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Статті в журналах з теми "Arteriopathy"

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Автор: Grafiati

Опубліковано: 7 липня 2024

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1

Chen, Alan M., Kunal B. Karani, J. Michael Taylor, Bin Zhang, Andrew Furthmiller, Gabriel De Vela, James L. Leach, Sudhakar Vadivelu, and Todd A. Abruzzo. "Cervicocerebral quantitative arterial tortuosity: a biomarker of arteriopathy in children with intracranial aneurysms." Journal of Neurosurgery: Pediatrics 24, no. 4 (October 2019): 389–96. http://dx.doi.org/10.3171/2019.5.peds1982.

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OBJECTIVEAlthough intracranial arterial aneurysms (IAAs) of childhood are usually idiopathic, it is possible that underlying arteriopathy escapes detection when using conventional diagnostic tools. Quantitative arterial tortuosity (QAT) has been studied as a biomarker of arteriopathy. The authors analyzed cervicocerebral QAT in children with idiopathic IAAs to assess the possibility of arteriopathy.METHODSCases were identified by text-string searches of imaging reports spanning the period January 1993 through June 2017. QAT of cervicocerebral arterial segments was measured from cross-sectional studies using image-processing software. Other imaging and clinical data were confirmed by retrospective electronic record review. Children with idiopathic IAAs and positive case controls, with congenital arteriopathy differentiated according to aneurysm status (with and without an aneurysm), were compared to each other and to healthy controls without vascular risk factors.RESULTSCervicocerebral QAT was measured in 314 children: 24 with idiopathic IAAs, 163 with congenital arteriopathy (including 14 arteriopathic IAAs), and 127 healthy controls. QAT of all vertebrobasilar segments was larger in children with IAAs (idiopathic and arteriopathic forms) (p < 0.05). In children with congenital arteriopathy without an aneurysm, QAT was decreased for the distal cervical vertebral arteries and increased for the supraspinal vertebral artery relative to healthy children. QAT of specific cervicocerebral segments correlated with IAA size and rupture status.CONCLUSIONSCervicocerebral QAT is a biomarker of arteriopathy in children with IAA, even in the absence of other disease markers. Additional findings suggest a correlation of cervicocerebral QAT with IAA size and rupture status and with the presence of IAA in children with congenital arteriopathy.

2

Rafay, Mubeen F., Kevin A. Shapiro, Ann-Marie Surmava, Gabrielle A. deVeber, Adam Kirton, Heather J. Fullerton, Catherine Amlie-Lefond, et al. "Spectrum of cerebral arteriopathies in children with arterial ischemic stroke." Neurology 94, no. 23 (May 26, 2020): e2479-e2490. http://dx.doi.org/10.1212/wnl.0000000000009557.

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ObjectiveTo determine that children with arterial ischemic stroke (AIS) due to an identifiable arteriopathy are distinct from those without arteriopathy and that each arteriopathy subtype has unique and recognizable clinical features.MethodsWe report a large, observational, multicenter cohort of children with AIS, age 1 month to 18 years, enrolled in the International Pediatric Stroke Study from 2003 to 2014. Clinical and demographic differences were compared by use of the Fisher exact test, with linear step-up permutation min-p adjustment for multiple comparisons. Exploratory analyses were conducted to evaluate differences between cases of AIS with and without arteriopathy and between arteriopathy subtypes.ResultsOf 2,127 children with AIS, 725 (34%) had arteriopathy (median age 7.45 years). Arteriopathy subtypes included dissection (27%), moyamoya (24.5%), focal cerebral arteriopathy–inflammatory subtype (FCA-i; 15%), diffuse cerebral vasculitis (15%), and nonspecific arteriopathy (18.5%). Children with arteriopathic AIS were more likely to present between 6 and 9 years of age (odds ratio [OR] 1.93, p = 0.029) with headache (OR 1.55, p = 0.023), multiple infarctions (OR 2.05, p < 0.001), sickle cell anemia (OR 2.9, p = 0.007), and head/neck trauma (OR 1.93, p = 0.018). Antithrombotic use and stroke recurrence were higher in children with arteriopathy. Among arteriopathy subtypes, dissection was associated with male sex, older age, headache, and anticoagulant use; FCA-i was associated with hemiparesis and single infarcts; moyamoya was associated with seizures and recurrent strokes; and vasculitis was associated with bilateral infarctions.ConclusionSpecific clinical profiles are associated with cerebral arteriopathies in children with AIS. These observations may be helpful indicators in guiding early diagnosis and defining subgroups who may benefit most from future therapeutic trials.

3

Joyal, France, and Pascal Margaroli. "Calcific Arteriopathy." New England Journal of Medicine 352, no. 26 (June 30, 2005): e24. http://dx.doi.org/10.1056/nejmicm040777.

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4

Wagenvoort, C. A. "Plexogenic arteriopathy." Thorax 49, Suppl (September 1, 1994): S39—S45. http://dx.doi.org/10.1136/thx.49.suppl.s39.

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5

Mitchell, Richard N. "Allograft arteriopathy." Cardiovascular Pathology 13, no. 1 (January 2004): 33–40. http://dx.doi.org/10.1016/s1054-8807(03)00108-x.

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6

Gupta, R. K. "Transplant Arteriopathy." Transplantation Proceedings 39, no. 3 (April 2007): 763–65. http://dx.doi.org/10.1016/j.transproceed.2007.01.068.

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7

Smith, Edward R. "Moyamoya Arteriopathy." Current Treatment Options in Neurology 14, no. 6 (August 3, 2012): 549–56. http://dx.doi.org/10.1007/s11940-012-0195-4.

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8

Kothur, Kavitha, Christopher Troedson, Richard Webster, Sushil Bandodkar, Stephanie Chu, Louise Wienholt, Alun Pope, Mark T. Mackay, and Russell C. Dale. "Elevation of cerebrospinal fluid cytokine/chemokines involved in innate, T cell, and granulocyte inflammation in pediatric focal cerebral arteriopathy." International Journal of Stroke 14, no. 2 (September 13, 2018): 154–58. http://dx.doi.org/10.1177/1747493018799975.

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Aim To determine the role of inflammation in pediatric transient focal cerebral arteriopathy using cerebrospinal fluid cytokine/chemokines as biomarkers. Methods We measured 32 cytokine/chemokines in acute cerebrospinal fluid collected from children with stroke due to focal cerebral arteriopathy (n = 5) using multiplex immunoassay and compared with two patients with arterial ischemic stroke due to other causes (non-focal cerebral arteriopathy group, vertebral dissection, n = 1; cryptogenic, n = 1), pediatric encephalitis (n = 43), and non-inflammatory neurological disease controls (n = 20). Results Median age in the focal cerebral arteriopathy group was 9.3 years (range, 2.8–13 years). In the focal cerebral arteriopathy group (n = 5), four patients had middle cerebral ± distal carotid arteriopathy; one patient had posterior circulation arteriopathy. The median time from symptom onset to cerebrospinal fluid sampling was four days (range, 0.6–7 days). Only IL-6, IL-8, CXCL1, and CXCL10 levels were significantly higher in the acute cerebrospinal fluid of focal cerebral arteriopathy patients compared to non-inflammatory neurological disease controls and non-focal cerebral arteriopathy stroke. In contrast to focal cerebral arteriopathy, a broad array of Th1, Th2, Treg, Th17, B-cell related, and other broad spectrum cytokine/chemokines were elevated in encephalitis. Conclusion The elevated cerebrospinal fluid cytokine/chemokines support innate, T cell, and granulocyte inflammatory mechanisms in children with focal cerebral arteriopathy. This warrants larger cohort studies to discriminate primary inflammatory signals of the arteriopathy from secondary inflammation due to the stroke itself.

9

Cuoco, Joshua A., Christopher M. Busch, Brendan J. Klein, Michael J. Benko, Rachel Stein, Andrew D. Nicholson, and Eric A. Marvin. "ACTA2 Cerebral Arteriopathy: Not Just a Puff of Smoke." Cerebrovascular Diseases 46, no. 3-4 (2018): 159–69. http://dx.doi.org/10.1159/000493863.

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Background: Missense mutations in the gene that codes for smooth muscle actin, ACTA2, cause diffuse smooth muscle dysfunction and a distinct cerebral arteriopathy collectively known as multisystemic smooth muscle dysfunction syndrome (MSMDS). Until recently, ACTA2 cerebral arteriopathy was considered to be a variant of moyamoya disease. However, recent basic science and clinical data have demonstrated that the cerebral arteriopathy caused by mutant ACTA2 exhibits genetic loci, histopathology, neurological sequelae, and radiographic findings unique from moyamoya disease. We conducted a literature review to provide insight into the history, clinical significance, and neurosurgical management of this recently described novel cerebral arteriopathy. Summary: We performed a literature search using PubMed with the key words “ACTA2 mutation,” “ACTA2 cerebral arteriopathy,” and “multisystemic smooth muscle dysfunction syndrome.” Case reports with confirmed ACTA2 mutations and cerebral arteriopathy were included in our review. Our literature search revealed 15 articles (58 cases) of confirmed ACTA2 cerebral arteriopathy. Distinctive features of this arteriopathy included an aberrant internal carotid circulation with dilatation of the proximal segments, occlusive disease at the distal segments, and dolichoectasia. As such, mutant ACTA2 predisposed patients to ischemic strokes as children. Direct and indirect cerebral revascularization procedures are the mainstay treatment options with varying degrees of success. Key Messages: ACTA2 cerebral arteriopathy is a recently described novel cerebrovascular disease seen in patients with MSMDS. Patients currently diagnosed with moyamoya disease who also have dysfunction of smooth muscle organs may benefit from reevaluation by a medical geneticist and ACTA2 genotyping.

10

Olivero, Juan Jose, Juan Jorge Olivero, Peter Nguyen, and Anna Kagan. "Nephrogenic Calcific Arteriopathy." Methodist DeBakey Cardiovascular Journal 7, no. 4 (October 1, 2011): 33. http://dx.doi.org/10.14797/mdcvj.304.

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11

Veinot, John P., and Virginia M. Walley. "Cardiac Transplant Arteriopathy." American Journal of Surgical Pathology 19, no. 6 (June 1995): 727. http://dx.doi.org/10.1097/00000478-199506000-00014.

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12

Edwards, W. D. "Plexogenic pulmonary arteriopathy." Histopathology 17, no. 2 (August 1990): 188a—189. http://dx.doi.org/10.1111/j.1365-2559.1990.tb00704.x.

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13

Heath, D., and A. W. Caslin. "Plexogenic pulmonary arteriopathy." Histopathology 17, no. 2 (August 1990): 189. http://dx.doi.org/10.1111/j.1365-2559.1990.tb00705.x.

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14

Wu, Mei-Han, Shang-Feng Yang, and Yao-Ping Lin. "Calcific Uremic Arteriopathy." American Journal of the Medical Sciences 347, no. 2 (February 2014): 146. http://dx.doi.org/10.1097/maj.0b013e31826b2d2f.

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15

Olivero, Juan Jose, Juan Jorge Olivero, Peter Nguyen, and Anna Kagan. "Nephrogenic Calcific Arteriopathy." Methodist DeBakey Cardiovascular Journal 7, no. 4 (October 2011): 33–36. http://dx.doi.org/10.14797/mdcj-7-4-33.

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16

Finsterer, J., and S. Zarrouk Mahjoub. "Primary mitochondrial arteriopathy." Nutrition, Metabolism and Cardiovascular Diseases 22, no. 5 (May 2012): 393–99. http://dx.doi.org/10.1016/j.numecd.2012.01.002.

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17

Steinlin, Maja, Sandra Bigi, Belinda Stojanovski, Jay Gajera, Maria Regényi, Marwan El-Koussy, and Mark T. Mackay. "Focal Cerebral Arteriopathy." Stroke 48, no. 9 (September 2017): 2375–82. http://dx.doi.org/10.1161/strokeaha.117.016818.

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18

Dlamini, Nomazulu, Dawn E. Saunders, Michael Bynevelt, Sara Trompeter, Timothy C. Cox, Romola S. Bucks, and Fenella J. Kirkham. "Nocturnal oxyhemoglobin desaturation and arteriopathy in a pediatric sickle cell disease cohort." Neurology 89, no. 24 (November 8, 2017): 2406–12. http://dx.doi.org/10.1212/wnl.0000000000004728.

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Objective:The purpose of this study of sickle cell disease (SCD) was to determine whether arteriopathy, measurable as intracranial vessel signal loss on magnetic resonance angiography (MRA), was associated with low nocturnal hemoglobin oxygen saturation (SpO2) or hemolytic rate, measurable as reticulocytosis or unconjugated hyperbilirubinemia.Methods:Ninety-five East London children with SCD without prior stroke had overnight pulse oximetry, of whom 47 (26 boys, 39 hemoglobin SS; mean age 9.1 ± 3.1 years) also had MRA, transcranial Doppler (TCD), steady-state hemoglobin, and reticulocytes within 34 months. Two radiologists blinded to the other data graded arteriopathy on MRA as 0 (none) or as increasing severity grades 1, 2, or 3.Results:Grades 2 or 3 arteriopathy (n = 24; 2 with abnormal TCD) predicted stroke/TIA compared with grades 0 and 1 (log-rank χ2 [1, n = 47] = 8.1, p = 0.004). Mean overnight SpO2 correlated negatively with reticulocyte percentage (r = −0.387; p = 0.007). Despite no significant differences across the degrees of arteriopathy in genotype, mean overnight SpO2 was higher (p < 0.01) in those with grade 0 (97.0% ± 1.6%) than those with grades 2 (93.9 ± 3.7%) or 3 (93.5% ± 3.0%) arteriopathy. Unconjugated bilirubin was not associated but reticulocyte percentage was lower (p < 0.001) in those with grade 0 than those with grades 2 and 3 arteriopathy. In multivariable logistic regression, lower mean overnight SpO2 (odds ratio 0.50, 95% confidence interval 0.26–0.96; p < 0.01) predicted arteriopathy independent of reticulocyte percentage (odds ratio 1.47, 95% confidence interval 1.15–1.87; p = 0.003).Conclusion:Low nocturnal SpO2 and reticulocytosis are associated with intracranial arteriopathy in children with SCD. Preventative strategies might reduce stroke risk.

19

Rutledge, W. Caleb, Omar Choudhri, Brian P. Walcott, Arnau Benet, Christine K. Fox, Nalin Gupta, and Michael T. Lawton. "Indirect and direct revascularization of ACTA2 cerebral arteriopathy: feasibility of the superficial temporal artery to anterior cerebral artery bypass with posterior auricular artery interposition graft: case report." Journal of Neurosurgery: Pediatrics 18, no. 3 (September 2016): 339–43. http://dx.doi.org/10.3171/2016.3.peds15694.

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Mutations in the smooth muscle–specific isoform of alpha actin (ACTA2) cause smooth muscle dysfunction in arteries. This rare loss-of-function mutation may cause a diffuse occlusive cerebral arteriopathy, resulting in stroke. While ACTA2 arteriopathy is often described as moyamoya-like, it has a distinct phenotype characterized by dilation of the proximal internal carotid artery (ICA) and occlusion of the terminal ICA and proximal middle cerebral artery. Intracranial arteries have an abnormally straight course, often with small aneurysms. There is limited experience with revascularization procedures for ACTA2 arteriopathy, and the safety and efficacy of these procedures are unknown. In this paper the authors present a symptomatic 6-year-old patient with ACTA2 cerebral arteriopathy who underwent both indirect revascularization and direct cerebrovascular bypass. Postoperatively, the patient suffered an ischemic infarct in a neighboring vascular territory. While direct cerebrovascular bypass is technically feasible, patients with ACTA2 arteriopathy may be at increased risk for perioperative stroke compared with patients with moyamoya disease.

20

Nordstrom, Matthew, Erin Felton, Katherine Sear, Benita Tamrazi, Joseph Torkildson, Karen Gauvain, Daphne A. Haas-Kogan, et al. "Large Vessel Arteriopathy After Cranial Radiation Therapy in Pediatric Brain Tumor Survivors." Journal of Child Neurology 33, no. 5 (March 26, 2018): 359–66. http://dx.doi.org/10.1177/0883073818756729.

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Among childhood cancer survivors, increased stroke risk after cranial radiation therapy may be caused by radiation-induced arteriopathy, but limited data exist to support this hypothesis. Herein, we assess the timing and presence of cerebral arteriopathy identified by magnetic resonance angiography (MRA) after cranial radiation therapy in childhood brain tumor survivors. In a cohort of 115 pediatric brain tumor survivors, we performed chart abstraction and prospective annual follow-up to assess the presence of large vessel cerebral arteriopathy by MRA. We identified 10 patients with cerebral arteriopathy. The cumulative incidence of arteriopathy 5 years post–cranial radiation therapy was 5.4% (CI 0.6%-10%) and 10 years was 16% (CI 4.6%-26%). One patient had an arterial ischemic stroke 2.4 years post–cranial radiation therapy in the distribution of a radiation-induced stenotic artery. We conclude that large vessel arteriopathies can occur within a few years of cranial radiation therapy and can become apparent on MRA in under a year.

21

Oka, Masahiko, Ivan F. McMurtry, and Kaori Oshima. "How does pulmonary endarterectomy cure CTEPH: a clue to cure PAH?" American Journal of Physiology-Lung Cellular and Molecular Physiology 311, no. 4 (October 1, 2016): L766—L769. http://dx.doi.org/10.1152/ajplung.00288.2016.

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Chronic thromboembolic pulmonary hypertension (CTEPH) is a hot topic in the field of pulmonary hypertension because many CTEPH patients are now curable by surgical pulmonary endarterectomy. However, there are still uncertainties regarding the pathogenesis of CTEPH, specifically how and where the small vessel arteriopathy that is indistinguishable from that in pulmonary arterial hypertension (plexogenic arteriopathy) develops and how pulmonary endarterectomy improves hemodynamics and possibly cures CTEPH. Based on our recent experimental finding that hemodynamic stress is fundamental for the development of plexogenic arteriopathy, we discuss the uncertainties of CTEPH and potential implication of the effectiveness of pulmonary endarterectomy for reversing plexogenic arteriopathy and possibly providing a novel approach to cure pulmonary arterial hypertension.

22

Wang, Hanlin L. "Carcinomatous Arteriopathy as an Unusual Feature of Pulmonary Spread of Cholangiocarcinoma Arising in Caroli Disease." Archives of Pathology & Laboratory Medicine 126, no. 6 (June 1, 2002): 717–20. http://dx.doi.org/10.5858/2002-126-0717-caaauf.

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Abstract Carcinomatous arteriopathy is a rare and distinct form of pulmonary spread of solid malignant tumors characterized by fibrointimal proliferation of small pulmonary arteries and arterioles initiated by tumor emboli. Although it has been reported in many types of adenocarcinomas, no case of carcinomatous arteriopathy induced by cholangiocarcinoma has been described in the literature. We report a unique case of cholangiocarcinoma that arose in Caroli disease. Postmortem examination revealed extensive pulmonary vascular spread in the form of carcinomatous arteriopathy.

23

Savitr Sastri, B. V., Bhagvatula Indira Devi, Jagathlal Gangadharan, and Dhaval Shukla. "Cerebral Aneurysmal Childhood Arteriopathy." Pediatric Neurosurgery 47, no. 3 (2011): 233–34. http://dx.doi.org/10.1159/000331571.

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24

Garcia, Julio H., and Khang-Loon Ho. "Pathology of Hypertensive Arteriopathy." Neurosurgery Clinics of North America 3, no. 3 (July 1992): 497–507. http://dx.doi.org/10.1016/s1042-3680(18)30641-7.

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25

Lou, Min, and Louis R. Caplan. "Vertebrobasilar dilatative arteriopathy (dolichoectasia)." Annals of the New York Academy of Sciences 1184, no. 1 (November 24, 2009): 121–33. http://dx.doi.org/10.1111/j.1749-6632.2009.05114.x.

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26

Bucci, F., F. Robert, L. Fiengo, and P. Plagnol. "Radiotherapy-related axillary arteriopathy." Interactive CardioVascular and Thoracic Surgery 15, no. 1 (March 28, 2012): 176–77. http://dx.doi.org/10.1093/icvts/ivr147.

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27

Jack, Andrew S., Michael M. Chow, Loretta Fiorillo, Thea Chibuk, Jerome Y. Yager, and Vivek Mehta. "Bilateral pial synangiosis in a child with PHACE syndrome." Journal of Neurosurgery: Pediatrics 17, no. 1 (January 2016): 70–75. http://dx.doi.org/10.3171/2015.5.peds1578.

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The acronym PHACE has been used to denote a constellation of abnormalities: posterior fossa anomalies, facial hemangiomas, arterial anomalies, cardiac anomalies, and eye abnormalities. Approximately 30% of patients with large facial hemangiomas have PHACE syndrome, with the vast majority having intracranial arteriopathy. Few reports characterize neurological deterioration from this intracranial arteriopathy, and even fewer report successful treatment thereof. The authors report on a case of a child with PHACE syndrome who presented with an ischemic stroke from a progressive intracranial arteriopathy and describe her successful treatment with bilateral pial synangiosis. An 8-month old girl diagnosed with PHACE syndrome was found to have bilateral internal carotid artery stenosis. Although initially asymptomatic, a few months after diagnosis she suffered a right frontal and parietal stroke. MRI and cerebral angiography investigations demonstrated progressive intracranial arterial stenosis and occlusion. The patient then underwent indirect cerebral revascularization surgery. At 2-year follow-up, she exhibited clinical improvement with persistent speech and motor developmental delay. Follow-up MRI and cerebral angiography showed no new ischemic events and robust extensive vascular collateralization from surgery. PHACE syndrome is an uncommon disease, and affected patients often have cerebral arteriopathy. Although the underlying natural history of cerebral arteriopathy in PHACE remains unclear, cerebral revascularization may represent a potential therapy for symptomatic patients.

28

Chabrier, Stéphane, Guillaume Sébire, and Joel Fluss. "Transient Cerebral Arteriopathy, Postvaricella Arteriopathy, and Focal Cerebral Arteriopathy or the Unique Susceptibility of the M1 Segment in Children With Stroke." Stroke 47, no. 10 (October 2016): 2439–41. http://dx.doi.org/10.1161/strokeaha.116.014606.

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29

Oesch, Gabriela, Francisco A. Perez, Mark S. Wainwright, Dennis W. W. Shaw, and Catherine Amlie-Lefond. "Focal Cerebral Arteriopathy of Childhood." Stroke 52, no. 7 (July 2021): 2258–65. http://dx.doi.org/10.1161/strokeaha.120.031880.

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Background and Purpose: Focal cerebral arteriopathy (FCA) of childhood with unilateral stenosis of the anterior circulation is reported to account for up to one-quarter of childhood arterial ischemic stroke, with stroke recurrence in 25% of cases. Limited knowledge regarding pathophysiology and outcome results in inconsistent treatment of FCA. Methods: Children with arterial ischemic stroke due to FCA between January 1, 2009, and January 1, 2019, were retrospectively identified at our institution which serves the US Pacific Northwest region. Electronic health record data, including neuroimaging studies, were reviewed, and the Pediatric Stroke Outcome Measure at 1 year was determined as the primary clinical end point. Results: Fifteen children were diagnosed with FCA, accounting for 19% of children with cerebral arteriopathies (n=77). Among children with FCA, the median age at the time of stroke was 6.8 years (Q1–Q3, 1.9–14.0 years). Four (20%) patients had worsening stroke, 3 of whom had concurrent infection. Three (20%) FCA cases were treated with steroids, one of whom had worsening stroke. Median Pediatric Stroke Outcome Measure at 1 year was 1.0 (Q1–Q3, 0.6–2.0). Variability in arteriopathy severity was observed within many patients. Patients with more severe arteriopathy using the Focal Cerebral Arteriopathy Severity Score had larger strokes and were more likely to have worsening stroke. The most common long-term neurological deficit was hemiparesis, which was present in 11 (73%) patients and associated with middle cerebral artery arteriopathy and infarcts. Conclusions: FCA may be less common than previously reported. Neuroimaging in FCA can help identify patients at greater risk for worsening stroke.

30

Kløw, N. E., K. Levorstad, S. Simonsen, and O. Geiran. "Coronary Arteriopathy after Heart Transplantation." Acta Radiologica 39, no. 6 (November 1998): 656–62. http://dx.doi.org/10.3109/02841859809175492.

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31

Millichap, J. Gordon. "Intracranial Arteriopathy and Ischemic Stroke." Pediatric Neurology Briefs 23, no. 3 (March 1, 2009): 18. http://dx.doi.org/10.15844/pedneurbriefs-23-3-3.

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32

Tanabe, Shigeru, Young-Sin Han, Tatsuya Nakatani, Taketoshi Kishimoto, Seiichi Suzuki, Hiroshi Amemiya, and Makiko Ueda. "OBLITERATIVE ARTERIOPATHY IN RENAL TRANSPLANTATION." Japanese Journal of Urology 84, no. 10 (1993): 1828–34. http://dx.doi.org/10.5980/jpnjurol1989.84.1828.

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33

&NA;. "Pathologic markers of allograft arteriopathy." Current Opinion in Cardiology 16, no. 3 (May 2001): 218. http://dx.doi.org/10.1097/00001573-200105000-00010.

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34

Sébire, Guillaume. "Transient cerebral arteriopathy in childhood." Lancet 368, no. 9529 (July 2006): 8–10. http://dx.doi.org/10.1016/s0140-6736(06)68944-7.

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35

Evans, D. J., S. J. Cashman, and M. Walport. "PROGRESSIVE SYSTEMIC SCLEROSIS: AUTOIMMUNE ARTERIOPATHY." Lancet 329, no. 8531 (February 1987): 480–82. http://dx.doi.org/10.1016/s0140-6736(87)92091-5.

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36

Voelkel, Norbert F., and Harm Jan Bogaard. "Adding complexity to plexogenic arteriopathy." European Respiratory Journal 48, no. 6 (November 30, 2016): 1553–55. http://dx.doi.org/10.1183/13993003.01867-2016.

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37

Fullerton, Heather J., Nicholas Stence, Nancy K. Hills, Bin Jiang, Catherine Amlie-Lefond, Timothy J. Bernard, Neil R. Friedman, et al. "Focal Cerebral Arteriopathy of Childhood." Stroke 49, no. 11 (November 2018): 2590–96. http://dx.doi.org/10.1161/strokeaha.118.021556.

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38

Perez-Atayde, A. R., D. I. Kearney, J. T. Bricker, S. D. Colan, K. A. Easley, S. Kaplan, W. W. Lai, et al. "Cardiac, Aortic, and Pulmonary Arteriopathy in HIV-Infected Children: The Prospective P2C2 HIV Multicenter Study." Pediatric and Developmental Pathology 7, no. 1 (January 2004): 61–70. http://dx.doi.org/10.1007/s10024-003-1001-9.

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Arteriopathy in human immunodeficiency virus (HIV)-infected patients is being increasingly recognized, especially in children. However, few studies have histologically evaluated the coronary arteries in HIV-infected children, and none have systematically assessed the aorta and pulmonary arteries. The coronary arteries, thoracic aorta, and the main and branch pulmonary arteries from the postmortem hearts of 14 HIV-infected children were systematically reviewed for vasculopathic lesions and compared with 14 age-matched controls. Findings from the HIV-infected children were compared with clinical, laboratory, and other postmortem findings. Coronary arteriopathy, seen in seven (50%) of the HIV-infected children, was primarily calcific, and it was associated with decreased CD3 and CD4 peripheral blood counts. Large vessel arteriopathy, seen in 9 (64%) of the 14 HIV-infected children, was primarily centered on the vasa vasorum and consisted mainly of medial hypertrophy and chronic inflammation. Large vessel lesions were associated with increased left ventricular mass z-scores ( P = 0.02), and 78% of patients with large vessel arteriopathy had postmortem cardiomegaly. Coronary and large vessel arteriopathies are common in pediatric HIV-infection and have different clinicopathologic features suggesting different pathogenesis.

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Wang, Zhen, Jingxuan Guo, Xian Wang, Yiming Zhao, and Lingfei Hou. "A Study of the Relationships between Serum Calcitonin Gene-Related Peptide, Sex Hormone, Homocysteine and Coronary Heart Disease in Postmenopausal Women." International Journal of Biomedical Science 2, no. 1 (March 15, 2006): 42–48. http://dx.doi.org/10.59566/ijbs.2006.2042.

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To investigate the relationships among serum calcitonin gene-related peptide (CGRP), homocysteine (Hcy), female hormone, and coronary arteriopathy in postmenopausal women. Method. In a cross-sectional study, serum CGRP, estrodiol (E2), progesterone（P）and Hcy levels of 144 postmenopausal women with coronary heart disease (CHD) and non-coronary heart disease (NCHD) were measured. Results. The mean serum CGRP level was significantly lower in CHD patients than in NCHD subjects. The mean serum E2 and P level were significantly lower in CHD patients than in NCHD subjects. The mean serum Hcy level was significantly higher in CHD patients than in NCHD subjects. By multivariate logistic regression, the OR of high Hcy level ≥1, p<0.01，which suggests that Hcy is an independent risk factor in the development of coronary arteriopathy. The OR of CGRP, E2 , and P are all≤1, indicating that CGRP , E2 and P are independent protective factor. Conclusion. The results of our study show that Hcy is an independent risk factor in the development of arteriopathy. CGRP and endogenous E2 are independent protective factors in the development of coronary arteriopathy. There are no relationships between Hcy, CGRP, and endogenous E2.

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Liu, Fang, Wei Wei, Gaoyi Yang, Cunxin Wang, Xin Yang, Yabei Jin, Chenghao Liu, and Fangjun Wang. "Therapeutic Effects and Finite Element Analysis of a Combined Treatment Using Laser Needle-Knife with Supine Repositioning Massage on Patients with Cervical Spondylotic Vertebral Arteriopathy." International Journal of Pattern Recognition and Artificial Intelligence 31, no. 11 (April 11, 2017): 1757008. http://dx.doi.org/10.1142/s0218001417570087.

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Objective: To investigate the effectiveness of combined laser needle-knife and massage on cervical spondylotic vertebral arteriopathy patients. Summary of background data: With the recent rise of electronic businesses, the incidence of cervical spondylosis has also risen rapidly. Methods: Cervical spondylotic vertebral arteriopathy patients were treated using laser needle-knife with massage, and compared to patients who only received the massage. A 3D anatomical and hemodynamic model was developed. Results: The symptomatic and functional overall scores were reduced by 71.43% after the combined treatment. Results from the finite element analysis indicated that the maximum flow rate of the left vertebral artery was improved by 47.52% and the right was improved by 38.67%. Conclusion: A combined treatment of cervical spondylotic vertebral arteriopathy using laser needle-knife and massage is an effective approach with a therapeutic mechanism closely related to hemodynamics.

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Furukawa, Yutaka, Peter Libby, Jennifer L. Stinn, Gerold Becker, and Richard N. Mitchell. "Cold Ischemia Induces Isograft Arteriopathy, but Does Not Augment Allograft Arteriopathy in Non-Immunosuppressed Hosts." American Journal of Pathology 160, no. 3 (March 2002): 1077–87. http://dx.doi.org/10.1016/s0002-9440(10)64928-0.

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Bulder, M., K. Braun, S. Chabrier, F. Kirkham, M. Tardieu, and G. Sébire. "SO01 Transient Cerebral Arteriopathy; follow up vascular imaging in 79 children with unilateral intracranial arteriopathy." European Journal of Paediatric Neurology 11 (September 2007): 22–23. http://dx.doi.org/10.1016/s1090-3798(08)70325-8.

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43

Low, Audrey, Elijah Mak, Maura Malpetti, Luca Passamonti, Nicolas Nicastro, James D. Stefaniak, George Savulich, et al. "In vivo neuroinflammation and cerebral small vessel disease in mild cognitive impairment and Alzheimer’s disease." Journal of Neurology, Neurosurgery & Psychiatry 92, no. 1 (September 11, 2020): 45–52. http://dx.doi.org/10.1136/jnnp-2020-323894.

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IntroductionAssociations between cerebral small vessel disease (SVD) and inflammation have been largely examined using peripheral blood markers of inflammation, with few studies measuring inflammation within the brain. We investigated the cross-sectional relationship between SVD and in vivo neuroinflammation using [11C]PK11195 positron emission tomography (PET) imaging.MethodsForty-two participants were recruited (according to NIA-AA guidelines, 14 healthy controls, 14 mild Alzheimer’s disease, 14 amyloid-positive mild cognitive impairment). Neuroinflammation was assessed using [11C]PK11195 PET imaging, a marker of microglial activation. To quantify SVD, we assessed white matter hyperintensities (WMH), enlarged perivascular spaces, cerebral microbleeds and lacunes. Composite scores were calculated for global SVD burden, and SVD subtypes of hypertensive arteriopathy and cerebral amyloid angiopathy (CAA). General linear models examined associations between SVD and [11C]PK11195, adjusting for sex, age, education, cognition, scan interval, and corrected for multiple comparisons via false discovery rate (FDR). Dominance analysis directly compared the relative importance of hypertensive arteriopathy and CAA scores as predictors of [11C]PK11195.ResultsGlobal [11C]PK11195 binding was associated with SVD markers, particularly in regions typical of hypertensive arteriopathy: deep microbleeds (β=0.63, F(1,35)=35.24, p<0.001), deep WMH (β=0.59, t=4.91, p<0.001). In dominance analysis, hypertensive arteriopathy score outperformed CAA in predicting [11C]PK11195 binding globally and in 28 out of 37 regions of interest, especially the medial temporal lobe (β=0.66–0.76, t=3.90–5.58, FDR-corrected p (pFDR)=<0.001–0.002) and orbitofrontal cortex (β=0.51–0.57, t=3.53–4.30, pFDR=0.001–0.004).ConclusionMicroglial activation is associated with SVD, particularly with the hypertensive arteriopathy subtype of SVD. Although further research is needed to determine causality, our study suggests that targeting neuroinflammation might represent a novel therapeutic strategy for SVD.

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Cospite, M., F. Ferrara, G. Milio, V. Scrivano, and F. Meli. "Ticlopidine in the Treatment of Multiple Atherosclerotic Arteriopathy: a Strain Gauge Plethysmography and Döppler Spectrum Analysis Evaluation." Journal of International Medical Research 15, no. 5 (September 1987): 303–11. http://dx.doi.org/10.1177/030006058701500506.

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The effect of ticlopidine was compared with flunarizine in patients with iliac–femoral and / or femoral–popliteal arteriosclerotic arteriopathy accompanied by lesions of the cervical arteries of no haemodynamic significance. In the lower limbs, plethysmography (strain gauge measurements) and Döppler ultrasonography integrated by spectral analysis of the cervical arteries showed qualitative and quantitative improvements of the regional haematic flow. Side-effects were negligible which suggests that ticlopidine is useful in the treatment of multiple arteriosclerotic arteriopathy.

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Alhadid, K., M. Kirby-Allen, G. DeVeber, W. Logan, and N. Dlamini. "P.054 Bone marrow transplant restores Cerebrovascular Reactivity (CVR) in Sickle Cell Disease (SCD): a case presentation." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 44, S2 (June 2017): S27. http://dx.doi.org/10.1017/cjn.2017.139.

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Background: A diagnosis of SCD in childhood confers a 200-fold increase in the risk of arterial ischemic stroke. Blood flow velocity measures provide better identification of ischemic risk compared to angiography. This indicates that steno-occlusive arteriopathy is not the singular causative factor. Cerebrovascular reactivity allows for augmentation of cerebral blood flow when needed. Kosinski et al in 2016 demonstrated a direct correlation between CVR and hematocrit levels in SCD. We report a case where CVR persistently normalized in an SCD patient following bone marrow transplant therapy (BMT). Methods: A nine-month-old SCD patient presented with right AIS. Angiography revealed a bilateral Moya-Moya like arteriopathy. A TCD study was normal while a CVR-MRI study revealed markedly impaired reactivity in the entire anterior circulation. Haemaglobin-S at that time was 20.2 %. BMT was performed at age four due to frequent sickle cell crises. Results: One year post-transplant, CVR had dramatically improved in areas previously shown to have impairment (haemoglobin-S 0%). Neuroimaging five years post-transplant showed no further arteriopathy and persistently normalized CVR. Conclusions: BMT therapy resulted in the arrest of progressive intracranial arteriopathy and persistently restored vascular reserve. SCD might not only produce global hematological effects but also triggers local processes such as endothelial dysfunction and vascular inflammation that impair cerebrovascular function.

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Hong, Ying, Annette Keylock, Barbara Jensen, Thomas S. Jacques, Olumide Ogunbiyi, Ebun Omoyinmi, Dawn Saunders, et al. "Cerebral arteriopathy associated with heterozygous variants in the casitas B-lineage lymphoma gene." Neurology Genetics 6, no. 4 (June 10, 2020): e448. http://dx.doi.org/10.1212/nxg.0000000000000448.

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ObjectiveTo report a series of patients with cerebral arteriopathy associated with heterozygous variants in the casitas B-lineage lymphoma (CBL) gene and examine the functional role of the identified mutant Cbl protein. We hypothesized that mutated Cbl fails to act as a negative regulator of the RAS-mitogen-activated protein kinases (MAPK) signaling pathway, resulting in enhanced vascular fibroblast proliferation and migration and enhanced angiogenesis and collateral vessel formation.MethodsWe performed whole-exome sequencing in 11 separate families referred to Great Ormond Street Hospital, London, with suspected genetic cause for clinical presentation with severe progressive cerebral arteriopathy.ResultsWe identified heterozygous variants in the CBL gene in 5 affected cases from 3 families. We show that impaired CBL-mediated degradation of cell surface tyrosine kinase receptors and dysregulated intracellular signaling through the RAS-MAPK pathway contribute to the pathogenesis of the observed arteriopathy. Mutated CBL failed to control the angiogenic signal relay of vascular endothelial growth factor receptor 2, leading to prolonged tyrosine kinase signaling, thus driving angiogenesis and collateral vessel formation. Mutant Cbl promoted myofibroblast migration and proliferation contributing to vascular occlusive disease; these effects were abrogated following treatment with a RAF-RAS-MAPK pathway inhibitor.ConclusionsWe provide a possible mechanism for the arteriopathy associated with heterozygous CBL variants. Identification of the key role for the RAS-MAPK pathway in CBL-mediated cerebral arteriopathy could facilitate identification of novel or repurposed druggable targets for treating these patients and may also provide therapeutic clues for other cerebral arteriopathies.

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McKenna, Mary Clare, Noel Fanning, and Simon Cronin. "Focal Cerebral Arteriopathy in Young Adult Patients With Stroke." Stroke 51, no. 5 (May 2020): 1596–99. http://dx.doi.org/10.1161/strokeaha.119.028343.

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Background and Purpose— Focal cerebral arteriopathy is monophasic inflammatory stenosis of the distal internal carotid artery or the proximal segment of the middle cerebral artery. It is one of the most common causes of acute arterial ischemic stroke in young children but is a less familiar entity for adult neurologists. Methods— We retrospectively reviewed stroke service radiology records at a tertiary referral center from January 2013 to December 2014. Focal cerebral arteriopathy was defined as nonprogressive unifocal and unilateral stenosis/irregularity of the distal internal carotid artery or its proximal branches. Only patients aged 16 to 55 years with stroke were included. Results— There were 5 cases of focal cerebral arteriopathy: 2 males and 3 females. Three cases were from the cohort of 123 acute presentations of young stroke, and 2 cases were outpatient referrals. The mean age (range) was 43 (32–55) years. The majority presented with recurrent transient ischemic attacks/minor strokes within a single vascular territory over days to weeks. All cases had characteristic radiological features. Interval imaging demonstrated resolution in 1 case and improvement in 3 cases. Functional outcome was excellent with discharge modified Rankin Scale score ranging from 0 to 1. Recurrence occurred in 1 case. Conclusions— Focal cerebral arteriopathy is a rare cause of arterial ischemic stroke in young adults. Follow-up intracranial imaging is essential to differentiate from progressive arteriopathies. Evidence-based treatment warrants further investigation. Prognosis is favorable.

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Minnelli, Carrie, Maziar Riazy, Ryuji Ohashi, Jolanta Kowalewska, Nicolae Leca, Behzad Najafian, Kelly D. Smith, Roberto F. Nicosia, Charles E. Alpers, and Shreeram Akilesh. "Early Transplant Arteriopathy in Kidney Transplantation." Transplantation Proceedings 53, no. 5 (June 2021): 1554–61. http://dx.doi.org/10.1016/j.transproceed.2021.02.019.

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Millichap, J. Gordon. "Prognosis of Cerebral Arteriopathy in Stroke." Pediatric Neurology Briefs 20, no. 4 (April 1, 2006): 28. http://dx.doi.org/10.15844/pedneurbriefs-20-4-5.

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Millichap, J. Gordon. "Cytokine Markers of Focal Cerebral Arteriopathy." Pediatric Neurology Briefs 26, no. 11 (November 1, 2012): 88. http://dx.doi.org/10.15844/pedneurbriefs-26-11-11.

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