Early Ischemia Research Articles

Advancing ischemic stroke diagnosis and clinical outcome prediction using improved ensemble techniques in DSC-PWI radiomics.

Ischemic stroke is a leading global cause of death and disability and is expected to rise in the future. The present diagnostic techniques, like CT and MRI, have some limitations in distinguishing acute from chronic ischemia and in early ischemia detection. This study investigates the function of ensemble models based on the dynamic radiomics features (DRF) from the dynamic susceptibility contrast perfusion-weighted imaging (DSC-PWI) ischemic stroke diagnosis, neurological impairment assessment, and modified Rankin Scale (mRS) outcome prediction). DRF is extracted from the 3D images, features are selected, and dimensionality is reduced. After that, ensemble models are applied. Two model structures were developed: a voting classifier with 6 bagging classifiers and a stacking classifier based on 4 bagging classifiers. The ensemble models were evaluated on three core tasks. The Stacking_ens_LR model performed best for ischemic stroke detection, the LR Bagging model for NIH Stroke Scale (NIHSS) prediction, and the NB Bagging model for outcome prediction. These outcomes illustrate the strength of ensemble models. The work showcases the role of ensemble models and DRF in the stroke management process.

Precision medicine in intestinal ischemia: the emerging role of biomarkers.

Intestinal ischemia (IIs) is a significant gastrointestinal condition characterized by reduced blood flow to the bowel, leading to inflammation and injury. Early diagnosis and management are crucial for preventing severe complications. Under this point of view, circulating biomarkers can enhance patient stratification and guide therapeutic decisions. Fatty acid-binding proteins (FABPs), specifically I-FABP and L-FABP, are small cytosolic proteins released upon enterocyte membrane integrity loss, with elevated plasma levels indicating early intestinal ischemia. Stromal Cell-Derived Factor-1 (SDF-1) regulates stem cell function and shows significantly higher levels in patients with IIs and cardiovascular disease compared to controls. D-Lactate, a bacterial fermentation byproduct, is another significant marker, with higher serum levels observed in intestinal ischemia cases. Alpha-glutathione S-transferase combats intracellular oxidative stress, with significantly elevated levels in acute mesenteric ischemia patients. Additionally, SM22, a small smooth muscle protein, shows higher plasma levels in patients with transmural ischemia compared to those with mucosal ischemic lesions and healthy controls. These biomarkers are promising for their roles in early detection and differentiation of IIs from other gastrointestinal conditions. Therapeutic strategies, including anti-inflammatory therapies, have shown efficacy in managing IIs symptoms and preventing recurrence. This review aims to inform clinicians and researchers about the current advancements in biomarker research and therapeutic approaches for IIs, emphasizing the importance of integrating these biomarkers and treatments into clinical practice to improve the management and prognosis of the disease.

Early Cardiac Ischemia–Reperfusion Injury: Interactions of Autophagy with Galectin-3 and Oxidative Stress

Background: Cardiovascular diseases are the leading cause of death worldwide, including the United Arab Emirates. Ischemia–reperfusion (IR) injury results in the death of cardiac myocytes that were viable immediately before myocardial reperfusion. We aim to investigate the role of galectin-3 (Gal-3) in autophagy during ischemia–reperfusion injuries. Methods: Male C57B6/J and Gal-3 knockout (KO) mice were used for the murine model of IR injury. Heart samples and serum were collected 24 h post-IR and were processed for immunohistochemical and immunofluorescent labeling and an enzyme-linked immunosorbent assay. Results: There was a significant increase in left ventricle (LV) concentrations of Gal-3 in Gal-3 wild-type mice compared to sham mice. There were significantly higher concentrations of LV autophagy proteins and phospho-AMPK in IR Gal-3 KO mice than in IR Gal-3 wild-type mice, compared to lower concentrations of LV phospho-mTOR and p62 in IR Gal-3 KO than in IR wild-type mice. Antioxidant activities were higher in the LVs of IR Gal-3 wild-type mice, while oxidative stress was higher in the LVs of IR Gal-3 KO mice. Conclusions: Our study supports the interaction of Gal-3 with autophagy proteins, oxidative stress, and antioxidant proteins and demonstrates that the absence of Gal-3 can enhance autophagy in the heart after IR injury.

Yap Is a Nutrient Sensor Sensitive to the Amino Acid L-Isoleucine and Regulates the Expression of Ctgf in Cardiomyocytes.

Myocardial infarction and reperfusion constitute a complex injury consisting of many distinct molecular stress patterns that influence cardiomyocyte survival and adaptation. Cell signalling, which is essential to cardiac development, also presents potential disease-modifying opportunities to recover and limit myocardial injury or maladaptive remodelling. Here, we hypothesized that Yap signalling could be sensitive to one or more molecular stress patterns associated with early acute ischemia. We found that Yap, and not Taz, expression patterns differed in a post-myocardial infarct compared to a peri-infarct region of rat hearts post-myocardial infarction, suggesting cell specificity that would be challenging to resolve for causation in vivo. Using H9c2 ventricular myotubes in vitro as a model, Yap levels were determined to be more sensitive to nutrient deprivation than other stress patterns typified by ischemia within the first hour of stress. Moreover, this is mediated by amino acid availability, predominantly L-isoleucine, and influences the expression of connective tissue growth factor (Ctgf)-a major determinant of myocardial adaptation after injury. These findings present novel opportunities for future therapeutic development and risk assessment for myocardial injury and adaptation.

Myointimal hyperplasia of the mesenteric veins mimicking inflammatory bowel disease in a 13‐year‐old patient

AbstractIdiopathic myointimal hyperplasia of the mesenteric veins (IMHMV) is a rare entity reported in adults, frequently mimicking inflammatory bowel disease (IBD). We report the first case of intestinal ischemia secondary to IMHMV presenting as IBD in a pediatric patient with Down syndrome. Chronic intestinal ischemia is rare in children, and this case emphasizes the need to consider this in the differential, when histopathology is suggestive. Clinical findings and colonoscopy in these patients may mimic IBD. The mucosal biopsies do not show classic features of IBD. Instead, there can be variable extent of mucosal changes such as dilated small capillaries in the lamina propria, edema, and early fibrosis. These changes may in fact represent early chronic ischemia. These findings should alert for vascular imaging and a full‐thickness biopsy to assess submucosal and subserosal larger vessels since medium‐ and large‐caliber veins in the colonic wall and mesentery are affected in IMHMV.

Early Bone Ischemia in Pediatric Acute Hematogenous Osteomyelitis and its Association With Progression to Chronic Osteomyelitis: New Insights From Gadolinium-enhanced Subtraction MRI.

Acute hematogenous osteomyelitis (AHO), the most common osteoarticular infection in children, carries a significant risk for chronic complications. Predicting chronic complications early in the course of disease is challenging. The underlying pathogenesis of complications is not fully understood. Children who presented to Sultan Qaboos University Hospital, Muscat, Oman between January 2015 and April 2022 for AHO were identified by a search of magnetic resonance imaging (MRI) records. Children between 1 month and 18 years of age who did not meet exclusion criteria, and whose MRI also included gadolinium-enhanced subtraction (GES) sequences were included in the analysis. Outcomes were compared between patients who showed early evidence of bone ischemia and those who did not. The analysis included 11 children who had GES MRI sequences from among 18 AHO cases in total. Median age was 5 years (IQR, 4-9), and 82% were males. Median duration of symptoms at presentation was 5 days (IQR, 3-7). GES sequences showed early bone ischemia in 6 of 11 (55%) patients. Patients with early bone ischemia were treated with significantly longer durations of IV antibiotics (median 23 vs. 10 days, P = 0.017) and oral antibiotics (median 134 vs. 29 days, P = 0.004), and required more surgical debridements (median 3 vs. 0 debridements, P = 0.017). Chronic osteomyelitis only developed among patients with early bone ischemia (5/6 vs. 0/5, P = 0.015). In pediatric AHO, GES MRI sequences revealed early bone ischemia in a significant proportion of patients. Early bone ischemia was strongly associated with progression to chronic osteomyelitis.

Impact of Carotid Siphon Calcification on the Course and Outcome of Patients With Aneurysmal Subarachnoid Hemorrhage.

Carotid siphon calcification (CSC) serves as a marker of atherosclerosis and therefore may influence the outcome after subarachnoid hemorrhage (aSAH). We aimed to analyze the impact of CSC on neurological outcomes, ischemia, and vasospasm. A total of 716 patients with aSAH were treated between December 2004 and June 2016 in our central European tertiary neurovascular care center in Essen, Germany. CSC was recorded using the Woodcock scale (grades 0-3) on a computed tomography scan. Study end points included an unfavorable outcome at 6 months post-aSAH (modified Rankin Scale score ≥4), vasospasm, and early cerebral ischemia (72 hours) and delayed cerebral ischemia (delayed cerebral ischemia; >72 hours) in the follow-up computed tomography scans. The associations were adjusted for patients' baseline characteristics and secondary complications. Finally, within a subgroup analysis, patients with and without daily aspirin intake after endovascular aneurysm occlusion were compared. Increasing grades of CSC were associated with lower rates of vasospasm in the anterior circulation. Severe CSC (grade 3) was independently related to the risk of an unfavorable outcome (adjusted odds ratio [aOR], 4.06 [95% CI, 1.98-8.33]; P<0.001) and early cerebral ischemia (aOR, 1.58 [95% CI, 1.03-2.43]; P=0.035) but not delayed cerebral ischemia (aOR, 1.08 [95% CI, 0.67-1.73]; P=0.763). In the aspirin subgroup analysis, the negative effect of severe CSC on functional outcome remained significant only in aSAH cases without aspirin (aOR, 5.47 [95% CI, 2.38-12.54]; P<0.001). In contrast, there was no association between severe CSC and unfavorable outcomes among individuals with daily aspirin intake (aOR, 0.84 [95% CI, 0.59-4.21]; P=0.603). Our data suggest CSC as a cerebrovascular risk factor resulting in higher rates of early cerebral ischemia and unfavorable outcomes after aSAH. However, by increasing arterial stiffness, CSC might lower the probability of vasospasm, which could explain the missing link between CSC and delayed cerebral ischemia. Additionally, aspirin intake seems to potentially mitigate the negative impact of CSC on aSAH outcome. Further investigations are needed to confirm the observations from the present study.

Frailty as an Independent Predictor of Adverse Outcomes in Patients Undergoing Direct Myocardial Revascularization.

The study included 387 patients admitted to the clinic for a scheduled primary CABG. A seven-item questionnaire, "PRISMA-7", was used to identify frail elderly patients before the procedure. We divided the study sample into two groups, taking into account the results of the survey: patients without frailty, n0 = 300 (77.5%), and patients with frailty, n1 = 87 (22.5%). The anamnestic and laboratory data, outcome of the surgical intervention, perioperative and early complications, and adverse outcomes were analyzed. We detected frailty in 22.5% of the patients with CAD before the procedure. According to the anamnestic data and paraclinical and intraoperative findings, the groups of patients with and without frailty were comparable. The differences were revealed in the intraoperative and early postoperative periods of CABG. Thus, postoperative rhythm disturbances (19.5% vs. 10.5%, p = 0.025, V = 0.115, respectively) and transient ischemic attacks/stroke (5.7% vs. 1.3%, p = 0.031, V = 0.122, respectively) occurred significantly more often among the frail patients. There were no significant differences between the groups in the frequency of other intraoperative and early postoperative complications. In the group of frail patients, four fatal outcomes due to early postoperative ischemia were recorded, and among patients without frailty, one fatal outcome was recorded (4.5% vs. 0.3%, p = 0.010, V = 0.156, respectively). At the 1-year follow-up visit, the presence of frailty in history served as a predictor of mortality (11.5% vs. 0.6%, p ˂ 0.001, V = 0.290, respectively). The presence of frailty can be used as an independent predictor of an unfavorable prognosis in patients with CAD, both in the perioperative and early survival period after CABG. It should be taken into account during surgical risk assessment.

A study to observe the association of left ventricular ejection fraction and wall motion score index with duration of early systolic lengthening in patients with non-ST-elevation acute coronary syndrome

Background: Management of non-ST elevation myocardial infarction acute coronary syndrome (NSTEMI ACS) patients is not well defined as that of ST elevation myocardial infarction. The accuracy of results of conventional echocardiography is significantly compromised when imaging is suboptimal, myocardial damage is in small areas, and compensatory hyperkinesias of healthy segment. Aims and Objectives: Duration of early systolic lengthening (DESL) may be employed to identify early myocardial ischemia and thus, may help to prepare treatment strategies for NSTEMI patients. Materials and Methods: A total of 57 patients with NSTEMI ACS attending the cardiology department were included in the study group. Results: More than 80% of patients of NSTEMI have normal or near normal ejection fraction and wall motion score index. In our study, the DESL is prolonged in a significant number of non-ST-elevation acute coronary syndrome patients. Conclusion: As DESL is afterload independent, it is superior to global longitudinal strain in assessing myocardial damage. Several studies including ourselves show that DESL of &lt;50 ms may be the cutoff value to reveal minimal myocardial damage.

Effects of a novel regimen of repetitive transcranial magnetic stimulation (rTMS) on neural remodeling and motor function in adult male mice with ischemic stroke

AbstractNeuroinflammation caused by excessive microglial activation plays a key role in the pathogenesis of ischemic stroke. Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive neuromodulatory technique that has recently been reported to regulate microglial functions and exert anti‐inflammatory effects. The intermittent burst stimulation (iTBS) regimen in rTMS improves neuronal excitability. However, whether iTBS exerts its anti‐inflammatory effects by stimulating neurons and thereby modulating microglial polarization remains unclear. Motor function was assessed after 1 week of rTMS (iTBS regimen) treatment in adult male mice with occlusion/reperfusion of the middle cerebral artery (MCAO/r) injury. We also investigated the molecular biological alterations associated with microglial polarization using a cell proliferation assay, multiplex cytokine bioassays, and immunofluorescence staining. iTBS regimen can improve balance and motor coordination function, increase spontaneous movement, and improve walking function in mice with early cerebral ischemia injury. Expression levels of IL‐1β, TNF‐α, and IL‐10 increased significantly in mice with MCAO injury. Especially, rTMS significantly increased the number of proliferating cells in the infarcted cortex. The fluorescence intensity of MAP2 in the peri‐infarct area of MCAO injured mice was low, but the signal was broader. Compared with MCAO group, the fluorescence intensity of MAP2 in rTMS group was significantly increased. rTMS inhibited pro‐inflammatory M1 activation (Iba1+/CD86+) and improved anti‐inflammatory M2 activation (Iba1+/CD206+) in the peri‐infarct zone, thus significantly changing the phenotypic ratio M1/M2. rTMS improves motor dysfunction and neuroinflammation after cerebral I/R injury in mice by regulating microglial polarization.

Exosomes-carried curcumin based on polysaccharide hydrogel promote flap survival

Flap grafting is a common technique used to repair skin defects in orthopedics and plastic and reconstructive surgeries. However, oxidative stress injury caused by ischemia and ischemia-reperfusion injury at the distal end of the skin flap can cause flap necrosis. Curcumin is a natural compound with anti-inflammatory and antioxidant properties that tackle oxidative stress. However, its applicability is limited by its poor water solubility. Exosomes are membranous vesicles that can be loaded with hydrophobic drugs. They are widely studied in drug delivery applications and can be investigated to augment curcumin efficiency. In this study, a self-healing oxidized pullulan polysaccharide-carboxymethylated chitosan composite hydrogel was used as a curcumin-loaded exosome delivery system to evaluate its impact on the viability of skin flaps. The hydrogel exhibited good self-healing properties that allowed the continuous and stable release of drugs. It had anti-inflammatory and antioxidant properties that could reduce oxidative stress damage due to early ischemia and hypoxia of the skin flap in vitro. Moreover, this composite hydrogel attenuated inflammatory responses, promoted angiogenesis, and reduced the distal necrosis of the flap in vivo. Therefore, our hydrogel provides a novel strategy for skin flap graft protection with reduced necrosis and the potential for broad clinical applications.

The underlying mechanism of calcium toxicity-induced autophagic cell death and lysosomal degradation in early stage of cerebral ischemia.

Cerebral ischemia is the important cause of worldwide disability and mortality, that is one of the obstruction of blood vessels supplying to the brain. In early stage, glutamate excitotoxicity and high level of intracellular calcium (Ca2+) are the major processes which can promote many downstream signaling involving in neuronal death and brain tissue damaging. Moreover, autophagy, the reusing of damaged cell organelles, is affected in early ischemia. Under ischemic conditions, autophagy plays an important role to maintain energy of the brain and its function. In the other hand, over intracellular Ca2+ accumulation triggers excessive autophagic process and lysosomal degradation leading to autophagic process impairment which finally induce neuronal death. This article reviews the association between intracellular Ca2+ and autophagic process in acute stage of ischemic stroke.

Study of Postmortem Pericardial Fluid Concentrations of Troponin T (cTnT) in Sudden Natural Death

Background: Cardiovascular diseases are the most common cause of sudden natural deaths. Cardiac troponin T is a specific biochemical marker of myocardial injury. It may help in diagnosis of early myocardial ischemia when macroscopic or microscopic evidence of necrosis is not available after autopsy. Aim of this study was to assess the effectiveness of pericardial fluid troponin T in predicting the cause of death in sudden natural death and in estimating the post mortem interval. Materials and methods: It was a pilot study. Sudden natural deaths brought to Forensic Medicine department of GMCH Nagpur for autopsy were included in this observational cross sectional study. Deaths were grouped into cardiac and non cardiac deaths. Pericardial fluid samples were collected by opening pericardial sac with sterile syringe and processed on Roche Cobas e411 autoanalyzer for estimation of levels of Troponin T. Results: There was a statistically significant difference seen for the values between the groups (p&lt;0.05) for Trop-T (ng/ml) with higher values in Cardiac cause. There was a statistically non significant correlation between postmortem interval vs Trop T (p&gt;0.05). Conclusion: Estimation of pericardial fluid Troponin-T may be used to predict the cause of death in sudden natural death.

Adenylate kinase 4 promotes neuronal energy metabolism and mitophagy in early cerebral ischemia via Parkin/PKM2 pathway

Mitochondrial dysfunction is closely related to brain injury and neurological dysfunction in ischemic stroke. Adenylate kinase 4 (AK4) plays a critical role in energy metabolism and mitochondrial homeostasis. However, the underlying mechanisms remain unclear. In the present study, we demonstrated an important role of AK4 in mitochondrial dysfunction in the early cerebral ischemia. Early focal cerebral ischemia induced decrease of AK4 protein expression in ischemic hemispheric brain tissue in mice. Exposure of cultured primary neuron to oxygen-glucose deprivation (OGD) also induced AK4 downregulation. Overexpression of AK4 in neuron using adeno-associated virus (AAV-AK4) in mice promoted neuronal survival reflected by decreased infarction volume and TUNEL staining. AK4 overexpression inhibited mitochondrial decline and downregulation of energy metabolism-associated proteins (p-AMPK and ATP1A3) induced by MCAO. Moreover, AK4 knock-in using lentivirus carried AK4 vector (LV-AK4) induced energy metabolism shift from glycolysis to oxidation in neuron. Using transmission electron microscope and western blot, we revealed that AK4 overexpression promoted mitophagy and mitophagy-associated proteins expression PINK1 and Parkin after MCAO. Mass spectrometry and co-immunoprecipitation revealed an interaction between AK4 and PKM2. Mechanistically, AK4 indirectly decreased PKM2 expression via enhancing its ubiquitination by increasing the interaction between PKM2 and its ubiquitin E3 ligase Parkin, and inhibits Parkin downregulation. In conclusion, our data demonstrate that AK4/ Parkin /PKM axis prevents cerebral ischemia damage via regulation of neuronal energy metabolism model and mitophagy. AK4 was a new target for intervention of early ischemic neuron injury.

Mapping tissue microstructure of brain white matter in vivo in health and disease using diffusion MRI

Abstract Diffusion magnetic resonance imaging offers unique in vivo sensitivity to tissue microstructure in brain white matter, which undergoes significant changes during development and is compromised in virtually every neurological disorder. Yet, the challenge is to develop biomarkers that are specific to micrometer-scale cellular features in a human MRI scan of a few minutes. Here, we quantify the sensitivity and specificity of a multicompartment diffusion modeling framework to the density, orientation, and integrity of axons. We demonstrate that using a machine learning-based estimator, our biophysical model captures the morphological changes of axons in early development, acute ischemia, and multiple sclerosis (total N = 821). The methodology of microstructure mapping is widely applicable in clinical settings and in large imaging consortium data to study development, aging, and pathology.

Clinical Applications of Dual‐Energy Computed Tomography for Acute Ischemic Stroke

Acute ischemic stroke is a leading cause for neurological disability worldwide, and treatment strategies are rapidly evolving. Patient selection for recanalization therapy and postintervention management relies heavily on diagnostic imaging. In this narrative review, we searched the existing literature for clinical applications of dual‐energy computed tomography for acute ischemic stroke. We summarized the current clinical evidence on the use of dual‐energy computed tomography for identifying early cerebral ischemia, detecting and predicting hemorrhagic transformations, and characterizing clots and stenotic plaques. We also highlight future opportunities for dual‐energy computed tomography to be used to address important diagnostic challenges during acute stroke triage and postintervention management. Dual‐energy computed tomography is a powerful tool that can be used to improve the diagnostic accuracy of ischemia, hemorrhage, and vascular lesions in the context of acute ischemic stroke.

Intraoperative AI-assisted early prediction of parathyroid and ischemia alert in endoscopic thyroid surgery.

The preservation of parathyroid glands is crucial in endoscopic thyroid surgery to prevent hypocalcemia and related complications. However, current methods for identifying and protecting these glands have limitations. We propose a novel technique that has the potential to improve the safety and efficacy of endoscopic thyroid surgery. Our study aims to develop a deep learning model called PTAIR 2.0 (Parathyroid gland Artificial Intelligence Recognition) to enhance parathyroid gland recognition during endoscopic thyroidectomy. We compare its performance against traditional surgeon-based identification methods. Parathyroid tissues were annotated in 32 428 images extracted from 838 endoscopic thyroidectomy videos, forming the internal training cohort. An external validation cohort comprised 54 full-length videos. Six candidate algorithms were evaluated to select the optimal one. We assessed the model's performance in terms of initial recognition time, identification duration, and recognition rate and compared it with the performance of surgeons. Utilizing the YOLOX algorithm, we developed PTAIR 2.0, which demonstrated superior performance with an AP50 score of 92.1%. The YOLOX algorithm achieved a frame rate of 25.14 Hz, meeting real-time requirements. In the internal training cohort, PTAIR 2.0 achieved AP50 values of 94.1%, 98.9%, and 92.1% for parathyroid gland early prediction, identification, and ischemia alert, respectively. Additionally, in the external validation cohort, PTAIR outperformed both junior and senior surgeons in identifying and tracking parathyroid glands (p < 0.001). The AI-driven PTAIR 2.0 model significantly outperforms both senior and junior surgeons in parathyroid gland identification and ischemia alert during endoscopic thyroid surgery, offering potential for enhanced surgical precision and patient outcomes.

Wandering Spleen with Tortion – A Case Report

A 16-year-old male presented with abdominal pain over 12 months, that had acutely worsened over the 5 days pre-presentation. Preliminary outpatient investigations revealed thrombocytopaenia 90(platelets per microliter), and a pelvic spleen on abdominal ultrasound. Contrast enhanced CT of the abdomen and pelvis in the portal venous phase confirmed a pelvic spleen with torsion of the splenic hilum. The spleen appeared hypoechoic on ultrasound. On CT, the spleen had heterogeneous enhancement with some irregularly shaped regions of hypoenhancement. There was a swirl (at least two complete turns) in the splenic vascular pedicle in the left abdomen. The splenic artery demonstrated some enhancement, but no enhancement of the splenic vein. The pancreatic tail was also involved in the torted vascular pedicle. No pancreatic duct dilation, and no infarct of pancreatic parenchyma were found. A small amount of free fluid around the spleen was found with no free gas. The portal vein enhanced normally. Lack of convincing enhancement of the splenic vein and heterogenous appearance of the spleen were suspicious for early splenic ischaemia. Laparotomy revealed an engorged twisted spleen around its pedicles. The spleen was identified in the pelvis with a torted vascular pedicle, which was subsequently detorted and manipulated back into the left upper quadrant (LUQ), with a pre-peritoneal space formed in the LUQ, the spleen was inserted into this pocket.

Free Flap Perfusion in Microvascular Head and Neck Reconstruction: Influence of the Number of Ischemia Intervals and Ischemia Duration-A Retrospective Study.

In microvascular head and neck reconstruction, ischemia of the free flap tissue is inevitable during microsurgical anastomosis and may affect microvascular free flap perfusion, which is a prerequisite for flap viability and a parameter commonly used for flap monitoring. The aim of this study was to investigate the influence of the number of ischemia intervals and ischemia duration on flap perfusion. Intraoperative and postoperative flap blood flow, hemoglobin concentration, and hemoglobin oxygen saturation at 2 and 8 mm tissue depths, as measured with the O2C tissue oxygen analysis system, were retrospectively analyzed for 330 patients who underwent microvascular head and neck reconstruction between 2011 and 2020. Perfusion values were compared between patients without (control patients) and with a second ischemia interval (early or late) and examined with regard to ischemia duration. Intraoperative and postoperative flap blood flow at 8 mm tissue depth were lower in patients with early second ischemia intervals than in control patients [102.0 arbitrary units (AU) vs 122.0 AU, P = .030; 107.0 AU vs 128.0 AU, P = .023]. Both differences persisted in multivariable analysis. Intraoperative and postoperative flap blood flow at 8 mm tissue depth correlated weakly negatively with ischemia duration in control patients (r = -.145, P = .020; r = -.124, P = .048). Both associations did not persist in multivariable analysis. The observed decrease in microvascular flap blood flow after early second ischemia intervals may reflect ischemia-related vascular flap tissue damage and should be considered as a confounding variable in flap perfusion monitoring.

Point-Of-Care low-field MRI in acute Stroke (POCS): protocol for a multicentric prospective open-label study evaluating diagnostic accuracy

IntroductionFast and accurate diagnosis of acute stroke is crucial to timely initiate reperfusion therapies. Conventional high-field (HF) MRI yields the highest accuracy in discriminating early ischaemia from haemorrhages and mimics....