Search Results (132)

Background/Objectives: This study evaluates whether ultrawide-field optical coherence tomography angiography (UWF-OCTA) can guide navigated laser therapy for non-perfused areas (NPAs) in branch retinal vein occlusion (BRVO). It further explores whether the laser spots can be accurately placed according to plan, considering that the retina is three-dimensional (3D), while UWF-OCTA provides two-dimensional (2D) images. Methods: UWF-OCTA images from three devices—VG200, Xephilio OCT-S1, and Bmizar—guided the treatments. These images were superimposed onto NAVILAS^® system images to guide NPA treatments. Pre-treatment planning was strategically designed to avoid normal and collateral vessels, with immediate post-laser OCTA and en face images assessing the efficacy of the laser spots in avoiding these vessels as planned. The accuracy of navigated laser therapy was further analyzed by comparing the intended laser locations with the actual spots. Results: All montaged OCTA images from the three devices were seamlessly integrated into the navigated laser system without registration errors. All patients received treatments targeting the NPAs as planned. However, not all collateral or normal vessels were successfully avoided by the laser spots. A further analysis revealed that the actual locations of the laser spots deviated slightly from the planned locations, particularly in the mid-periphery areas. Conclusions: UWF-OCTA-guided navigated laser photocoagulation is feasible and precise for treating NPAs in BRVO. Nonetheless, minor deviations between planned and actual locations were observed. This discrepancy, particularly important when treating diseases of the macular area, should be carefully considered when employing OCTA-guided navigated laser photocoagulation. Full article

In this study, pharmacotherapies of abdominal compartment syndrome (ACS) and intra-abdominal hypertension (IAH) in animal studies were reviewed from the perspective of ACS/IAH as failed cytoprotection issues, as non-specific injuries, and from the point of view of the cytoprotection concept as resolution. Therefore, this review challenges the unresolved theoretical and practical issues of severe multiorgan failure, acknowledged significance in clinics, and resolving outcomes (i.e., open abdomen). Generally, the reported agents not aligned with cytoprotection align with current pharmacotherapy limitations and have (non-)confirmed effectiveness, mostly in only one organ, mild/moderate IAH, prophylactic application, and provide only a tentative resolution. Contrarily, stable gastric pentadecapeptide BPC 157 therapy, as a novel and relevant cytoprotective mediator having pleiotropic beneficial effects, simultaneously resolves many targets, resolving established disturbances, specifically compression/ischemia (grade III and grade IV), and decompression/advanced reperfusion. BPC 157 therapy rapidly activates collateral bypassing pathways, and, in ACS and IAH, and later, in reperfusion, there is a “bypassing key” (i.e., azygos vein direct blood flow delivery). This serves to counteract multiorgan and vessel failure, including lesions and hemorrhages in the brain, heart, lung, liver, kidney and gastrointestinal tract, thrombosis, peripherally and centrally, intracranial (superior sagittal sinus), portal and caval hypertension and aortal hypotension, occlusion/occlusion-like syndrome, advanced Virchow triad circumstances, and free radical formation acting as a membrane stabilizer and free radical scavenger. Likewise, not only in ACS/IAH resolving, but also in other occlusion/occlusion-like syndromes, this “bypassing key” could be an effect of the essential endothelial cytoprotective capacity of BPC 157 and a particular modulatory effect on the NO-system, and a rescuing impact on vasomotor tone. Full article

Moyamoya disease (MMD) is a rare yet clinically significant cerebrovascular disorder characterized by progressive stenosis of the distal internal carotid artery and/or its principal branches, accompanied by the development of characteristic collateral vessel networks. This disease demonstrates a complex multifactorial etiology with strong genetic determinants, as evidenced by its distinct geographical distribution patterns and familial clustering. Recent genetic researches have identified multiple pathogenic mutations contributing to MMD development through three principal mechanisms: progressive vascular stenosis, abnormal angiogenesis, and dysregulated inflammatory responses. Furthermore, moyamoya syndrome frequently occurs as a secondary vascular complication in various monogenic disorders. This review provides a comprehensive analysis of recent genetic advances in MMD in view of diverse pathogenic pathways, offering valuable perspectives on the molecular mechanisms underlying disease development and potential therapeutic targets. Full article

We present a rare case of a 16-year-old male who was admitted with bilateral tinnitus and subsequently underwent magnetic resonance imaging (MRI) and digital subtraction angiography (DSA) for further evaluation. The left internal carotid (ICA) artery had a normal caliber but ended as a stump at the C7 segment, with a network of filiform vessels from both the stump and right posterior communicating artery (PComm). The right PComm was hypertrophic and the right posterior cerebral artery (PCA) was mainly supplied by the right ICA. The right ICA’s bifurcation and the initial middle cerebral artery (MCA) segment were absent, while the MCA trunk was hypoplastic. The right PCA and pial branches vascularized the temporal lobe, with collaterals between the PCA and MCA. The left ICA was slightly enlarged with double fenestration at the left A1 segment. The right A1 segment of the anterior cerebral artery had double fenestration and while several diagnoses were considered, no single diagnosis fully explained all clinical findings. A thorough review of the existing literature yielded no comparable cases, highlighting the uniqueness of this presentation. This case emphasizes the complexity of cerebral vascular anomalies and the challenges associated with diagnosing such rare conditions, underscoring the need for careful assessment. Full article

Background: Nodal dendritic cells (DCs) and CD169-positive macrophages, possibly monocyte-derived, cross-present cancer antigens earlier in the proximal node than in the distal node. Methods: We performed immunohistochemical and morphometric analyses to show differences in the distributions of DC-SIGN-, CD68-, and CD169-positive cells in the paratracheal, subcarinal, and hilar nodes from 25 non-small cell lung cancer patients without metastasis. Results: CD169-positive and DC-SIGN-positive cells were colocalized in the subcapsular and paracortical sinuses, whereas CD68-positive, self-renewal alveolar macrophages were present in the medullary sinus. This complementary distribution was more evident in nodes other than hilar nodes. In hilar nodes, the proportion of CD68-positive macrophages usually exceeds 50%. Notably, the proportion of the overlapped cluster between CD169-positive cells and DC-SIGN-positive cells, which likely corresponds to the cross-presentation activity, was almost the same between the hilar and “next-upstream” node (i.e., the paratracheal node for the upper lobe and the subcarinal node for the lower lobe). Monocyte-derived cells occupied a significantly larger area in the hilar nodes of patients with upper lobe cancer than in patients with lower lobe cancer (p = 0.002–0.009). Conclusion: The specific site occupying the lung hilum with collateral vessels seemed to determine the hilar node composite cells. Full article

Background: Hyperintense vessels (HVs) visualized on FLAIR MRI are believed to reflect sluggish antegrade or retrograde flow in leptomeningeal collaterals that develop in response to major intracranial artery stenosis or occlusion. HV is frequently observed in conditions such as Moyamoya disease and symptomatic ICA/MCA steno-occlusion. However, the relationship between HV and cerebral hemodynamics—and the effect of STA-MCA bypass on HV—remains inadequately characterized. This study aimed to investigate the relationship between HV on FLAIR and cerebral vascular hemodynamic status, as measured by SPECT, in patients with Moyamoya disease and symptomatic ICA/MCA occlusion. The secondary goal was to assess the impact of recanalization through STA-MCA bypass surgery on the presence of HV. Methods: We retrospectively analyzed 49 patients with symptomatic ICA or MCA steno-occlusion who underwent STA-MCA bypass between 2015 and 2020. Pre- and postoperative FLAIR MRIs were evaluated, and HV presence was graded as negative (0), minimal (1), or positive (2). SPECT was utilized to assess cerebrovascular reserve (CVR) in regions exhibiting various HV intensities. Follow-up FLAIR imaging was performed 3–14 months postoperatively to correlate HV changes with hemodynamic improvements observed via SPECT. Result: HV was present in 74% (36/49) of affected hemispheres. Regions exhibiting minimal or positive HV demonstrated a significantly lower CVR compared to HV-negative areas, indicating compromised perfusion. Following bypass surgery, HV was reduced or resolved in 65% (32/49) of patients, and this regression corresponded with improved CVR as confirmed by both SPECT and perfusion MRI. Conclusions: HV presence on FLAIR imaging is associated with impaired cerebrovascular hemodynamics in patients with Moyamoya disease or symptomatic large-vessel steno-occlusion. HV-positive territories exhibit reduced CVR, while surgical revascularization via STA-MCA bypass leads to hemodynamic improvement and concurrent HV reduction. These findings support HV as a potential surrogate marker for treatment response. Full article

Background. Statins appear to be useful in patients with acute ischemic stroke. Our aim was to evaluate the association between premorbid statin treatment and CT perfusion characteristics of acute ischemic stroke. Methods. A retrospective analysis of patients with acute stroke secondary to occlusion of large vessels in the anterior circulation was performed to assess collateral flow, ischemic core volume, and ischemic penumbra using CT angiography and CT perfusion maps. Fisher’s exact test was used to compare baseline characteristics of patients in the two groups. The Wilcoxon rank-sum test for independent groups was used to compare all variables obtained for the two different groups with and without statin use. Results. We identified 61 patients, including 29 treated with statins and 32 not treated with statins before stroke onset matched by age, gender, and vascular risk factors except for hypercholesterolemia. The statin group showed lower National Institutes of health Stroke Scale scores at onset (14 ± 6.1 vs. 16 ± 4.5; p = 0.04) and lower volumes of brain tissue characterized by impaired cerebral blood flow (CBF), cerebral blood volume (CBV), and ${\mathrm{T}}_{\mathrm{m}\mathrm{a}\mathrm{x}}^{9.5-25\mathrm{s}}$; otherwise, no statistically significant difference was found in the volume of the ${\mathrm{T}}_{\mathrm{m}\mathrm{a}\mathrm{x}}^{16-25\mathrm{s}}$ between the two groups. Conclusions. Premorbid statin treatment is associated with a favorable imaging condition of acute ischemic stroke in terms of ischemic core and ischemic penumbra volume. Full article

Background: CT perfusion (CTP) overestimation of core volume >10 mL compared to the final infarct volume (FIV) size is the current definition of the ghost infarct core (GIC) phenomenon. However, subsequent infarct growth might influence FIV. We aimed to report a more reliable assessment of GIC occurrence, defined as no evidence of infarct at 24 h follow-up imaging, compared to CTP core volume at admission. This phenomenon was named absolute GIC (aGIC), and we investigated its prevalence and predictors. Methods: A total of 652 consecutive stroke patients with large vessel occlusion who achieved successful recanalization (mTICI 2b-3) after endovascular treatment (EVT) and non-contrast CT (NCCT) follow-up imaging at 24 h were retrospectively analyzed. Ischemic core volume was automatically generated from CTP, and FIV was manually determined on follow-up NCCT. Multivariable logistic regression was used to explore aGIC predictors. Results: We included 652 patients (53.3% female, median age 75 years), of whom 35 (5.3%) had an aGIC. The aGIC group showed higher ASPECTS (p < 0.001), shorter (<3 h) onset-to-imaging time (p < 0.016), poorer collaterals (p < 0.001), and higher hypoperfusion intensity ratio (p < 0.001) compared to the non-aGIC group. In multivariate analysis, ASPECTS (odds ratio (OR), 2.37; p <0.001), onset-to-imaging time (OR, 0.99; p = 0.034), collateral score (OR, 0.24; p < 0.001), and hypoperfusion intensity ratio (OR, 23.2; p < 0.001) were independently associated with aGIC. Conclusions: aGIC is a more reliable evaluation of infarct core volume overestimation assessed on admission CTP and represents a rare phenomenon, associated with ultra-early presentation and poor collaterals. Full article

Background and Objectives: The neutrophil-percentage-to-albumin ratio (NPAR) has been recognized as an independent risk factor for cardiovascular diseases. In our study, we investigated whether the NPAR is associated with the formation of coronary collateral circulation (CCC) in patients with chronic coronary syndrome (CCS). Materials and Methods: A total of 681 patients with CCS were included in this study. Of these patients, 571 had chronic total occlusion in at least one major vessel and developed collateral vessels. In total, 110 patients were in the control group, who had CCS but did not have complete occlusion in a major vessel and did not develop collateral vessels. Patients with collateral vessels on coronary angiography were divided into two groups according to the Rentrop score: poor CCC (Rentrop 0–1) and good CCC (Rentrop 2–3). Blood samples were taken for the NPAR and other biochemical parameters in all patients during hospitalization. The NPAR was calculated as the neutrophil-percentage-to-albumin ratio. Results: The group of patients with poor CCC had a higher white blood count (WBC), neutrophil, C-reactive protein (CRP), neutrophil–lymphocyte ratio (NLR), CRP/albumin ratio (CAR), and NPAR values than patients with good CCC (p < 0.001, for all). Multivariate logistic regression analysis showed that high NPAR levels were an independent predictor of poor CCC (OR: 2.79, 95% CI:1.7–4.6, p < 0.001), accompanied by neutrophil, CRP, CAR, and NLR levels. In the receiver operator characteristic curve (ROC analysis), the cut-off value for the NPAR to indicate poor CCC was 1.78 with a sensitivity of 76.6% and specificity of 81.4% (area under ROC curve = 0.804 95% CI (0.753–0.854), p < 0.001). Conclusions: We demonstrated that the NPAR may be an independent predictor of poor CCC development in clinical practice. Full article

Vascular steal refers to the diversion of blood flow between collateral vessels that share a common inflow restricted by arterial stenosis. Blood is diverted from the high-pressure to the low-pressure, low-resistance system. Vascular steal is associated with anatomical bypass or vasodilation in the collateral network and is called “the arterial steal”. However, we have demonstrated that in the presence of an outflow gradient (e.g., intra-extracranial), blood is shunted to a lower pressure system, a phenomenon we term “venous steal”. Using Thevenin’s equivalent, we generalized the concept of venous steal to apply it to any region of the vascular system with increased outflow pressure. Both arterial steal, caused by increased collateral network conductivity, and venous steal, resulting from lower collateral outflow pressure, reduce compartment perfusion. This occurs indirectly by increasing flow and the pressure gradient across the arterial stenosis, lowering the segmental compartment perfusion pressure—the difference between post-stenotic (inflow) and compartmental (outflow) pressures. Venous steal diverts blood flow from compartments with elevated pressure, such as intracranial, subendocardial, the ischemic core, and regions of focal edema due to inflammation, trauma, or external compression. In shock and low-flow states, it contributes to regional blood flow maldistribution. Treatment of venous steal addresses inflow stenosis, increased compartmental pressure and systemic loading conditions (arterial and venous pressure) to reverse venous steal malperfusion in the ischemic regions. Full article

Good leptomeningeal collaterals (LMCs) after large vessel occlusion (LVO) extend the time window for endovascular therapy. The mechanisms regulating LMC activation are not fully understood. The aim of this study was to investigate the potential role of two vasoactive molecules endothelin-1 (ET-1)—a vasoconstrictor agent—and nitric oxide (NO)—a vasodilator agent—in the regulation of post-stroke LMCs. Ischemic stroke patients within 6 h of LVO were included. Collateral status was assessed using the Menon scoring system based on computed tomography angiography scans. Patients were accordingly divided into three groups: poor, intermediate, and good LMCs. Recanalization was evaluated using the modified thrombolysis in cerebral infarction (mTICI) score. Serum levels of ET-1 and NO were measured at three time points: T0 (<6 h), T1 (24 h), and T2 (48 h). A total of 105 patients were enrolled (mean age 76 ± 12.8 years): 44 with good (46.2%), 36 with intermediate (37.8%), and 22 with poor LMCs (23.1%). NO values decreased, whereas ET-1 values increased from T0 to T1 in all groups of patients. No significant association was found between serum ET-1 levels and collateral status. Higher ET-1 levels at T1 correlated with poor outcome regardless of the LMC status or the degree of recanalization (p = 0.030). A significant linear positive correlation was revealed at T0 between high levels of ET-1 and the neutrophil count (Spearman’s rho = 0.236, p = 0.035). Subgroup analysis showed a significant inverse correlation at T1 between NO and the collateral score (Spearman’s rho = −0.251, p = 0.021). Although we observed no significant association between LMC score and serum ET-1 concentrations, at 24 h higher ET-1 serum levels were predictive of poor outcome and higher NO levels were correlated with poor collateral status. These findings may indicate an inadequate microvascular reperfusion, possibly due to ET-1-mediated vasoconstriction, neutrophil activation, and NO-mediated oxidative stress, suggesting their potential role in the no-reflow phenomenon. Full article

The epiligament (EL), described in 1990 as a connective tissue layer distinguishable from the ligament proper, has only recently gained recognition for its critical role in ligament function and repair. Previously overlooked, the EL is now understood to be a dynamic structure, particularly in the context of medial collateral ligament (MCL) healing. Rat model studies demonstrate that the EL actively contributes to ligament repair by serving as a source of cells and blood vessels, findings later corroborated in human studies. The EL’s role in spontaneous MCL healing highlights its importance, raising the question of whether differences in EL morphology and activity contribute to the poor healing capacity of the anterior cruciate ligament (ACL). Comparative studies reveal significant disparities in EL cellularity and activity between the ACL and MCL. The EL of the MCL is hypercellular, with robust expression markers like α-smooth muscle actin (α-SMA) and collagen types III and V, essential for tissue remodeling and structural integrity. Conversely, the ACL’s EL is less vascularized and exhibits weaker expression of these markers. While vascular endothelial growth factor (VEGF) promotes angiogenesis, its effectiveness is limited in the ACL due to restricted vascularization. Similarly, CD34, a progenitor cell marker, is more prominently expressed in the MCL’s EL, further supporting its superior healing potential. These findings suggest that the EL’s distinct structural and functional attributes are key determinants of ligament healing. Targeting the EL’s regenerative properties offers a promising therapeutic strategy, particularly for improving ACL repair outcomes. Further research is necessary to validate and expand these findings. Full article

Background/Objectives: Bilateral steno-occlusive disease of the internal carotid artery (ICA) carries an increased stroke risk with associated high morbidity and mortality. Management of these patients is often complex. In this study, we evaluate the value of non-invasive optimal vessel analysis quantitative magnetic resonance angiography (NOVA-qMRA) for studying flow and collateral patterns in patients with bilateral carotid steno-occlusive disease. Methods: Patients with bilateral ICA-stenosis ≥ 50% who received NOVA-qMRA were included in this study. The volume flow rates (VFRs) of the A2-segment of the anterior cerebral artery (A2-ACA), M1-segment of the middle cerebral artery (M1-MCA), and P2-segment of the posterior cerebral artery (P2-PCA) were analyzed. Demographic, clinical, and treatment data were collected. Results: Twenty-two patients (mean age ± SD: 68 ± 10 years) were included. Nineteen patients (86%) were symptomatic. Thirteen patients (59%) were revascularized; among them, M1-VFR was significantly lower (p-value = 0.01) on the side selected for revascularization (88 mL/min ± 53) compared to the contralateral one (130 mL/min ± 56). P2-VFR was significantly higher (p-value = 0.04) in the treated subgroup (108 mL/min ± 41) than in the non-treated one (83 mL/min ± 34). Conclusions: The present study supports the use of NOVA-qMRA to study flow and collateral patterns in patients with bilateral steno-occlusive carotid disease, especially M1- and P2-VFR. This information may be helpful for decision-making and to tailor revascularization treatment. Full article

Moyamoya disease (MMD) is a rare progressive cerebrovascular disorder characterized by the stenosis or occlusion of the terminal segments of the internal carotid arteries, leading to the development of abnormal collateral vascular networks. These networks are a compensatory mechanism for reduced blood flow to the brain. Despite extensive research, the exact etiology of MMD remains unknown, although recent studies suggest that immune system dysfunction plays a critical role in its pathogenesis. In particular, the involvement of immune cells such as T cells, macrophages, and dendritic cells has been increasingly recognized. These immune cells contribute to the inflammatory process and vascular remodeling observed in MMD patients, further complicating the disease’s progression. Inflammation and immune-mediated damage to the vessel walls may accelerate the narrowing and occlusion of arteries, exacerbating ischemic events in the brain. Additionally, studies have revealed that certain genetic and environmental factors can influence immune system activation in MMD, linking these pathways to disease development. This review aims to provide a comprehensive overview of the immune mechanisms at play in MMD, focusing on how immune cells participate in vascular injury and remodeling. Understanding these immunological processes may offer new therapeutic targets to halt or reverse disease progression, potentially leading to more effective treatment strategies for MMD. Full article

Introduction: The e-STROKE study is a prospective, multicenter observational study designed to assess the impact of various CT parameters (including e-ASPECT, CT perfusion (CTP), collateral flow status, and the size and location of the ischemic lesion) on the clinical outcomes of patients with ischemic stroke, as evaluated by the modified Rankins Scale (mRS) three months post-stroke. This study also aims to investigate whether the use of multimodal CT imaging increases the number of patients eligible for recanalization therapy. The analysis will integrate data from the RES-Q registry and radiological data from the e-STROKE system provided by Brainomix Ltd. Aims: The primary aim is to determine the predictive value of CT parameters (e-ASPECTS, CTP, collateral vessel status, and ischemic lesion volume and location) on three-month functional outcomes, as defined by the mRS, in patients with non-lacunar stroke following recanalization treatment (IVT and/or MT). The secondary aim is to evaluate whether multimodal CT examination leads to an increase in the number of patients eligible for recanalization therapy. Additionally, this study seeks to assess the specificity and sensitivity of multimodal CT in distinguishing stroke mimics from actual strokes. Methods: This multicenter observational study involves patients with suspected acute ischemic stroke and a premorbid mRS ≤ 4, who are treated with endovascular thrombectomy (EVT), intravenous thrombolysis (IVT), or managed conservatively in stroke centers within the Czech Stroke Research Network (STROCZECH), which is part of the Czech Clinical Research Infrastructure Network (CZECRIN). Data collection includes demographic, clinical, and imaging data variables such as age, sex, ethnicity, risk factors, treatment times (OTT, DNT, and OGT), TICI scores, post-treatment hemorrhage (ECAS II), mRS outcome, stroke etiology, e-ASPECTS, acute ischemic volume (AIV), thrombus length on NCCT, CTA collateral score and collateral vessel density, location of large vessel occlusion, ischemic core, hypoperfusion volume, mismatch ratio and volume, final infarct volume, hemorrhage volume, and MRI in case of negative follow-up NCCT. Conclusions: We anticipate collecting robust clinical and radiological data from approximately 2000 patients across 22 centers over a 12-month period. The results are expected to enhance the precision of diagnostic and prognostic radiological markers in managing acute stroke. Full article