Artery Occlusion Research Articles

Dynamic monitoring of the endothelium function in pregnant women at high risk of preeclampsia during pathogenetic prevention of its development

BACKGROUND: Today, preclinical diagnosis of preeclampsia presents significant difficulties. In widespread practice, it is diagnosed based on existing clinical signs and laboratory and functional research methods. Most of them are invasive and expensive, which makes it difficult to use them in widespread clinical practice for diagnosis and, especially, for monitoring the effectiveness of therapy over the dynamics of the disease. It is known that the pathogenesis of preeclampsia can have two independent development paths, converging in a common resulting link — the formation of endothelial dysfunction. Methods for studying endothelial function include determining markers of its imbalance in blood samples and non-invasive functional tests. Non-invasive diagnosis of endothelial dysfunction using the EndoPAT test allows us to quantify endothelium-mediated changes in vascular tone during 5-minute occlusion of the brachial artery. AIM: The aim of this study was to evaluate the method for determining the endothelium function in the first, second and third trimesters of pregnancy during ongoing pathogenetic prevention of preeclampsia. MATERIALS AND METHODS: This interventional uncontrolled study of the effectiveness of preventing preeclampsia using non-invasive assessment of vascular endothelial dysfunction during pregnancy was conducted at the Research Institute of Obstetrics, Gynecology and Reproductology named after D.O. Ott, St. Petersburg, Russia. The study involved 108 pregnant women at high risk of developing preeclampsia. All pregnant women underwent a cuff test to determine endothelial dysfunction using the peripheral arterial tonometry technique on the Endo-PAT 2000 device. The dynamic study was carried out in the first, second and third trimesters of pregnancy. As a result of the study, when endothelial dysfunction was detected [logarithmic transformation of reactive hyperemia peripheral arterial tonometry index (LnRHI) less 0.51], a complex glycosaminoglycan was additionally added to the basic prophylaxis with acetylsalicylic acid at a dosage of 250 MU (one capsule three times a day for eight weeks), then a cuff test was monitored after 6–12 weeks. Statistical analysis was performed using the IBM SPSS Statistics 20 software. All tests for significance were two-tailed, and differences were considered significant at p 0.05. RESULTS: Endothelial dysfunction was detected in the first trimester in 59 (55%) patients, then during ongoing complex therapy in the second trimester (n = 72) in 46 (64%) patients and in the third trimester (n = 46) in 4 (1%) patients. Moderate preeclampsia in the third trimester (35–39 weeks of gestation) developed in 28 (25.9%) patients out of 108. At the same time, at the start of the study, 15 patients with endothelial dysfunction received complex therapy, and 13 individuals only took acetylsalicylic acid. Among 46 patients who observed the dynamics of the entire pregnancy, only 4 (8.7%) women developed preeclampsia. After complex treatment prescribed based on the first trimester parameters, out of 36 patients who discontinued complex therapy and did not undergo a functional test subsequently, preeclampsia developed in 16 (44.4%) women. In the second trimester, out of 26 patients who stopped complex therapy, preeclampsia developed in 8 (30.8%) people. Thus, constant monitoring and complex therapy reduced the frequency of preeclampsia. In the group with a history of preeclampsia, the disease developed in 13 (39.4%) women. In the group with a high risk of preeclampsia according to the results of combined prenatal screening in the first trimester, with the exception of a history of preeclampsia (blood pressure test, placental growth factor level in the blood serum, lowest uterine artery pulsatility index value calculated to assess the individual risk of preeclampsia with a titer less than 1 : 100), preeclampsia occurred in 4 (13.3%) women. In the group with extragenital pathology associated with the risk of preeclampsia, including obesity, pregestational diabetes mellitus, chronic arterial hypertension, and chronic kidney disease, with the exception of a history of preeclampsia and a high risk of preeclampsia according to the results of perinatal screening, preeclampsia occurred in 11 (24.4%) women. In the high–risk groups for preeclampsia, we identified the highest-risk group, namely, one with the presence of preeclampsia in the anamnesis. CONCLUSIONS: The effectiveness of the functional method for determining endothelial dysfunction in the first, second and third trimesters of pregnancy during pathogenetic prevention of preeclampsia has been proven.

Acute mesenteric ischemia secondary to complete AV block and acute systolic heart failure: a case report

BackgroundAcute mesenteric ischemia (AMI) usually presents with abrupt and severe abdominal pain associated with nausea and vomiting. This case is notable due to the occurrence of AMI secondary to acute systolic heart failure caused by new onset complete heart block.Case PresentationA 65-year-old male presented with sudden onset epigastric pain. ECG showed complete AV block and acute ischemia, and a subsequent CTA revealed complete occlusion of the mid superior mesenteric artery. His emergent left heart catheterization showed non-occlusive coronary artery disease. The patient underwent emergent laparotomy and SMA thrombectomy. Postoperative complications included worsening congestive heart failure and persistent bradycardia, requiring a permanent pacemaker. The patient was discharged to a skilled nursing facility in stable condition.ConclusionsThis case highlights the diagnostic challenges of AMI in the setting of acute heart failure and new onset AV block mimicking acute cardiac events and emphasizes the importance of a multidisciplinary approach in managing such complex cases.

Unraveling the complexities of ısolated cecal necrosis: a comprehensive presentation clinical symptoms, management strategies, and outcomes in a series of patients

Isolated cecal necrosis (ICN) represents a rare yet clinically significant variant of ischemic colitis, characterized by ischemic injury to the cecal region due to prolonged disruption of intestinal blood flow. While ICN can arise from various causes, including atherothrombotic occlusions in cecal arteries and non-occlusive factors such as shock or chronic diseases, its pathogenesis remains multifactorial. Clinical presentation often mirrors acute appendicitis, with patients typically presenting with sudden right lower quadrant abdominal pain. Prompt diagnosis and surgical intervention are paramount to mitigate the risk of cecal perforation and improve patient outcomes. However, preoperative diagnosis can be challenging due to non-specific radiological findings, necessitating urgent surgical resection of the affected intestine. Despite documented cases in the literature, knowledge regarding ICN remains limited, underscoring the importance of detailed case reporting to enhance disease understanding and refine diagnostic and therapeutic approaches. Here, we present a retrospective analysis of 7 ICN cases diagnosed in our hospital between 2019 and 2024, aiming to contribute insights into the clinical spectrum, management strategies, and outcomes associated with ICN. Our study revealed a diverse array of clinical presentations, radiological features, surgical interventions, and pathological findings among ICN patients. Hypertension and diabetes mellitus emerged as common comorbidities, with acute abdomen and abdominal pain being predominant symptoms. Radiologically, cecal wall thickening was frequently observed. Surgical management predominantly involved right hemicolectomy, with varying techniques employed. Pathological examination unveiled histological alterations indicative of ischemic necrosis, inflammation, and perforation. Our findings underscore the importance of considering ICN in the differential diagnosis of acute abdominal pain, particularly in elderly patients with predisposing risk factors. Further research efforts are warranted to elucidate its pathophysiological mechanisms and optimize therapeutic approaches.

A new angiographic scoring for grading the difficulty of recanalization for symptomatic non-acute middle cerebral artery occlusions.

Endovascular recanalization is a feasible option for treating symptomatic non-acute middle cerebral artery occlusion (MCAO) patients. Hence, we aimed to establish a new angiographic scoring to grade the recanalization difficulty of MCAO to determine the suitable patients for endovascular treatment. We retrospectively analyzed a total of 113 consecutive recurrent symptomatic non-acute MCAO patients who underwent endovascular recanalization from July 2015 to August 2021 in four Chinese comprehensive stroke centers. All patients were reappraised using a new angiographic scoring based on the stump morphology, the MCA occlusion length, MCA bend, and the distal vascular bed of MCAO. We used the final results to establish the patients' outcomes. The total successful recanalization and perioperative complication rates were 83.2% (94/113) and 15.9% (18/113), respectively. No deaths occurred within 30 days. Moreover, 96.9, 90, 87.5, 52.6, and 50% of the patients achieved recanalization with scores of 0, 1, 2, 3, and 4 (p < 0.001), respectively. However, the perioperative complication rate showed the opposite trend. (3.1% vs. 7.5% vs. 6.3% vs. 52.6% vs. 50%; p < 0.001). The median time of successful microwire crossing of the occlusion lesion (TMO) in the score 0 group was shorter than the other groups (2 min, 9 min, 8.5 min, 14 min, and 20 min; p < 0.001). When a score of 2 was used as the optimal cut-off point, the sensitivity and specificity were 86.2 and 63.2%, respectively. The new angiographic scoring can effectively predict the successful recanalization rate, perioperative complication rate, and TMO of endovascular recanalization for non-acute MCAO. It can also be used as an effective clinical evaluation tool to determine the suitable non-acute MCAO patients for recanalization, especially with a score ≤ 2.

Ling gui shen fu decoction ameliorates cardiac injury in ischemic heart disease rats by regulating ANP32A/HIF2α/HMGB1 signal route

Purpose: To investigate the effect of ling gui shen fu decoction (LGSFD) on cardiac injury and cardiomyocyte apoptosis in rats with ischemic heart disease (IHD), and to elucidate the underlying molecular mechanism. Methods: An IHD rat model was established by performing coronary artery occlusion surgery on the left anterior descending (LAD) of rats. The rats were assigned equally to 5 groups: sham-operated group (sham group), IHD group, IHD + perindopril group, IHD + low- dose LGSFD group (IHD + LGSFD-L group), and IHD + high-dose LGSFD group (IHD+LGSFD-H group). The LGSFD was given via gavage. A hypoxia-induced cardiomyocyte model was established by subjecting H9C2 cells to hypoxia. Then, LGSFD-containing serum or blank serum was used to treat the hypoxic rat cardiomyocytes (H9C2). The severity of cardiac injury and extent of apoptotic changes in cardiomyocytes was determined using hematoxylin-eosin (H&amp;E) staining and TUNEL staining, while immunoblotting was used to measure the protein expressions of ANP32A, p-AKT, AKT, HIF-2α, p-mTOR, mTOR and HMGB1. Results: The cardiac injury of rats in the LGSFD groups was significantly reversed, relative to the IHD group (p &lt; 0.05). Moreover, LGSFD reduced the level of apoptosis in hypoxia- induced H9C2 cells and upregulated the concentrations of ANP32A, p-AKT, HIF-2α and p-mTOR. However, the expression levels of HMGB1 were decreased in the heart tissues of IHD rats and hypoxic H9C2 cells. Silencing of ANP32A with ANP32A siRNA (siANP32A) down- regulated ANP32A, p-AKT, HIF-2α and p-mTOR, but up-regulated apoptosis and expression levels of HMGB1 in hypoxic H9C2 cells. Conclusion: LGSFD ameliorates cardiac injury in IHD rats by inhibiting cardiomyocyte apoptosis via the ANP32A/HIF-2α/HMGB1 axis. Further investigations are recommended into the specific mechanism of LGSFD effect using clinical samples, in order to facilitate its clinical development.

Neuroprotective effects of psilocybin in a rat model of stroke

BackgroundPsilocybin is a psychedelic 5HT2A receptor agonist found in “magic mushrooms”. Recent studies have indicated that 5HT2A agonists, such as dimethyltryptamine, given before middle cerebral artery occlusion (MCAo), improve staircase behavior, increased BDNF expression, and reduce brain infarction in stroke rats. The objective of this study is to determine the protective effect of psilocybin in cellular and animal models of stroke.MethodsAdult male and timed-pregnant Sprague-Dawley rats were used for this study. The neural protective effects of psilocybin were determined in primary rat cortical neurons and adult rats. Rats were subjected to a 60-min middle cerebral artery occlusion. Brain tissues were collected for histological and qRTPCR analysis.ResultsPsilocybin reduced glutamate-mediated neuronal loss in rat primary cortical neuronal cultures. Psilocybin-mediated protection in culture was antagonized by the BDNF inhibitor ANA12. Pretreatment with psilocybin reduced brain infarction and neurological deficits in stroke rats. Early post-treatment with psilocybin improved locomotor behavior, upregulated the expression of MAP2 and synaptophysin, and down-regulated the expression of IBA1 in the stroke brain. ANA12 significantly attenuated psilocybin-mediated reduction in brain infarction and improvements in locomotor behavior.ConclusionsPsilocybin reduced brain infarction and improved locomotor behavior in stroke rats; the protective mechanisms involve regulating BDNF expression. Our data support a novel therapeutic approach of psilocybin in stroke.

Glycyrrhizic Acid Inhibits Hippocampal Neuron Apoptosis by Activating the PI3K/ AKT Signaling Pathway.

Glycyrrhizic acid (GA), one of the main active substances in Glycyrrhiza, has anti-inflammatory, anti-viral, and neuroprotective effects. GA can significantly reduce cerebral infarction size in middle cerebral artery occlusion (MCAO) rats and suppress inflammatory responses. However, the underlying mechanism by which GA protects the neuronal system remains poorly understood. Cell proliferation and viability were tested using CCK-8 and Edu assays. The effects of GA on apoptosis were detected using flow cytometry and Tunel assays. Western blotting was performed to assess protein expression. Behavioral experiments were conducted using the Morris water maze and rotation tests. Infarct size was observed using TTC staining. We report that GA protects neurons by inhibiting apoptosis, mainly through the PI3K/AKT pathway in oxygen-glucose deprivation/reoxygenation (OGD/R) and MCAO rat models. GA increases the viability and proliferation of oxygen- and glucose-deprived hippocampal neurons. Hippocampal neuron apoptosis decreased after GA treatment in vitro and in vivo. Furthermore, we determined that GA treatment increased the active state of PI3K and its downstream protein p-AKT, whereas when using a specific inhibitor of PI3K, Y294002, the levels of p-PI3K and p-AKT decreased. Finally, we showed that GA treatment improved spatial memory and motor coordination in MCAO rats, while TTC staining showed that GA decreased cerebral infarct size in MCAO rats. We reveal that GA protects hippocampal neurons by inhibiting their apoptosis, mainly through the PI3K/AKT signaling pathway.

Phenotyping vestibulocochlear manifestations in Susac syndrome: a cohort study.

To characterize vestibulocochlear involvement in patients with Susac syndrome (SuS), a rare immune-mediated endotheliopathy of cerebral, retinal and inner ear microvasculature causing a triad of encephalopathy, branch retinal artery occlusions and sensorineural hearing loss. The electronic patient files of 21 patients with SuS are reviewed for data on demography, clinical presentation, disease course and audiovestibular testing. All 21 patients experienced some form of audiovestibular complaints during the disease course, with vertigo and instability being most frequently reported, followed by hearing loss, tinnitus and aural fullness. These audiovestibular symptoms did not always coincide. Fifteen patients had objectified predominant low- to midfrequency sensorineural hearing loss and 8 out of 18 patients showed abnormalities on vestibular testing, most frequently vestibular evoked myogenic potential-abnormalities, indicating otolith dysfunction. Treatment protocols consisted of uniformly extensive immunosuppressive therapy and hearing loss remained mostly mild. Audiovestibular involvement is very common in patients with SuS. Characteristic findings include a "reverse-slope" configuration on audiological testing and otolith dysfunction on vestibular testing. Aggressive immunosuppression may prevent severe audiovestibular dysfunction. Symptoms as aural fullness and otolith dysfunction may indicate an underlying hydrops. Further investigations are necessary to elucidate the histopathological mechanisms underlying these preferentially involved cochleovestibular areas. Early recognition and treatment of SuS are important to stabilize or decrease disease activity and might also have beneficial effects on inner ear outcome. THE SUBMITTED MANUSCRIPT REPORTS DATA DERIVED FROM CLINICAL OBSERVATIONS IN HUMANS: Consent for the research was provided by the Ethics Committee of Ghent University hospital (application number 2019/1443, registration date 31/12/2021, principal investigator Guy Laureys).

Utility of automated CT perfusion software in acute ischemic stroke with large and medium vessel occlusion.

Early diagnosis of large vessel occlusion (LVO) in acute stroke often requires CT angiography (CTA). Automated CT perfusion (CTP) software, which identifies blood flow abnormalities, enhances LVO diagnosis and patient selection for endovascular thrombectomy (EVT). This study evaluates the sensitivity of automated CTP images in detecting perfusion abnormalities in patients with acute ischemic stroke (AIS) and LVO or medium vessel occlusion (MeVO), compared to CTA. We screened acute ischemic stroke patients presenting within 24 h who underwent CT, CTA, and CTP as per institutional protocol. RAPID AI software processed CTP images, while neuroradiologists reviewed CTA for intracranial arterial occlusions. Sensitivity, specificity, and accuracy of automated CTP maps in detecting occlusions were assessed. Of 790 screened patients, 31 were excluded due to lack of RAPID CTP data or poor-quality scans, leaving 759 for analysis. The median age was 71 years (IQR: 61-81), with 47% female. Among them, 678 had AIS, and 81 had AIS ruled out. CTA identified arterial occlusion in 562 patients (74%), with corresponding CTP abnormalities in 537 patients (Tmax > 6 sec). In the 197 without occlusion, CTP was negative in 161. Automated CTP maps had a sensitivity of 95.55% (CI 95: 93.50-97.10%), specificity of 81.73% (CI 95: 75.61-86.86%), negative predictive value of 98.22% (CI 95: 97.39-98.79%), positive predictive value of 63.54% (CI 95: 56.46-70.09%), and overall accuracy of 85.18% (CI 95: 82.45-87.64%). Automated CTP maps demonstrated high sensitivity and negative predictive value for LVOs and MeVOs, suggesting their usefulness as a rapid diagnostic tool, especially in settings without expert neuroradiologists.

Percutaneous Deep Venous Arterialization by Balloon Angioplasty without Stent Implantation for Patients with Chronic Limb-Threatening Ischemia Undergoing Hemodialysis: A Retrospective Cohort, Single-Center, Single-Arm Study.

This retrospective, single-center study aimed to determine the efficacy of percutaneous deep venous arterialization in patients on hemodialysis with chronic limb-threatening ischemia. Twenty-one consecutive limbs on hemodialysis with chronic limb-threatening ischemia were treated with percutaneous deep venous arterialization using balloon angioplasty following a failed pedal arterial reconstruction between May 2021 and June 2022. An arteriovenous fistula near the ankle joint was created to ensure sufficient venous flow reversal to the pedal veins. In case of occlusion of the tibial artery, a guidewire was advanced (subintimal) to the ankle joint vicinity was technically important. The primary outcome measures were the 6-month complete wound healing and freedom from major amputation rates; the secondary outcome measure was the 6-month amputation-free survival. Occlusion of all pedal arteries was observed in 17 limbs (81.0%). Arteriovenous fistulas were predominantly created at the distal portions of the posterior tibial artery and vein in 18 limbs (85.7%). No extravasation at the fistulas was observed. Re-intervention was required in 16 limbs (76.2%) due to tibial artery or deep vein occlusion. The 6-month complete wound healing rate was 42.9% (nine limbs), with a median healing time of 85 days (interquartile range: 58-151 days). The 6-month freedom from major amputation and amputation-free survival rates were 90.5% (19 limbs) and 61.9% (13 limbs), respectively. Balloon angioplasty without stent implantation for percutaneous deep venous arterialization is promising for improving the complete wound healing and amputation-free survival rates after pedal artery reconstruction failure. Level 3b, retrospective cohort study.

Acute middle cerebral artery occlusion due to a small internal carotid aneurysm cavity with blood stagnation: illustrative case.

In cerebral large vessel occlusion, even when an aneurysm is close to the target vessel, if the aneurysm is relatively small and angiography shows no thrombus within the aneurysm, it is difficult to identify the aneurysm as the embolic source. A 67-year-old man with a history of two left-sided cerebral infarctions developed a small left-sided cerebral infarction. On hospital day 3, he developed a left M2 occlusion and underwent thrombectomy with retraction of a stent retriever into an aspiration catheter at the proximal end of the thrombus. A red thrombus was retrieved, and M2 recanalization was successfully achieved. Angiography revealed a large partially thrombotic aneurysm with a small cavity with blood stagnation in the left cervical internal carotid artery, which was considered the embolic source. Stent-assisted coil embolization was performed on the aneurysm, and no recurrent cerebral infarction was observed after embolization. In cerebral large vessel occlusion, an aneurysm cavity with blood stagnation may be the embolic source. Using an aspiration catheter alone or retracting a stent retriever into an aspiration catheter could be a useful technique and help to avoid interference between the aneurysm and the stent retriever. https://thejns.org/doi/10.3171/CASE24406.

Fabry disease in female monozygotic twins with complex intronic haplotype variants: a case report

BackgroundFabry disease is an X-linked lysosomal storage disease caused by the impairment of α-galactosidase A. The complex intronic haplotype (CIH) variants, located in promoter and intronic regulatory lesions, has been found in patients with classical forms of Fabry disease. We present a case of Fabry disease in female monozygotic twins exhibiting the CIH mutation and classical manifestations.Case presentationA 61-year-old woman with a history of stroke, carotid artery occlusion, hypertrophic cardiomyopathy, and chronic kidney disease was referred to the nephrology clinic for management of her chronic kidney disease. Her monozygotic twin sister also presented with hypertrophic cardiomyopathy, atrial flutter, carotid stenosis, and proteinuria. Clinical symptoms and a comprehensive family history strongly suggested the presence of Fabry disease. Genetic analysis revealed the presence of 5 variants within a complex intronic haplotype (CIH): c.−10 C > T, c.369 + 990 C > A, c.370 − 81_370–77delCAGCC, c.640–16 A > G, and c.1000–22 C > T. We conducted a review of the patient’s previous kidney biopsy findings, which demonstrated the presence of lamellated inclusion bodies in electron microscopy. Remarkably, both the monozygotic twin sister and her son exhibited the same genetic mutation. Enzyme replacement therapy was initiated for the patient. Her kidney function decreased throughout a thorough 2-year follow-up period, while there was a slight decrease in the left ventricular mass index.ConclusionsThis is the first reported case of female monozygotic twins with the CIH variants representing cardiac, cerebrovascular, and renal manifestations suggestive of Fabry disease.

Ocular Ultrasound, a neglected tool in the diagnosis of central retinal artery occlusion.

Purpose: To discuss the practical utility of ocular ultrasound in central retinal artery occlusion (CRAO). Methods: Ocular ultrasound was obtained in 4 patients with CRAO using a 20 MHz Annular Array Probe of the ABSolu (Quantel Medical, Texas, USA) ultrasound machine. Results: The causative embolus occluding the central retinal artery was detected on ocular ultrasound imaging in four patients with CRAO. Conclusion: Ocular ultrasound, including newer generation, higher frequency ultrasound probes, aids in the detection of the “retrobulbar spot sign”, a finding that seems to be related to embolic central retinal artery occlusion. This sign will orient investigations towards finding an embolic source.

Reliable infarction of the middle cerebral artery territory in C57BL/6 mice using pterygopalatine artery ligation and filament optimization - The PURE-MCAo model.

Current techniques for inducing intraluminal filamentous middle cerebral artery occlusion (fMCAo) in mice produce highly variable results and often cause additional infarcts in the posterior cerebral artery (PCA) territory. The aim of the current study was to develop a novel procedure to overcome these shortcomings. Male C57BL/6 mice were subjected to 60 min of fMCAo with cerebral blood flow monitored by laser Doppler flowmetry. The influence of the length of the occlusion filament coating and the combination of common carotid artery (CCA) or pterygopalatine artery (PPA) ligation on lesion volume and functional outcome 24 h after reperfusion was evaluated. The use of appropriate filament and PPA ligation while maintaining CCA perfusion prevented the development of infarcts in the PCA area, resulted in pure MCA infarcts (68.3 ± 14.5 mm3) and reduced the variability of infarct volumes by more than half (from 26-38% to 14% standard deviation/mean). Using an improved fMCAo procedure, we were able to produce PCA area-unaffected reproducible (PURE) infarcts exclusively in the MCA territory. Thus PURE-MCAo reduced outcome variability by more than 50%. Our results may thus help to reduce the number of animals in preclinical stroke research and to increase the reproducibility of the fMCAo model.

Analysis of the brain transcriptome, microbiome and metabolome in ketogenic diet and experimental stroke

The ketogenic diet (KD) has been shown to be effective in treating various brain pathologies. In this study, we conducted detailed transcriptomic and metabolomic profiling of rat brains after KD and ischemic stroke in order to investigate the effects of KD and its underlying mechanisms. We evaluated the effect of a two-month KD on gene expression in intact brain tissue and after middle cerebral artery occlusion (MCAO). We analyzed the effects of KD on gut microbiome composition and blood metabolic profile as well as investigated the correlation between severity of neurological deficits and KD-induced changes. We found transcriptional reprogramming in the brain after stroke and KD treatment. The KD altered the expression of genes involved in the regulation of glucose and fatty acid metabolism, mitochondrial function, the immune response, Wnt-associated signaling, stem cell development, and neurotransmission, both in intact rats and after MCAO. The KD led to a significant change in the composition of gut microbiome and the levels of amino acids, acylcarnitines, polyunsaturated fatty acids, and oxylipins in the blood. However, the KD slightly worsened the neurological functions after MCAO, so that the therapeutic effect of the diet remained unproven.

Detecting cardiac states with wearable photoplethysmograms and implications for out-of-hospital cardiac arrest detection.

Out-of-hospital cardiac arrest (OHCA) is a global health problem affecting approximately 4.4million individuals yearly. OHCA has a poor survival rate, specifically when unwitnessed (accounting for up to 75% of cases). Rapid recognition can significantly improve OHCA survival, and consumer wearables with continuous cardiopulmonary monitoring capabilities hold potential to "witness" cardiac arrest and activate emergency services. In this study, we used an arterial occlusion model to simulate cardiac arrest and investigated the ability of infrared photoplethysmogram (PPG) sensors, often utilized in consumer wearable devices, to differentiate normal cardiac pulsation, pulseless cardiac (i.e., resembling a cardiac arrest), and non-physiologic (i.e., off-body) states. Across the classification models trained and evaluated on three anatomical locations, higher classification performances were observed on the finger (macro average F1-score of 0.964 on the fingertip and 0.954 on the finger base) compared to the wrist (macro average F1-score of 0.837). The wrist-based classification model, which was trained and evaluated using all PPG measurements, including both high- and low-quality recordings, achieved a macro average precision and recall of 0.922 and 0.800, respectively. This wrist-based model, which represents the most common form factor in consumer wearables, could only capture about 43.8% of pulseless events. However, models trained and tested exclusively on high-quality recordings achieved higher classification outcomes (macro average F1-score of 0.975 on the fingertip, 0.973 on the finger base, and 0.934 on the wrist). The fingertip model had the highest performance to differentiate arterial occlusion pulselessness from normal cardiac pulsation and off-body measurements with macro average precision and recall of 0.978 and 0.972, respectively. This model was able to identify 93.7% of pulseless states (i.e., resembling a cardiac arrest event), with a 0.4% false positive rate. All classification models relied on a combination of time-, power spectral density (PSD)-, and frequency-domain features to differentiate normal cardiac pulsation, pulseless cardiac, and off-body PPG recordings. However, our best model represented an idealized detection condition, relying on ensuring high-quality PPG data for training and evaluation of machine learning algorithms. While 90.7% of our PPG recordings from the fingertip were considered of high quality, only 53.2% of the measurements from the wrist passed the quality criteria. Our findings have implications for adapting consumer wearables to provide OHCA detection, involving advancements in hardware and software to ensure high-quality measurements in real-world settings, as well as development of wearables with form factors that enable high-quality PPG data acquisition more consistently. Given these improvements, we demonstrate that OHCA detection can feasibly be made available to anyone using PPG-based consumer wearables.

8291 Graves’ Disease and Moyamoya Syndrome: A Complex Case of Thyroid Dysfunction and Neurovascular Abnormalities

Abstract Disclosure: A. Jamil: None. Q.V. Luong: None. A. Llorens Bonilla: None. A. Siddiqui: None. Background: Moyamoya disease is a cerebrovascular disease characterized by progressive stenosis and occlusion of cerebral arteries, particularly the internal carotid arteries, proximal anterior and middle cerebral arteries associated with a net-like collateral vessel formation. Moyamoya disease in association with certain systemic conditions (e.g. Graves’ disease, sickle cell anemia, neurofibromatosis type 1, and Down Syndrome) has been referred to as moyamoya syndrome. Graves’ disease is an autoimmune disease in which the development of thyroid-stimulating hormone (TSH) receptor autoantibodies leads to overproduction of thyroid hormones. Although the pathophysiology is unclear, Graves’ disease can adversely impact the clinical course of moyamoya syndrome.Clinical Case: A 26-year-old woman diagnosed with Graves’ disease at the age of 20 years who was in remission presented to the ED with right upper extremity weakness and headache. A stroke work-up was performed, and an initial CT head without contrast showed an acute infarct in the left temporal area. Extensive workup for hypercoagulability and cardiac causes were negative. MRI brain showed multiple infarcts of the left cerebral hemisphere with ivy sign, which are prominent linear or punctate high intensity areas in the subarachnoid space reflecting the development of collaterals that occurs in moyamoya disease. TSH at the time was noted to be &amp;lt;0.01 uIU/mL (range: 0.30-4.20 uIU/mL), indicating a thyrotoxic state. She was discharged on methimazole and antiplatelet therapies. However, the patient continued to have hypertension and headaches which did not resolve with the return to euthyroidism. At age 29, she again developed acute right upper and lower extremity weakness, and consequently presented to the ED. Imaging studies showed multiple punctate infarcts in her bilateral frontal lobes and bilateral ICA stenosis consistent with moyamoya disease. However, her biochemical studies showed euthyroidism. Ultimately, she underwent right frontotemporal craniotomy and direct parietal superficial temporal artery to middle cerebral artery bypass by neurosurgery to decrease her future stroke risk for her moyamoya syndrome, and her Graves’ disease remains in remission.Conclusions: The coexistence of Graves’ disease in moyamoya syndrome may suggest a pathophysiologic connection. It has been suggested that hemodynamic changes in cerebrovascular flow due to thyrotoxicosis might contribute to ischemic neurologic deficits. Surgical intervention for revascularization procedures should be attempted after optimal control of thyrotoxicosis, as this may help to prevent further ischemic events in the future and improve patient outcomes. Presentation: 6/1/2024

Life-threatening presentation of an acute cerebellar ischemic stroke secondary to a protein C deficiency.

Acute cerebellar ischemic stroke is a rare disease in children. Typically, patients present with ataxia and cranial nerve palsy. Rarely, some patients show a severe intracranial hypertension syndrome with a life-threatening clinical presentation. We report a case of a 2-year-old male child who was admitted for deterioration of his consciousness level and vomiting. Cerebral imaging revealed a right cerebellar and brainstem infarction with an obstructive hydrocephalus and a tonsillar herniation. Angiography identified an occlusion of the right anterior inferior cerebellar artery. The child was referred to a neurosurgeon for the treatment of acute hydrocephalus and posterior fossa craniectomy. Etiological investigations revealed a protein C deficiency. Initially, the patient was maintained under fluid restriction and received mannitol several times as he had clinical and radiological signs of intracranial hypertension. He was also kept on mechanical ventilation and monitored. However, the evolution was complicated by the occurrence of a thrombosis of the vena cava and the renal vein.

TCD-Guided management in carotid endarterectomy: a retrospective study

BackgroundːStroke, primarily resulting from ischemic conditions, is the foremost cause of mortality and long-term impairment and is frequently associated with narrowing of the carotid arteries. Although carotid endarterectomy (CEA) is the treatment of choice, it carries the risk of cerebral ischemia and reduced blood flow. Transcranial Doppler (TCD) ultrasound offers a nonintrusive method to assess cerebral blood circulation during CEA, potentially enhancing surgical outcomes. The objective of this study was to assess the clinical utility and safety of TCD monitoring during CEA and to identify factors influencing postoperative complications.MethodsThis retrospective analysis included 158 CEA patients (from January 2021–August 2023) who underwent TCD monitoring and whose data were compared to historical standard care data. The primary outcomes were operation duration and artery occlusion time. Secondary outcomes included carotid shunt usage, seven-day postoperative complications, and six-month carotid artery patency. Logistic regression identified factors linked to adverse reactions, and a predictive model was evaluated with a receiver operating characteristic (ROC) curve.ResultsːComparative analysis indicated significant reductions in both the duration of surgery (113.26 ± 7.29 min) and artery occlusion time (21.85 ± 2.92 min) for patients monitored with TCD (P < 0.001) and an increase in carotid shunt implementation (25% as opposed to traditional care). The observed postoperative complications were minor, with a nonsignificant trend that favored the use of TCD-monitored procedures (1% vs. historical rates). Factors such as patient age and plaque echogenicity were found to be predictive of postoperative issues, with plaque echogenicity emerging as a significant predictive factor (OR = 10.70, 95% CI: 2.14–202, P = 0.02) upon multivariate analysis. The predictive model exhibited high precision (AUC = 0.93).ConclusionThis retrospective evaluation suggested that TCD monitoring in the CEA may reduce procedural time and potentially decrease postoperative complications, supporting its use for personalized surgical planning.

APMCG-1 attenuates ischemic stroke injury by reducing oxidative stress and apoptosis and promoting angiogenesis via activating PI3K/AKT pathway

Ischemic stroke (IS) is a major cause of mortality and morbidity worldwide. Beyond thrombolysis, strategies targeting anti-oxidative apoptosis and angiogenesis are considered prospective therapeutic strategies. Nevertheless, existing natural and clinical remedies have limited efficacy in the management of IS. Moreover, despite their millennial legacy of IS remediation, natural remedies such as ginseng incur high production costs. The novel glycopeptide APMCG-1, extracted from mountain-cultivated ginseng dregs in our previous study, is a potent therapeutic candidate for IS. This study investigated APMCG-1's remedial mechanisms against IS injury using an H2O2-induced oxidative stress paradigm in human umbilical vein endothelial cells (HUVECs) emulating ischemic endothelial cells, in a ponatinib-induced zebrafish IS model, and in rat middle cerebral artery occlusion (MCAO) prototypes. Cellular assays confirmed the proficiency of APMCG-1 in preventing oxidative stress and cell death, fostering regeneration, and facilitating neovascularization within the H2O2-stressed HUVECs framework. Moreover, APMCG-1 augmented hemodynamic velocity, oxidative stress mitigation, apoptosis reduction, and motor enhancement in a zebrafish model of IS. In MCAO rats, APMCG-1 ameliorated neurological deficits and cerebral injury, as evidenced by increased neurological scores and diminished infarct dimensions. In cells and animal models, APMCG-1 activated the PI3K/AKT signaling pathway, modulating factors such as Nrf2, Bcl-2, Caspase 3, eNOS, and VEGFA, thereby ameliorating cellular oxidative distress and catalyzing angiogenesis. Collectively, these results demonstrate the potential protective effects of APMCG-1 in IS pharmacotherapy and its prospective utility as an herbal-derived IS treatment modality.