Background: Hyperperfusion syndrome (HPS) is a critical complication after carotid artery stenting (CAS) and carotid endarterectomy (CEA).
Objective: To identify predictors of HPS before and immediately after CAS.
Methods: We analyzed patients who underwent elective CAS from 2005 to 2008, and underwent single-photon emission computed tomography (SPECT) and transcranial color-coded real-time sonography before and immediately after CAS. HPS was defined as post-CAS deteriorating neurological conditions with headache not secondary to cerebral ischemia. We assessed the measures of blood flow between the two cortical hemispheres by taking the ratio of cerebral blood flow (CBF) of the affected to unaffected hemisphere excluding any ischemic/infarcted areas (asymmetry index); the measures of blood flow within each cortical hemisphere by comparing the CBF in the affected cortical hemispheric area to the CBF in the ipsilateral cerebellar hemisphere (middle cerebral artery [MCA]-to-cerebellar activity ratio); cerebral vasoreactivity (CVR); MCA mean blood flow velocity in the affected hemisphere; and MCA mean blood flow velocity ratio (preoperative to postoperative).
Results: Sixty-four patients were analyzed retrospectively. Nine patients presented with HPS. Logistic regression analysis showed that CVR (P<.01) and MCA mean blood flow velocity (P<.05) were the significant predictors among the pre-CAS variables, and that MCA mean blood flow velocity ratio (P<.05) and MCA-to-cerebellar activity ratio change (P<.05) were significant predictors among the post-CAS variables.
Conclusion: SPECT and transcranial color-coded real-time sonography studies are useful in predicting HPS.
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http://dx.doi.org/10.1227/NEU.0b013e3182077ed8 | DOI Listing |
Bioconjug Chem
January 2025
Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-5127, United States.
Red blood cells (RBCs) serve as natural transporters and can be modified to enhance the pharmacokinetics and pharmacodynamics of a protein cargo. Affinity targeting of Factor IX (FIX) to the RBC membrane is a promising approach to improve the (pro)enzyme's pharmacokinetics. For RBC targeting, purified human FIX was conjugated to the anti-mouse glycophorin A monoclonal antibody Ter119.
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January 2025
The Trauma and Neuroscience Institutes, St. John's Hospital and Medical Center, Tulsa, Oklahoma.
Background: Direct carotid-cavernous fistulas (CCFs) are relatively rare but dangerous complications of penetrating traumatic brain injury or maxillofacial trauma. A variety of clinical signs have been described, including ophthalmological and neurological ones. In some cases, severely altered cerebral blood flow can present as massive life-threatening bleeding through the nose, subarachnoid hemorrhage, and/or intraparenchymal hemorrhage.
View Article and Find Full Text PDFT-cell prolymphocytic leukemia (T-PLL) is an aggressive lymphoid malignancy with limited treatment options. To discover new treatment targets for T-PLL, we performed high-throughput drug sensitivity screening on 30 primary patient samples ex-vivo. After screening over 2'800 unique compounds, we found T-PLL to be more resistant to most drug classes, including chemotherapeutics, compared to other blood cancers.
View Article and Find Full Text PDFAngiotensin II (Ang II) is the most active peptide hormone produced by the renin-angiotensin system (RAS). Genetic deletion of genes that ultimately restrict Ang II formation has been shown to result in marked anemia in mice. In this study, adult mice with a genetic deletion of the RAS precursor protein angiotensinogen (Agt-KO) were used.
View Article and Find Full Text PDFInt J Surg
January 2025
Division of Cardiology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Background: This study tested the hypothesis that extracorporeal shockwave therapy (ECSWT) effectively rescues critical limb ischemia (CLI) in mice through the upregulation of GPR120, which protects against inflammation and angiogenesis to restore blood flow in the ischemic area.
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