Vessel Wall Magnetic Resonance Imaging for Evaluating Stroke

Total Page:16

File Type:pdf, Size:1020Kb

Vessel Wall Magnetic Resonance Imaging for Evaluating Stroke REVIEW ARTICLE Ann Clin Neurophysiol 2021;23(1):17-28 https://doi.org/10.14253/acn.2021.23.1.17 ANNALS OF CLINICAL NEUROPHYSIOLOGY Targeting the culprit: vessel wall magnetic resonance imaging for evaluating stroke Seung Min Kim1, Sang Hee Ha2, Hanim Kwon2, Yeon Jung Kim2, Sung Ho Ahn3, Bum Joon Kim2 1Department of Neurology, Veterans Health Service Medical Center, Seoul, Korea 2Department of Neurology, Asan Medical Center, Seoul, Korea 3Department of Neurology, Pusan National University Yangsan Hospital, Yangsan, Korea Received: February 2, 2021 Revised: February 21, 2021 The pathogenesis of many strokes originates in the vessel wall. Despite this, most traditional Accepted: February 24, 2021 imaging focuses on the vascular lumen. Vessel-wall magnetic resonance imaging (VWMRI) is useful for establishing the etiology of intracranial stenosis. It also provides information regard- ing atherosclerotic plaque composition and thus plaque vulnerability, which is an indication of its potential to cause a stroke. In this review we focus on the characteristics of VWMRI findings in various arteriopathies related to intracranial artery stenosis, and discuss the clinical implica- Correspondence to tions of these findings. Bum Joon Kim Department of Neurology, Asan Medical Key words: Vessel-wall magnetic resonance imaging; Ischemic stroke; Intracranial athero- Center, 88 Olympic-ro 43-gil, Songpa-gu, Seoul 05505, Korea sclerosis; Dissection; Moyamoya disease Tel: +82-2-3010-3981 Fax: +82-2-474-4691 E-mail: [email protected] INTRODUCTION ORCID Seung Min Kim Ischemic stroke is a cerebrovascular event caused by occlusion or stenosis of the cerebral https://orcid.org/0000-0001-5228-6512 arteries that supply blood flow to the brain parenchyma. Sudden interruption of this blood Sang Hee Ha flow causes ischemia and subsequent permanent damage to the involved brain tissue, https://orcid.org/0000-0002-2926-2368 Hanim Kwon resulting in a focal neurological deficit. More than 40% of arterial occlusions are attribut- https://orcid.org/0000-0003-1340-9529 able to arterial pathology, and predominantly atherosclerosis.1 Various etiologies of arterial Yeon Jung Kim stenosis, and stenosis of the intracranial arteries in particular, may cause ischemic stroke. https://orcid.org/0000-0002-6081-890X Sung Ho Ahn To date, neuroimaging for stroke has focused on the brain parenchyma, as for other https://orcid.org/0000-0002-8376-545X neurological diseases that primarily involve this brain region. Although parenchymal im- Bum Joon Kim aging is useful for evaluating the underlying stroke mechanism, predicting the prognosis, https://orcid.org/0000-0002-3278-3252 and aiding treatment decision-making, it neglects the true culprit of arterial-wall pathol- ogy. Various modalities including computed tomography angiography (CTA), magnetic http://www.e-acn.org Copyright © 2021 The Korean Society of Clinical Neurophysiology This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http:// pISSN 2508-691X creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, eISSN 2508-6960 provided the original work is properly cited. Annals of Clinical Neurophysiology Volume 23, Number 1, April 2021 resonance angiography (MRA), and digital subtraction angi- ly the distal internal carotid artery (ICA), is more commonly ography (DSA) have been used to locate and measure ste- associated with artery-to-artery embolism, whereas local noses in the intra- and extracranial arteries. However, these branch occlusion is prevalent in posterior-circulation ICAS, conventional vascular imaging modalities do not provide especially in the basilar artery (BA).4 In the middle cerebral ar- adequate information regarding vessel pathology.2 Carotid tery (MCA), the mechanism differs according to the location duplex sonography does reveal the vessel-wall pathology and severity of the atherosclerotic lesion. In proximal MCA of extracranial cervical arteries,3 but is of limited use for eval- disease, and particularly in the case of proximal MCA occlu- uating intracranial artery stenosis, which is a major cause of sion, stroke most commonly results from a combination of stroke in Asian patients. mechanisms. This can be explained by plaque rupture with The use of high-resolution vessel-wall magnetic reso- occlusion causing both perforator infarction and embolism. nance imaging (VWMRI) to evaluate intracranial arterial-wall In the case of distal MCA atherosclerotic disease, artery-to-ar- pathologies is increasing in many centers. Since treatment tery embolism is the most common mechanism of stroke decision-making for ischemic stroke depends primarily on because of the location, being associated with turbulence the mechanism, it is critical to identify the true culprit. This at the distal MCA bifurcation. A longer stenosis is associated review focuses on the usefulness of VWMRI for identifying with the occurrence of a local branch occlusion.8 the etiology of arterial stenosis and for evaluating intracra- nial atherosclerotic stenosis (ICAS). The pitfalls and future Imaging techniques in VWMRI directions for the use of VWMRI in the field of stroke care are High-spatial-resolution in VWMRI is essential for character- also discussed. izing vessel-wall pathologies, enabling visualization of the morphology of both the plaque and its components. In terms of hardware, a magnetic field strength of at least 3 T VWMRI IN ICAS is needed to perform VWMRI.9 For vessel-wall assessment, a combination of multiple magnetic resonance sequences Stroke mechanism of ICAS such as T1-weighted imaging (T1WI), T2-weighted imaging It has been demonstrated that the high prevalence of ICAS (T2WI), and proton-density (PD) and time of flight (TOF) im- in Asians may be at least partially explained by vulnerability aging are used in VWMRI. Multiple tissue-weighted images to certain risk factors, levels of antioxidant enzyme activi- such as obtained in T1WI, T2WI, and PD imaging are used ty,4,5 and greater intracranial arterial tortuosity than in other for better characterization of the individual lesion, whereas races.6 The stroke mechanism also differs according to the TOF imaging is used mainly to characterize luminal abnor- location of the atherosclerosis, and most strokes related to malities and locate and assess the site of vessel narrowing. extracranial atherosclerosis are caused by artery-to-artery In brain tissue, the signal intensity (SI) on T1WI is highest for embolism. ICAS is associated with more diverse mechanisms lipids, followed in decreasing order by cerebral white matter, based on the lesion pattern presented on diffusion-weight- cerebral gray matter, and cerebrospinal fluid (CSF). Subacute ed imaging: 1) local branch occlusion, 2) artery-to-artery hemorrhages and high-protein-containing lesions such as embolism, 3) in situ thrombosis, and 4) hemodynamic. Local mucoceles also have a high SI. On T2WI, the SI in the brain is branch occlusion is caused by obliteration of the perforator’s highest in the CSF, which has the longest T2 relaxation time, orifice by the atheroma. Artery-to-artery embolism manifests followed in decreasing order by gray matter and white mat- as infarcts distal to the stenosis in the territory of the relevant ter. Brain edema, demyelinating lesions, cerebral infarcts, and artery, usually with small scattered lesions. In situ thrombosis tumors also have long T2 relaxation times and thus a high involves infarcts with extensive involvement of most or even SI on T2WI. Conversely, acute or chronic hemorrhage, calci- all of the diseased arterial territory. With a hemodynamic fication, fibrosis, and high-protein-containing lesions have a impairment, the infarcts are located in the border-zone areas low SI on T2WI. PD imaging has a better signal-to-noise ratio associated with perfusion deficits distal to the stenotic or oc- than T1WI, while contrast enhancement is less evident.9 cluded artery.4,7 ICAS in the anterior circulation, and especial- 18 https://doi.org/10.14253/acn.2021.23.1.17 http://www.e-acn.org Seung Min Kim, et al. Vessel wall MRI in stroke Typical findings of VWMRI of ICAS pears hyperintense on T2WI and may show enhancement. Atherosclerosis develops in the inner curvature of the arterial In contrast, a hypointense and nonenhanced layer in the vessel wall, where the shear stress is low.10 Atherosclerotic adjacent area is often observed on T2WI. A third, thin layer plaques are composed of lipid, fibrous components, cellular with enhancement is often observed in the periphery. These material, connective tissue matrix, and calcification. Evalu- layers observed on carotid VWMRI are correlated with find- ating these components can aid the diagnosis of vascular ings obtained from carotid endarterectomy specimens. The pathologies, thus helping to identify “vulnerable” plaques enhanced layer immediately adjacent to the lumen is the that are at high risk of causing stroke.11 ICAS lesions are often fibrous cap, the outer nonenhanced layer indicates the lipid multiple and exhibit eccentric thickening with or without a core, and the outer peripheral thin rim of enhancement rep- focal enhancement (Fig. 1). Positive vessel-wall remodeling resents an increased area of vasa vasorum in the arterial ad- can be also observed in some cases.12 Symptomatic plaques ventitia (Table 1).13 However, not all intracranial atheroscle- are associated with more positive vessel-wall remodeling,
Recommended publications
  • Pathogenetic Mechanisms in Vascular Dementia
    lnt J Clin Lab Res 24: 15-22, 1994 Springer-Verlag 1994 Pathogenetie mechanisms in vascular dementia Lueilla Parnetti 1, Daniela Mari 2, Patrizia Mecocci 1, and Umberto Senin 1 1 Sezione di Gerontologia e Geriatria, Dipartimento di Medicina Clinica, Patologia e Farmacologia, Universitfi degli Studi di Perugia, Via Eugubina 42, 1-06122 Perugia, Italy 2 Istituto di Medicina Interna, UniversitY. degli Studi di Milano, Milan, Italy Summary. Vascular dementia accounts for approximately figures reach and surpass prevalence rates for DAT [62]. 20% of all cases of dementia and for about 50% in VD is the commonest cause of dementia in Japan, being subjects over 80 years. Thromboembolism with multiple responsible for up to 50% of all clinical cases and for cerebral infarcts was considered to be almost the only 54%-65% of all autopsy-confirmed dementias world- pathogenetic pathway of vascular dementia, with multi- wide [88]. While degenerative dementias are currently un- infarct dementia as its clinical manifestation. However, treatable, there is, in contrast, a definite potential for the there is a great heterogeneity of vascular dementia syn- prevention and treatment of cerebrovascular diseases. dromes and pathological subtypes, as documented by the The varied clinical presentations and the multiple number of pathogenetic mechanisms now known to un- causes of dementia syndrome make clinical diagnosis derlie the clinical picture. They include thromboem- quite difficult. In 1984, a Work Group on the Diagnosis bolism and extracerebral and cerebral factors. Among of Alzheimer's Disease established by the National Insti- the extracerebral factors are ischemic hypoxic dementia tute of Neurological and Communicative Disorders and (i.e., dementia due to hypoperfusion), vasculitis, hyper- Stroke and the Alzheimer's Disease and Related Disor- viscosity and abnormalities of hemostasis.
    [Show full text]
  • Intracranial Angioplasty & Stenting
    Position Statement Intracranial Angioplasty & Stenting for Cerebral Atherosclerosis: A Position Statement of the American Society of Interventional and Therapeutic Neuroradiology, Society of Interventional Radiology, and the American Society of Neuroradiology Stroke is the third leading cause of death and the 20) with the definitive National Institutes of Health leading cause of adult disability in North America, (NIH) study demonstrating a first year ischemic Europe, and Asia (1, 2). Intracranial cerebral athero- stroke rate in the pertinent vascular territory of at sclerosis accounts for approximately 8–10% of all least 11% (17). ischemic strokes with a higher reported incidence in the Asian, African, and Hispanic descent populations (3–5). Risk factors include insulin-dependent diabe- Review of Studies tes mellitus, hypercholesterolemia, hypertension, and Surgical Revascularization—EC/IC Bypass Trial cigarette smoking (6–8). In the United States, it is (Extracranial to Intracranial): In 1985, the EC/IC By- estimated that 40,000–60,000 new strokes per year pass Study Group published the results of a trial that are due to intracranial cerebral atherosclerosis. attempted to prove benefit for a surgical approach to treating intracranial atherosclerotic stenoses or occlu- Intracranial Atherosclerosis sion (18). This extracranial to intracranial arterial bypass trial was a prospective, multicenter, interna- Etiology tional study involving 1377 patients and attempted to Four mechanisms for ischemic stroke secondary to show that patients with an intracranial atherosclerotic intracranial atherosclerosis have been proposed: (1) stenosis or occlusion could benefit by an EC/IC by- hypoperfusion; (2) thrombosis at the site of stenosis pass. This trial failed for all subgroups, and in partic- due to plaque rupture, intraplaque hemorrhage, or ular for those with middle cerebral artery stenosis.
    [Show full text]
  • Diagnostic and Therapeutic Approach of Carotid and Cerebrovascular Plaque on the Basis of Vessel Imaging
    Review J Lipid Atheroscler 2017 June;6(1):15-21 https://doi.org/10.12997/jla.2017.6.1.15 JLA pISSN 2287-2892 • eISSN 2288-2561 Diagnostic and Therapeutic Approach of Carotid and Cerebrovascular Plaque on the Basis of Vessel Imaging Dong Hyun Lee, Jong-Ho Park Department of Stroke Neurology, Seonam University Myongji Hospital, Goyang-si, Korea Atherosclerosis, characterized by chronic systemic inflammation with plaque formation, is one of the major causes of cerebrovascular disease. Recent advances in imaging technologies can help further understand the overall process and biology of plaque formation and rupture. Thus, these imaging techniques could aid clinicians to make better decision for risk stratification, therapeutic planning, and prediction of future cerebrovascular event. Ultrasonography, magnetic resonance imaging, and positron emission tomography are the rapidly-evolving imaging modalities dealing with assessment of atherosclerotic plaque. By advances in imaging technology for evaluating plaque, we can characterize the vulnerability of plaque in-vivo, understand the composition and activity of plaque, assess therapeutic response to treatment, and ultimately predict the overall risk of future cerebrovascular episodes. In this review, we will introduce current understanding of various advanced imaging modalities and clinical application of these imaging technologies. (J Lipid Atheroscler 2017 June;6(1):15-21) Key Words: Atherosclerosis, Plaque, Imaging, Carotid artery disease, Cerebrovascular disease INTRODUCTION vascular episodes, and reliably monitor the therapeutic response to medication. Atherosclerosis is a chronic systemic inflammatory Recent advances in imaging technologies can help disease with an insidious process caused by multiple further understand the overall process in atherosclerosis pathological changes triggering lipoprotein dysregulation including molecular biology of plaque formation and and immunocyte activation within the arterial system.1 rupture.
    [Show full text]
  • Search for Reliable Circulating Biomarkers to Predict Carotid Plaque Vulnerability
    International Journal of Molecular Sciences Review Search for Reliable Circulating Biomarkers to Predict Carotid Plaque Vulnerability Núria Puig 1,2, Elena Jiménez-Xarrié 3,*, Pol Camps-Renom 3,* and Sonia Benitez 2,* 1 Department of Biochemistry and Molecular Biology, Faculty of Medicine, Building M, Autonomous University of Barcelona (UAB), 08193 Cerdanyola del Vallès, Barcelona, Spain; [email protected] 2 Cardiovascular Biochemistry, Biomedical Research Institute Sant Pau (IIB-Sant Pau), 08041 Barcelona, Spain 3 Stroke Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau (IIB-Sant Pau), 08041 Barcelona, Spain * Correspondence: [email protected] (E.J.-X.); [email protected] (P.C.-R.); [email protected] (S.B.); Tel.: +34-93-553-7595 (S.B.) Received: 2 October 2020; Accepted: 1 November 2020; Published: 3 November 2020 Abstract: Atherosclerosis is responsible for 20% of ischemic strokes, and the plaques from the internal carotid artery the most frequently involved. Lipoproteins play a key role in carotid atherosclerosis since lipid accumulation contributes to plaque progression and chronic inflammation, both factors leading to plaque vulnerability. Carotid revascularization to prevent future vascular events is reasonable in some patients with high-grade carotid stenosis. However, the degree of stenosis alone is not sufficient to decide upon the best clinical management in some situations. In this context, it is essential to further characterize plaque vulnerability, according to specific characteristics (lipid-rich core, fibrous cap thinning, intraplaque hemorrhage). Although these features can be partly detected by imaging techniques, identifying carotid plaque vulnerability is still challenging. Therefore, the study of circulating biomarkers could provide adjunctive criteria to predict the risk of atherothrombotic stroke.
    [Show full text]
  • VIEW Open Access the Overlap Between Vascular Disease and Alzheimer’S Disease – Lessons from Pathology Johannes Attems1* and Kurt a Jellinger2
    Attems and Jellinger BMC Medicine 2014, 12:206 http://www.biomedcentral.com/1741-7015/12/206 Vascular risk factors and Alzheimer’s Disease REVIEW Open Access The overlap between vascular disease and Alzheimer’s disease – lessons from pathology Johannes Attems1* and Kurt A Jellinger2 Abstract Recent epidemiological and clinico-pathological data indicate considerable overlap between cerebrovascular disease (CVD) and Alzheimer’s disease (AD) and suggest additive or synergistic effects of both pathologies on cognitive decline. The most frequent vascular pathologies in the aging brain and in AD are cerebral amyloid angiopathy and small vessel disease. Up to 84% of aged subjects show morphological substrates of CVD in addition to AD pathology. AD brains with minor CVD, similar to pure vascular dementia, show subcortical vascular lesions in about two-thirds, while in mixed type dementia (AD plus vascular dementia), multiple larger infarcts are more frequent. Small infarcts in patients with full-blown AD have no impact on cognitive decline but are overwhelmed by the severity of Alzheimer pathology, while in early stages of AD, cerebrovascular lesions may influence and promote cognitive impairment, lowering the threshold for clinically overt dementia. Further studies are warranted to elucidate the many hitherto unanswered questions regarding the overlap between CVD and AD as well as the impact of both CVD and AD pathologies on the development and progression of dementia. Keywords: Alzheimer’s disease, Cerebrovascular lesions, Cerebral amyloid angiopathy, Cognitive impairment, Lacunes, Microinfarcts, Small vessel disease, White matter lesions Introduction risk factors, e.g., atrial fibrillation and congestive heart fail- The interaction between cerebrovascular disease (CVD) ure, have also been linked to the pathogenesis and progres- and Alzheimer’s disease (AD) is a topic of considerable sion of AD and are among the most important modifiable current interest.
    [Show full text]
  • Use of High-Resolution 3.0-T Magnetic Resonance Imaging to Characterize Atherosclerotic Plaques in Patients with Cerebral Infarction
    2424 EXPERIMENTAL AND THERAPEUTIC MEDICINE 10: 2424-2428, 2015 Use of high-resolution 3.0-T magnetic resonance imaging to characterize atherosclerotic plaques in patients with cerebral infarction PENG XU1*, LULU LV2*, SHAODONG LI1, HAITAO GE1, YUTAO RONG1, CHUNFENG HU1 and KAI XU1 1Department of Radiology, Affiliated Hospital of Xuzhou Medical College, Xuzhou, Jiangsu 221006; 2Department of Computed Tomography and Magnetic Resonance Imaging, Xuzhou Central Hospital, Xuzhou, Jiangsu 221009, P.R. China Received November 12, 2014; Accepted September 1, 2015 DOI: 10.3892/etm.2015.2815 Abstract. The present study aimed to evaluate the utility of Introduction high-resolution magnetic resonance imaging (MRI) in the characterization of atherosclerotic plaques in patients with Cerebral atherosclerosis is an important risk factor for ischemic acute and non-acute cerebral infarction. High-resolution MRI stroke, and is the cause of stroke in 8-15% of patients (1). Factors of unilateral stenotic middle cerebral arteries was performed that lead to stroke and that are associated with cerebral artery to evaluate the degree of stenosis, the wall and plaque areas, stenosis include intraluminal embolus, perforating artery occlu- plaque enhancement patterns and lumen remodeling features sion and low perfusion (2). Currently, common techniques used in 15 and 17 patients with acute and non-acute cerebral infarc- for cerebrovascular evaluation include computed tomography tion, respectively. No significant difference was identified in angiography, magnetic resonance angiography (MRA) and the vascular stenosis rate between acute and non-acute patients. digital subtraction angiography (DSA); however, the majority of Overall, plaque eccentricity was observed in 29 patients, these only examine the vascular lumen.
    [Show full text]
  • Intracranial Atherosclerosis: from Microscopy to High-Resolution Magnetic Resonance Imaging
    Journal of Stroke 2017;19(3):249-260 https://doi.org/10.5853/jos.2016.01956 Special Review Intracranial Atherosclerosis: From Microscopy to High-Resolution Magnetic Resonance Imaging Wen-jie Yang, Ka-sing Wong, Xiang-yan Chen Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Prince of Wales Hospital, Sha Tin, Hong Kong Intracranial atherosclerosis is one of the leading causes of ischemic stroke and occurs more Correspondence: Xiangyan Chen Department of Medicine and commonly in patients of Asian, African or Hispanic origin than in Caucasians. Although the Therapeutics, The Chinese University histopathology of intracranial atherosclerotic disease resembles extracranial atherosclerosis, there of Hong Kong, Prince of Wales Hospital, General Office, 9/F, Clinical are some notable differences in the onset and severity of atherosclerosis. Current understanding of Sciences Building, Sha Tin, Hong Kong intracranial atherosclerotic disease has been advanced by the high-resolution magnetic resonance Tel: +852-26352130 imaging (HRMRI), a novel emerging imaging technique that can directly visualize the vessel wall Fax: +852-26493761 E-mail: [email protected] pathology. However, the pathological validation of HRMRI signal characteristics remains a key step to depict the plaque components and vulnerability in intracranial atherosclerotic lesions. The Received: December 8, 2016 Revised: February 26, 2017 purpose of this review is to describe the histological features of intracranial atherosclerosis and to Accepted: March
    [Show full text]
  • Cerebral Atherosclerosis Contributes to Alzheimer's Dementia
    bioRxiv preprint doi: https://doi.org/10.1101/793349; this version posted October 13, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Cerebral atherosclerosis contributes to Alzheimer’s dementia independently of its hallmark amyloid and tau pathologies Aliza P. Wingo1,2,#, Wen Fan3, Duc M. Duong4, Ekaterina S. Gerasimov3, Eric B. Dammer4, Bartholomew White5, Madhav Thambisetty6, Juan C. Troncoso5, Julie A. Schneider7, James J. Lah3, David A. Bennett7, Nicholas T. Seyfried4,#, Allan I. Levey3,#, Thomas S. Wingo3,# Affiliations 1Division of Mental Health, Atlanta VA Medical Center, Decatur, GA 30033, USA 2Department of Psychiatry, Emory University School of Medicine, Atlanta, GA 30322, USA 3Department of Neurology, Emory University School of Medicine, Atlanta, GA 30322, US 4Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322, USA 5Johns Hopkins School of Medicine, Baltimore, MD 21205, USA 6Clinical and Translational Neuroscience Section, Laboratory of Behavioral Neuroscience, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA 7Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, Illinois, USA #Corresponding authors [email protected] (T.S.W.) [email protected] (A.I.L.) [email protected] (N.T.S.) [email protected] (A.P.W.) Emory University Center for Neurodegenerative Disease 505K Whitehead Building 615 Michael Street NE Atlanta, GA 30322-1047 1 bioRxiv preprint doi: https://doi.org/10.1101/793349; this version posted October 13, 2019.
    [Show full text]
  • Hypertension-Induced Cognitive Impairment: from Pathophysiology to Public Health
    REVIEWS Hypertension-induced cognitive impairment: from pathophysiology to public health Zoltan Ungvari1,2,3, Peter Toth1,2,4, Stefano Tarantini1,2,3, Calin I. Prodan 5,6, Farzaneh Sorond 7, Bela Merkely8 and Anna Csiszar1,9 ✉ Abstract | Hypertension affects two-thirds of people aged >60 years and significantly increases the risk of both vascular cognitive impairment and Alzheimer’s disease. Hypertension compromises the structural and functional integrity of the cerebral microcirculation, promoting microvascular rarefaction, cerebromicrovascular endothelial dysfunction and neurovascular uncoupling, which impair cerebral blood supply. In addition, hypertension disrupts the blood–brain barrier, promoting neuroinflammation and exacerbation of amyloid pathologies. Ageing is characterized by multifaceted homeostatic dysfunction and impaired cellular stress resilience, which exacerbate the deleterious cerebromicrovascular effects of hypertension. Neuroradiological markers of hypertension-induced cerebral small vessel disease include white matter hyperintensities, lacunar infarcts and microhaemorrhages, all of which are associated with cognitive decline. Use of pharmaceutical and lifestyle interventions that reduce blood pressure, in combination with treatments that promote microvascular health, have the potential to prevent or delay the pathogenesis of vascular cognitive impairment and Alzheimer’s disease in patients with hypertension. Vascular cognitive impairment (VCI) and Alzheimer’s mechanisms, including regulation of cerebral blood disease (AD) are major obstacles to healthy ageing and flow and microvascular pressure. Third, ageing is asso- the principal causes of chronic disability and decreased ciated with impaired cellular stress resilience, which quality of life among elderly people in the industrialized exacerbates cellular and molecular damage resulting world. The prevalence of AD and VCI is projected to from hypertension-induced haemodynamic and oxi- quadruple in the next 50 years owing to rapid ageing dative stress.
    [Show full text]
  • Medical & Surgical Treatment of Intracranial Cerebral
    Brain Summit 2020 Virtual Symposium October 31, 2020 MEDICAL & SURGICAL TREATMENT OF INTRACRANIAL CEREBRAL ATHEROSCLEROSIS MARK D. JOHNSON, MD DEPARTMENT OF NEUROLOGY UT SOUTHWESTERN Fibrous and Adipose component: Solid arrows Fibrous Component: Dotted Arrow White component is calcification and Red component is necrosis A. H & E; B. 7T; C:. Intravascular Sonography Lancet 2014:383: 984-98 1 Brain Summit 2020 Virtual Symposium October 31, 2020 DISCLOSURES • I have participated in several of the clinical trials related to this lecture including WASID, SAMMPRIS, and MyRIAD as co-investigator or principal investigator in our institution. 2 Brain Summit 2020 Virtual Symposium October 31, 2020 ATHEROSCLEROTIC LARGE ARTERY INTRACRANIAL STENOSIS - EPIDEMIOLOGY • Particularly prevalent in black, Asian, Hispanic, and Indian populations. Also in some Arabic countries.* • High rate of vascular risk factors • 90% have multiple risk factors • 75% HTN, 50% DM, 65% CAD, 65% smokers, and 40% hypercholesterolemia • Genetic factors undetermined – • 30-50% of strokes in Asian people (China, Japan, South Korea, India) • 5%-10% of strokes in white people • 11% in Hispanics • 11%-22% in Japanese (Nishimaru*; Brust*; Kieffer*) • 50% present with TIAs • Hypertension and diabetes are most important risk factors • Age-specific prevalence of intracranial and extracranial stenosis (A) 50–99% symptomatic, asymptomatic, and no intracranial stenosis. • It is a marker of CAD in white patients (B) Proximal extracranial internal carotid artery stenosis, extracranial vertebral
    [Show full text]
  • Of 33 Appendix
    Appendix: Algorithms used to identify variables in the study titled: Rosiglitazone use and post-discontinuation glycaemic control in two European countries, 2000-2010 Diagnostic codes used to Abstract the Danish National Registry of Patients Disease/condition ICD-8 code ICD-10 code Diabetes type 1 249.00; 249.06; 249.07; 249.09 E10.0, E10.1; E10.9 Diabetes type 2 250.00; 250.06; 250.07; 250.09 E11.0; E11.1; E11.9 Acute myocardial infarction 410 I21, I22, I23 Ischemic heart disease (acute 411-414 I20, I24, I25 and chronic) Congestive heart failure 427.09, 427.10, 427.11, I50, I11.0, I13.0, I13.2 427.19, 428.99, 782.49; Other cardiac disease 393–398, 400–404 I05–I09 Peripheral vascular disease 440, 441, 442, 443, 444, 445 I70, I71, I72, I73, I74, I77 Ischemic stroke 430-438 (cerebrovascular I63-64 disease) Alcoholism 291, 303, 577.10, 571.09, F10.1-F10.9, G31.2, G62.1, 571.10 G72.1, I42.6, K29.2, K86.0, Z72.1 Obesity 277.99 E65-E66 Mild liver disease 571, 573.01, 573.04 B18, K70.0–K70.3, K70.9, K71, K73, K74, K76.0 Moderate to severe liver 070.00, 070.02, 070.04, B15.0, B16.0, B16.2, B19.0, disease 070.06, 070.08, 573.00, K70.4, K72, K76.6, I85 456.00–456.09 Deep vein thrombosis 451.00 I81, I82 Pulmonary embolism 450.99 I26 ICD-8: http://www.sst.dk/Indberetning%20og%20statistik/Klassifikationer/SKS_download.aspx ICD-10: http://apps.who.int/classifications/apps/icd/icd10online/ Page 1 of 33 Diagnostic codes used to compute Charlson Comorbidity Index Disease ICD-8 code ICD-10 code Myocardial infarction 410 I21;I22;I23 Congestive heart failure
    [Show full text]
  • Pilot Study of Pre-Ischemic Conditioning for Intracranial Atherosclerosis
    Pilot Study of Pre-Ischemic Conditioning for Intracranial Atherosclerosis Study Protocol Principal Investigators Marc I. Chimowitz MBChB Professor of Neurology Medical University of South Carolina David C Hess M.D Chairman and Professor of Neurology Medical College of Georgia Augusta University Funding for this Pilot Clinical Trial is through a Pilot Grant from the South Carolina Clinical & Translational Research (SCTR) Institute at the Medical University of South Carolina. SCTR is funded through a UL1 grant from NIH / NCATS. Version: February 6, 2017 February 6, 2017 page 1 of 17 TABLE OF CONTENTS 1. Study Rationale ………………………………………………………………………….. 3 2. Primary Aims and Long-Term Goal ………………………………………………….. 3 3. Overview of Study Design ……………………………………………………………... 4 4. Subject Selection Criteria ……………………………………………………………… 4 Inclusion Criteria 5 Exclusion Criteria 5 5. Screening, Informed Consent, Randomization and Enrollment of Subjects 6 6. RLIC Device And Ischemic Conditioning Regimen……………………………… 6 7. Aggressive Medical Management …………………………………………………. 7 8. Blood Biomarker Measurements…………………………………………………… 7 9. MRI Measurements Of CBF And Other Perfusion Parameters………………… 8 10. Assessment Of Feasibility, Tolerability And Adherence To RLIC……………. 8 11. Randomization, Blinding, And Data Management………………………………. 8 12. Statistical Analyses…………………………………………………………………… 8 13. Protection Of Human Subjects……………………………………………………… 8 Bibliography……………………………………………………………………………. 12 Appendix 1. Adverse Event Questionnaire……………………………………….. 15 Appendix 2. Subject
    [Show full text]