Stroke Science and Care Since the Founding of the American Heart Association
2024; Lippincott Williams & Wilkins; Volume: 149; Issue: 19 Linguagem: Inglês
10.1161/circulationaha.123.065471
ISSN1524-4539
Autores Tópico(s)Intracranial Aneurysms: Treatment and Complications
ResumoHomeCirculationVol. 149, No. 19Stroke Science and Care Since the Founding of the American Heart Association Free AccessArticle CommentaryPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessArticle CommentaryPDF/EPUBStroke Science and Care Since the Founding of the American Heart Association Mitchell S.V. Elkind Mitchell S.V. ElkindMitchell S.V. Elkind Correspondence to: Mitchell S.V. Elkind, MD, MS, Neurological Institute, 710 West 168th St, New York, NY 10032. Email E-mail Address: [email protected] American Heart Association, Dallas, TX. Department of Neurology, Vagelos College of Physicians and Surgeons, and Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY. Originally published6 May 2024https://doi.org/10.1161/CIRCULATIONAHA.123.065471Circulation. 2024;149:1469–1470The past century witnessed dramatic advances in the field of cerebrovascular disease, many spurred by the American Heart Association and American Stroke Association. Early advances included the 1927 use by Antonio Egas Moniz of x-rays and contrast angiography to produce in vivo images of human cerebral arteries, followed 10 years later by the first cerebral aneurysm clipping by Walter Dandy. The original successful carotid endarterectomies were performed in the 1950s by DeBakey in the United States and Eastcott in the United Kingdom. In the 1950s and 1960s, astute clinicians such as C. Miller Fisher described and recognized the implications of clinical syndromes, including transient monocular blindness, transient ischemic attack, lacunar stroke, and carotid occlusive disease; atrial fibrillation was discovered to be an important and preventable cause of stroke. Another 10 years brought the development, in 1972, by Godfrey Hounsfield and Allan Cormack, of computerized tomography, revolutionizing brain imaging and permitting direct visualization of cerebral infarction and the immediate distinction between ischemic and hemorrhagic stroke. A decade later, in 1981, Astrup, Siesjö, and Symon introduced the concept of the "ischemic penumbra," a stunned and vulnerable, but not yet completely dead, area of brain tissue adjacent to a core of infarction; neurosurgeon George Ojemann, around the same time, first demonstrated the reversibility of cerebral ischemia.Building on these advances over more than half a century, and with evolution of the modern multicenter randomized controlled clinical trial, the stage was set for rapid advances in stroke prevention and acute therapy. Large definitive trials demonstrated the efficacy of anticoagulation in preventing strokes among patients with atrial fibrillation, and carotid endarterectomy was proven to prevent stroke among those with atherosclerotic stenosis of the carotid artery. In December 1995, investigators demonstrated that intravenous thrombolysis administered within 3 hours improved outcomes after ischemic stroke.1 Twenty years later, in 2015, endovascular therapy was convincingly shown to benefit patients with middle cerebral artery occlusion in a stunning session of presentations of results from 5 separate clinical trials2 at the American Heart Association/American Stroke Association International Stroke Conference in Nashville; investigators were met with standing ovations. Only 3 years later, trials demonstrated the potential for advanced neuroimaging to identify patients with salvageable brain tissue up to 24 hours after symptom onset.3 At the same time, American Heart Association/American Stroke Association quality improvement programs focused on stroke systems of care, such as Target: Stroke, ensured the timely delivery of acute therapies. Acute stroke treatment had come full circle: neurologists could now rapidly recognize and diagnose stroke, neuroradiologists could image stroke and characterize brain tissue, and interventionalists and surgeons could remove obstructing thrombi using techniques reliant on those Moniz first developed a century earlier.These crucial clinical advances were matched by sophisticated study of stroke pathophysiology, leading to recognition that, contrary to impressions given by the word "stroke," evoking images of lightning, stroke evolves over days. This insight led to the search for neuroprotective medications and other novel therapies, such as sphenopalatine ganglion stimulation, that interfere with neuronal injury after ischemia. These discoveries have not yet led to approved medications in the United States, but the search continues.Over the past century, moreover, the connections between heart, brain, body, and mind grew more apparent. Cardiac disease, particularly atrial fibrillation, is a clear precipitant of stroke. Recognition of this association led to increased efforts to search for atrial fibrillation in patients with recent stroke using implanted cardiac monitors, development of an expanding array of antithrombotic agents, including increasingly specific coagulation factor inhibitors, and advances in interventional procedures, such as left atrial exclusion devices, to prevent embolism. The connection is bidirectional, because brain and mental health are increasingly recognized to contribute to cardiac function, both chronically and acutely. For instance, stroke can trigger acute heart failure ("takotsubo cardiomyopathy") through sudden increases in sympathetic activation; advanced neuroimaging studies now suggest that individuals with preexisting amygdala activation, indicative of propensity to fear, are at greater risk of experiencing this form of cardiomyopathy during acute stress.4Laboratory advances and growing awareness of patient experiences, moreover, highlight chronic, delayed, and even progressive poststroke neurological effects. Long-term complications include depression, anxiety, cognitive decline, dementia, pain, gait difficulty, and movement disorders. Mechanisms for delayed manifestations after stroke may include blood-brain barrier changes, accelerated neurodegeneration, neuroinflammation, remote immune effects, altered brain circuitry, and metabolic disruption. For example, chronic inflammation may persist much longer after stroke than previously appreciated and stroke may accelerate amyloid deposition characteristic of Alzheimer disease. Other chronic stroke consequences, not specifically neurological, include osteoporosis, falls and fractures, incontinence, and frailty. Recognizing stroke as not only an acute event but also an initiator of chronic and progressive conditions has potential to reshape approaches to poststroke care. Greater emphasis will need to be placed on continuing rehabilitation, monitoring for decline, and comprehensive support for survivors.Injury to the brain, growing evidence shows, is also tightly related to health and dysfunction of organs distinct from the vasculature. Historically, the brain was regarded as privileged, ensconced in and protected from the rest of the body by the skull and blood-brain barrier. The blood-brain barrier, comprising tight junctions between cells in the brain's vasculature, restricts the passage of harmful substances while allowing in essential nutrients. This traditional conception implied a brain functioning in isolation, apart from and unaffected by vulnerabilities faced by other organ systems. Recent breakthroughs, however, reveal complex interconnections between the brain and other organs. Ripple effects of cerebral damage influence other major organs, including lungs, liver, kidneys, spleen, intestines, and immune system. Sophisticated neuroimaging research provides evidence that systemic bodily functions, such as cardiac rhythm, the stress-related hyperglycemic response, and response to infection, localize to different brain regions, much like aphasia and motor function.5 The inflammatory response triggered by stroke releases signaling molecules that disrupt distant organs, leading to lung infiltration by leukocytes and dysfunction of cilia that protect the airways. Stroke-induced immune dysregulation makes the body more susceptible to infections. These systemic changes may contribute to the progressive, chronic consequences of stroke discussed above.This emerging holistic understanding of stroke underscores the intricate interdependence of the body's organ systems and challenges the long-held belief of the brain's exclusivity. Recognizing the multifaceted effect of stroke suggests that vascular neurologists of the future will need to be vigilant about the effects of stroke on other organs and related potential secondary complications to provide comprehensive care to patients experiencing stroke.ARTICLE INFORMATIONSources of FundingNone.Disclosures Dr Elkind discloses employment by the American Heart Association; receipt of study drug in kind from BMS-Pfizer Alliance for Eliquis and ancillary funding from Roche for a National Institutes of Health–funded trial of stroke prevention; royalties from UpToDate for chapters on stroke; and honoraria from the Atria Academy of Science and Medicine.FootnotesThe American Heart Association celebrates its 100th anniversary in 2024. This article is part of a series across the entire AHA Journal portfolio written by international thought leaders on the past, present, and future of cardiovascular and cerebrovascular research and care. To explore the full Centennial Collection, visit https://www.ahajournals.org/centennialThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.For Sources of Funding and Disclosures, see page 1470.Circulation is available at www.ahajournals.org/journal/circCorrespondence to: Mitchell S.V. Elkind, MD, MS, Neurological Institute, 710 West 168th St, New York, NY 10032. Email mse13@columbia.eduREFERENCES1. National Institute of Neurological Disorders and Stroke rt-PA Stroke Group. Tissue plasminogen activator for acute ischemic stroke.New Engl J Med. 1995; 333:1581–1587. doi: 10.1056/NEJM199512143332401CrossrefMedlineGoogle Scholar2. Goyal M, Menon BK, van Zwam WH, Dippel DW, Mitchell PJ, Demchuk AM, Dávalos A, Majoie CBLM, van der Lugt A, de Miquel MA, et al; HERMES collaborators. Endovascular thrombectomy after large-vessel ischaemic stroke: a meta-analysis of individual patient data from five randomised trials.Lancet. 2016; 387:1723–1731. doi: 10.1016/S0140-6736(16)00163-XCrossrefMedlineGoogle Scholar3. Nogueira RG, Jadhav AP, Haussen DC, Bonafe A, Budzik RF, Bhuva P, Yavagal DR, Ribo M, Cognard C, Hanel RA, et al. Thrombectomy 6 to 24 hours after stroke with a mismatch between deficit and infarct.N Engl J Med. 2018; 378:11–21. doi: 10.1056/NEJMoa1706442CrossrefMedlineGoogle Scholar4. Radfar A, Abohashem S, Osborne MT, Wang Y, Dar T, Hassan MZO, Ghoneem A, Naddaf N, Patrich T, Abbasi T, et al. Stress-associated neurobiological activity associates with the risk for and timing of subsequent Takotsubo syndrome.Eur Heart J. 2021; 42:1898–1908. doi: 10.1093/eurheartj/ehab029CrossrefMedlineGoogle Scholar5. Arsava EM, Chang K, Tawakol A, Loggia ML, Goldstein JN, Brown J, Park K-Y, Singhal AB, Kalpathy-Cramer J, Sorensen AG, et al. Stroke-related visceral alterations: a voxel-based neuroanatomic localization study.Ann Neurol. 2023; 94:1155–1163. doi: 10.1002/ana.26785CrossrefMedlineGoogle Scholar eLetters(0)eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.Sign In to Submit a Response to This Article Previous Back to top Next FiguresReferencesRelatedDetails May 7, 2024Vol 149, Issue 19 Advertisement Article InformationMetrics © 2024 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.123.065471PMID: 38709839 Originally publishedMay 6, 2024 Keywordscerebrovascular disordersdementianeuroinflammatory diseasesstrokethrombectomythrombolytic therapyPDF download Advertisement SubjectsCerebrovascular Disease/StrokeCognitive ImpairmentComputerized Tomography (CT)Magnetic Resonance Imaging (MRI)Neuroprotectants
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