sequencing identified a novel homozygous missense variant (POC1B:NM_172240.3:c.1391T>C;p.L464P) in the proband. Existing evidence supported pathogenicity of the identified variant in the family. Conclusion In conclusion, we document a first-ever Pakistani family with POC1B-related cone dystrophy.

Abstract 428: The Unusual Suspect ‐ Hypereosinophilia as the Cause for Acute Stroke

Background Eosinophilic granulomatosis with polyangiitis (EGPA) causes inflammation of small blood vessels. EGPA is rare, with an annual incidence of 1 per million, with a mean age of onset of 40‐60 years. EGPA is divided into 2 phenotypes, ANCA‐positive vasculitis type and ANCA‐negative eosinophilia type. There is an overlap between other hypereosinophilic syndromes and EGPA. There are no diagnostic criteria for EGPA, however clinical features of asthma, chronic rhinosinusitis with polyps, eosinophilia, neuropathy, lung infiltrates, and eosinophilic cardiomyopathy or gastroenteritis are supportive. Central nervous system involvement manifests as cerebral infarcts and subarachnoid hemorrhages. Case: Here we present a 53‐year‐old Caucasian female with no past medical history who presented with chest pain and shortness of breath. She reported dyspnea on exertion for 8 months prior, and more recently paroxysmal nocturnal dyspnea and orthopnea, with minimal relief from inhalers. She was noted to have pansinusitis and was started on amoxicillin‐clavulanic acid without improvement. She noted acute right upper extremity weakness. Initial workup showed elevated troponin and a white blood cell (WBC) count of 28.4 with 11.64 eosinophils. CT chest showed bilateral bronchial wall thickening with bilateral nodular consolidative opacities in the right upper lobe and left lower lobe. She was started on a heparin drip. Coronary angiography was negative, and the initial echocardiogram revealed mild circumferential pericardial effusion without tamponade. CT head showed an 11 mm right cerebellar hemorrhage. Heparin was stopped. MRI brain revealed multiple scattered areas of restricted diffusion in bilateral cerebral hemispheres and a right cerebellar hemisphere. CTA head and neck showed normal vessels, and after transfer to our facility, a repeat MRI brain revealed scattered new infarcts in the left parietal and occipital regions. A repeat echocardiogram showed a small loculated pericardial effusion anterior to the right ventricle but no intracardiac shunt. The patient was exposed to wildfire smoke before symptom onset, raising suspicion of fungal infection. The patient underwent fungal evaluation in both serum and sinus aspirate, including beta‐D‐glucan in the serum, which was negative, and a bronchoscopy, which revealed white plaques and nodules with negative fungal and tuberculosis studies. Lumbar puncture revealed an elevated opening pressure of 30 mmHg but otherwise unremarkable infectious studies. Antibiotic therapy included vancomycin, cefepime, and amphotericin, but with consistently elevated WBCs of more than 24 with eosinophilic predominance. Endomyocardial biopsy showed numerous eosinophils. Subsequent endobronchial biopsy showed eosinophilic infiltrates and features suspicious for vasculitis. ANCA and bone marrow biopsy were negative. The primary diagnosis was considered hypereosinophilic syndrome. She was started on pulse dose steroids, and WBC count fell from 24.1 to 11.8 with a decrease in eosinophils from 13.05 to 0.01. Outpatient rheumatology was planned to initiate cyclophosphamide or rituximab. Dual antiplatelet therapy was initiated before discharge. Conclusion Central nervous system sequelae of EGPA are rare, but this diagnosis should be considered in patients with symptoms of sinusitis, elevated eosinophils, and acute stroke, especially without other risk factors. Since ANCA is only positive in about 30‐40% of patients, an early biopsy is needed for confirmation and early treatment with steroids.

Label-free classification of atherosclerosis plaque via OCT and ultraviolet autofluorescence spectroscopy.

We proposed a label-free method for the identification and classification of atherosclerosis plaques by combining optical coherence tomography (OCT) with ultraviolet autofluorescence spectroscopy (uFLS). By aligning the OCT source and the FLS excitation beams, we were able to illuminate the same spot on plaques fixed to the integrated probe, which underwent rotational scanning. This setup enabled the detection of both OCT images and uFLS spectra of the plaques in a co-localized manner. In our approach, a 1300 nm centered swept laser source was utilized for OCT imaging, while a 355 nm laser source, along with a lensed multimode fiber, served as the fluorescence probe for uFLS. The successful acquisition of OCT-uFLS images provided complementary information regarding the tomographic internal structure and biochemical components within the vessels, allowing for comprehensive identification and classification of atherosclerosis plaques. Furthermore, we achieved quantitative measurements and analysis of fluorescence spectra from three main component channels, corresponding to collagen, elastin, and lipid. This enabled us to differentiate atherosclerosis from normal vessel walls and determine the specific types. With the implementation of this dual-modal OCT-uFLS technique, it is possible to facilitate the label-free classification of various histopathological types of atherosclerosis plaques, which holds the potential for both diagnosis and image-guided ablation therapy applications.

Coronary Computed Tomographic Angiography (CCTA) in non-ST elevation acute coronary syndromes

Abstract Background In patients presenting with an acute coronary syndrome (ACS), a diverse range of coronary artery disease is observed from structurally normal vessels to non-obstructive atherosclerosis and severe/obstructive coronary artery disease (CAD). In current clinical practice guidelines, the main diagnostic route for optimal management of patients with non-ST segment elevation acute coronary syndrome is invasive coronary angiography. However, in 30-40% of cases, no significant coronary lesions are evident. The purpose of this study is to describe the role of coronary computed tomographic angiography (CCTA) in non-ST elevation acute coronary syndromes in low and intermediate risk patients. Methods We describe the results of 504 patients evaluated with a protocol that includes the use of CCTA in patients with ACS. Patients over 18 years of age with a diagnosis of ACS without ST elevation who did not meet high-risk criteria (hemodynamic instability, dynamic changes in the ST segment or T wave, ventricular arrhythmia, GRACE score &amp;gt;140, refractory angina, heart failure or cardiorespiratory arrest) were included. They underwent CCTA as the initial coronary evaluation. Data collection was carried out between May 11, 2022 and February 20, 2024. Results 504 patients were included, with a mean age of 58 years, of which 44% were women and 56% men. Among the admission diagnoses, 26% were NSTEMI and 74% were unstable angina according to the 4th universal definition of acute myocardial infarction (AMI). The median high-sensitivity cardiac troponin T value was 7 nanograms per liter (interquartile range, 7 to 15) for the first troponin measurement. CCTA was performed in 93% of the patients. It was observed that 28% did not have any coronary lesions or plaques. 36% had non-obstructive coronary artery disease (plaques &amp;lt;50%). The rest had significant lesions in at least one vessel (27%), predominantly in the left anterior descending artery, or were nondiagnostic (9%). 31% had myocardial bridges, while in 13% of the patients a high-risk plaque was found. 38% of the patients included underwent invasive coronary angiography and 23% required revascularisation. Conclusion This study shows that the prevalence of ACS with coronary arteries without significant lesions by CCTA was 28%, which suggests CCTA could have a predominant role in the diagnostic algorithm of acute coronary syndromes without high-risk criteria, implying a decrease in the need of invasive studies in these patients. Only 38% required invasive coronary angiography, while revascularisation was performed in 23% of the patients. Furthermore, CCTA allowed a better detection of non-obstructive coronary artery disease (NOCAD) in 36% of the patients, and a more complete characterization of the atherosclerotic plaque, which could prompt to an initiation of preventive therapies or the optimization of medical treatment in these patients.Table 1CCTA findings

Plaque phenotyping using deep learning in optical coherence tomography imaging

Abstract Background Artificial intelligence (AI) techniques have emerged as powerful tools in various computer vision tasks, particularly in classification, detection, and segmentation. Purpose This study aimed to develop a deep learning model for categorizing optical coherence tomography (OCT) frames into different plaque phenotypes, including thin-cap fibroatheroma (TCFA) and fibroatheroma. Methods A prospective multicenter observational study enrolled 168 patients who underwent percutaneous coronary intervention (PCI) and received OCT imaging for non-target lesions with angiographically estimated diameter stenosis greater than 30% (177 vessels). Among them, 129 patients (135 vessels) underwent follow-up OCT imaging at 1 year. A total of 45,072 OCT frames were randomly divided into training and validation sets in a 4:1 ratio. An EfficientNet-B3 convolutional neural network model was developed to classify OCT frames into TCFA, thick-cap fibroatheroma, non-fibroatheroma, adaptive intimal thickening, and normal vessel categories. Results A confusion matrix comparing manually assessed plaque phenotypes with AI-predicted phenotypes was presented in Table. In the validation datasets (9,015 frames), the overall accuracy of the model was 85.1%. For predicting the presence of TCFA, sensitivity was 81.1%, specificity was 98.8%, positive predictive value was 63.9%, and negative predictive value was 99.5%. Regarding the presence of fibroatheroma, sensitivity was 90.3%, specificity was 89.4%, positive predictive value was 93.1%, and negative predictive value was 85.4%. Conclusions The deep learning algorithm demonstrated high accuracy in detecting TCFA and fibroatheroma with excellent reproducibility. This automated process enables operators to promptly identify high-risk lesions during PCI, potentially leading to improved clinical outcomes.

Clinical case of an atypical variant of Labbe's vein structure in a patient with pharmacoresistant temporal epilepsy

Among the commonly recognised structural lesions that cause drug-resistant temporal lobe epilepsy, such as mesial temporal sclerosis, focal cortical dysplasia, benign intracerebral tumors, arteriovenous malformations and cavernous angiomas, researchers have recently noted other pathologies, such as, encephalocele. There are a number of publications on the connection between epilepsy and cerebral venous angiomas. However, there are no published cases of the influence of the abnormal structure and location of normal cerebral vessels on the development of epilepsy. This article presents a case of an atypically large and unusually located vein of Labbe that may have been involved in epileptogenesis and also complicated an anteromedial temporal lobectomy. Forced coagulation and excision of the Labbe vein during surgery did not lead to venous infarction and neurological deficit.

A recurrent typical angina pectoris without any finding in coronary angiography: Microvascular angina.

Microvascular angina (MVA) can present with recurrent chest pain and normal coronary angiography. Recognizing MVA is crucial as it significantly impacts patient morbidity and mortality. Early diagnosis and management with antianginal medications are essential for improving outcomes and quality of life. Cardiovascular diseases are still the main cause of death in many parts of the world. Chest pain and dyspnea are always concerning due to the implications of cardiovascular disease. However, in patients with the involvement of the small coronary vessels (Microvascular Angina), symptoms might be recurrent and persistent despite the presence of normal coronary vessel evaluations. A 45-year-old man with a 25-year smoking history presented with recurrent chest pain, especially during physical activity, and mild shortness of breath. He was admitted, and a coronary angiography the next day appeared normal. However, a cardiac PET scan revealed the involvement of small coronary vessels not visible on angiography. The Patient was a 45-year-old man who presented with recurrent chest pain, more prominent during physical activity. He also had mild shortness of breath. The patient was admitted, and the next day, he underwent normal coronary angiography. The cardiac positron emission tomography (PET scan) showed the involvement of small coronary vessels that were not obvious on angiography.

A rare spatial relation of the great arteries in patients with transposition of the great arteries: Posterior aorta and its effect on outcomes.

This study aimed to evaluate patients diagnosed with posterior transposition of the great arteries (TGA) in detail. This retrospective study included 192 patients (155 males, 37 females; mean age: 0.4±0.9 month; range, 0.1 to 6 month) with TGA who were followed between August 1, 2016, and August 1, 2022. Patients with ventriculoarterial discordance, normal vessel relationship, and mitral-aortic continuity were considered posterior TGA. Demographic features, clinical findings, echocardiographic data, and surgical results of each patient were recorded. Posterior TGA was present in 11 (5.7%) of the patients. The median age of patients with posterior TGA at the time of surgery was two months (interquartile range [IQR], 1-3 months), and their median body weight was 6.2 kg (IQR, 5-7.2 kg). The median oxygen saturation of the patients was 85% (IQR, 80-90%). A ventricular septal defect was present in all patients on echocardiography. There was also nonrestrictive atrial septal defect and patent ductus arteriosus in four patients, and one patient had arcus aorta hypoplasia. A coronary anomaly was determined in eight of the patients during surgery. These were 1LRCA2Cx in three cases, 1LRCx in three cases, 1R2LCx in one case, and 1L2RCx in one case. Arterial switch operation and ventricular septal defect closure was performed in 10 patients initially and in one patient after a pulmonary banding operation. The median cardiopulmonary bypass time was 190 min (IQR, 170-210 min). The Lecompte maneuver was not performed in any of the patients. The median stay in the intensive care unit and the hospital was 7 days (IQR, 5-10 days) and 16 days (IQR, 14-18 days), respectively. Two patients died in the early postoperative period. In patients with suspected congenital heart disease, a segmental echocardiographic evaluation should be performed, and it should be kept in mind that the aorta may be located posteriorly as a rare spatial relationship in patients with TGA.