Brain Microbleeds, Amyloid Plaques, Intellectual Deterioration, and Arterial Stiffness
2008; Lippincott Williams & Wilkins; Volume: 51; Issue: 3 Linguagem: Inglês
10.1161/hypertensionaha.107.109199
ISSN1524-4563
Autores Tópico(s)Dementia and Cognitive Impairment Research
ResumoHomeHypertensionVol. 51, No. 3Brain Microbleeds, Amyloid Plaques, Intellectual Deterioration, and Arterial Stiffness Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBBrain Microbleeds, Amyloid Plaques, Intellectual Deterioration, and Arterial Stiffness Michael F. O'Rourke Michael F. O'RourkeMichael F. O'Rourke St Vincent's Clinic, University of New South Wales, Sydney, Australia Originally published4 Feb 2008https://doi.org/10.1161/HYPERTENSIONAHA.107.109199Hypertension. 2008;51:e20Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: February 4, 2008: Previous Version 1 To the Editor:The article by Henskens et al1 on brain microbleeds supports a view2 that cerebral microvascular disease in hypertensive patients is responsible for intellectual deterioration and is caused by abnormal flow pulsations extending into the small cerebral vessels as a consequence of aortic stiffening. The relationship between cognitive decline and aortic stiffness and pulse pressure, suspected previously on mechanistic grounds,2 has been confirmed by Waldstein et al3 for the Baltimore Longitudinal Study of Aging in the same issue of Hypertension. MRI studies have confirmed an association between cerebral white matter hyperintensities and high-flow pulsations in the cerebral vasculature and have referred to the former as caused by "pulse wave encephalopathy."4 Histological studies have shown that the amyloid deposits characteristic of Alzheimer's dementia can be attributed to previous microbleeds.5 Our own work2 suggests that microbleeds, white matter hyperintensities, and lacunar infarcts are caused by the damaging forces of high pulsatile pressure and flow in cerebral microvessels, as first pointed out by Byrom in Sydney, and by a similar mechanism in the pulmonary circulation of children with congenital left to right shunts, as pointed out by Edwards from the Mayo Clinic 50 years ago.These mechanisms may help explain other recent findings. Increased circulating endothelial cell fragments in persons with aortic stiffening6 may be caused by such microvascular damage in brain and kidney.2 High C-reactive protein levels in older persons may be a consequence of inflammation caused by small vessel damage rather than a cause of large artery damage. Even the findings of highest value of nocturnal blood pressure in outcomes by Henskens et al1 and by Fagard et al7 in the same issue of Hypertension may be due in part to cerebral arteries being exposed to the highest blood pressure during sleep when persons are recumbent and the brain less protected from hydrostatic (gravitational) forces than when a person is erect or sitting.The article by Henskens et al1 and others in the same issue of Hypertension provide more evidence to support a cerebral microvascular mechanism for intellectual deterioration in older persons with arterial stiffening.DisclosuresM.F.O. is a founding director of AtCor Medical Pty Ltd, manufacturer of systems for analyzing the arterial pulse.1 Henskens LHG, van Oostenbrugge RJ, Kroon AA, de Leeuw P, Lodder J. Brain microbleeds are associated with ambulatory blood pressure levels in a hypertensive population. Hypertension. 2008; 51: 62–68.LinkGoogle Scholar2 O'Rourke MF, Safar ME. Relationship between aortic stiffening and microvascular disease in brain and kidney: cause and logic of therapy. Hypertension. 2005; 46: 200–204.LinkGoogle Scholar3 Waldstein SR, Rice SC, Thayer JF, Najjar SS, Scuteri A, Zonderman AB. Pulse pressure and pulse wave velocity are related to cognitive decline in the Baltimore Longitudinal Study of Aging. Hypertension. 2008; 51: 99–104.LinkGoogle Scholar4 Henry-Feugeas MC, De Marco G, Idy-Peretti I, Godon-Hardy S, Fredy D, Schouman-Claeys E. age-related cerebral white matter changes and pulse-wave encephalopathy: observations with three-dimensional MRI. Magn Reson Imaging. 2005; 23: 145–165.Google Scholar5 Cullen KM, Kocsi Z, Stone J. Microvascular pathology in the aging human brain: evidence that senile plaques are sites of microhemorrhages. Neurobiol Aging. 2006; 27: 1786–1796.CrossrefMedlineGoogle Scholar6 Wang JM, Huang YJ, Wang Y, Xu MG, Wang LC, Wang SH, Tao J. Increased circulating CD31+/CD42− microparticles are associated with impaired systemic artery elasticity in healthy subjects. Am J Hypertens. 2007; 20: 957–964.CrossrefMedlineGoogle Scholar7 Fagard RH, Celis H, Thijsh L, Staessen JA, Clement DL, De Buyzere ML, De Bacquer D. Daytime and nighttime blood pressure as predictors of death and cause-specific cardiovascular events in hypertension. Hypertension. 2008; 51: 55–61.LinkGoogle 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 FiguresReferencesRelatedDetailsCited By Bernal M, Saldarriaga J, Cabeza C, Negreira C, Bustamante J and Brum J (2019) Development and evaluation of anisotropic and nonlinear aortic models made from clinical images for in vitro experimentation , Physics in Medicine & Biology, 10.1088/1361-6560/ab2db5, 64:16, (165006) Liu J, Xia S, Hanks R, Wiseman N, Peng C, Zhou S, Haacke E and Kou Z (2016) Susceptibility Weighted Imaging and Mapping of Micro-Hemorrhages and Major Deep Veins after Traumatic Brain Injury, Journal of Neurotrauma, 10.1089/neu.2014.3856, 33:1, (10-21), Online publication date: 1-Jan-2016. Abe Y, Sudo R, Ikeda M and Tanishita K (2012) Steady and pulsatile shear stress induce different three-dimensional endothelial networks through pseudopodium formation, Journal of Biorheology, 10.1007/s12573-012-0056-5, 27:1-2, (38-48), Online publication date: 1-Nov-2013. Li M, Tan Y, Stenmark K and Tan W (2012) High Pulsatility Flow Induces Acute Endothelial Inflammation Through Overpolarizing Cells to Activate NF-κB, Cardiovascular Engineering and Technology, 10.1007/s13239-012-0115-5, 4:1, (26-38), Online publication date: 1-Mar-2013. Ochi N, Kohara K, Tabara Y, Nagai T, Kido T, Uetani E, Ochi M, Igase M and Miki T (2010) Association of Central Systolic Blood Pressure With Intracerebral Small Vessel Disease in Japanese, American Journal of Hypertension, 10.1038/ajh.2010.60, 23:8, (889-894), Online publication date: 1-Aug-2010. Vemuri P and Jack C (2009) Iron imaging in neurodegenerative disorders Clinical MR Neuroimaging, 10.1017/CBO9781139193481.044, (642-652) Henskens L, van Oostenbrugge R, Kroon A, de Leeuw P and Lodder J (2008) Response to Brain Microbleeds, Amyloid Plaques, Intellectual Deterioration, and Arterial Stiffness, Hypertension, 51:3, (e21-e21), Online publication date: 1-Mar-2008. March 2008Vol 51, Issue 3 Advertisement Article InformationMetrics https://doi.org/10.1161/HYPERTENSIONAHA.107.109199PMID: 18250358 Originally publishedFebruary 4, 2008 PDF download Advertisement SubjectsCerebrovascular Disease/StrokeComputerized Tomography (CT)Hypertension
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