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• W2143684672 abstract "HomeHypertensionVol. 57, No. 4Cerebrovascular Challenges in Diabetic Patients Free AccessArticle CommentaryPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessArticle CommentaryPDF/EPUBCerebrovascular Challenges in Diabetic PatientsThe Pressure Is on to Maintain Perfusion Jill N. Barnes and Michael J. Joyner Jill N. BarnesJill N. Barnes From the Department of Anesthesiology, Mayo Clinic, Rochester, MN. Search for more papers by this author and Michael J. JoynerMichael J. Joyner From the Department of Anesthesiology, Mayo Clinic, Rochester, MN. Search for more papers by this author Originally published28 Feb 2011https://doi.org/10.1161/HYPERTENSIONAHA.110.168070Hypertension. 2011;57:674–675Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2011: Previous Version 1 See related article, pp 738–745In this edition of Hypertension, Kim et al1 report that cerebral perfusion is differentially effected by pharmacological blood pressure treatment in hypertensive patients, uncomplicated type II diabetics, and type II diabetics with microvascular complications. Specifically, they reported a progressive decrease in cerebral blood flow after 6 months of antihypertensive medication in diabetics with microvascular complications, whereas cerebral blood flow in hypertensive or uncomplicated diabetics was only marginally reduced by treatment. In addition, the diabetics with microvascular complications demonstrated a blunted cerebral responsiveness to CO2 but similar middle cerebral artery blood velocity compared with hypertensives and uncomplicated diabetics before treatment for their hypertension. However, it is unknown whether the blunted cerebral vasodilator responses at baseline were caused by the same mechanisms that reduced middle cerebral artery blood velocity after blood pressure treatment.When the findings of Kim et al1 are viewed in an epidemiological context, it is interesting to note that, in middle-aged and older humans, obesity, diabetes mellitus, hypertension, and physical inactivity frequently coexist in the same patients. All of these conditions are associated with vascular dysfunction in both large conduit vessels and the microcirculation, and all have emerged as major risk factors for mild cognitive impairment and Alzheimer disease.2,3 Furthermore, reduced brain volume associated with any of these conditions may mediate the decline in cognitive function.4 By contrast, recent evidence suggests that physical activity might be protective against mild cognitive impairment and Alzheimer disease,5,6 although the mechanisms are unknown. Extrapolation of the data from Kim et al1 suggests a potential physiological link between so-called vascular risk factors and cognitive decline in patients with long-standing diabetes mellitus and hypertension.In this context, a few questions come to mind. First, because diabetes mellitus is associated with macrovascular and microvascular dysfunction, is it possible that high resting blood pressure in complicated diabetes mellitus is a compensatory mechanism to maintain adequate cerebral perfusion? This concept has emerged for other critical organs like the heart and kidneys, but does it also operate in the brain? Second, does reduced cerebral vasodilator responsiveness to CO2 mean that cerebral vasodilator responses to increased neural activity will also be blunted? Third, is the reduced cerebral vasodilator response attributed to the effects of hyperglycemia, per se, or does it reflect a more long-term maladaptive response to diabetes mellitus? Fourth, will blunted cerebral vasodilator responses to increased neural activity eventually cause brain atrophy? Finally, will this lead to a vicious cycle of reduced cerebral perfusion, brain atrophy, and lower metabolic demand? In addition, whereas increases in perfusion pressure in the short run might maintain cerebral blood flow, over time they might evoke so-called end organ damage and further deteriorate the inherent ability of the cerebral microvessels to dilate in response to chemical, autoregulatory, or metabolic stimuli. Thus, how do we maintain blood flow in the normal range and enhance local vasodilator responses in the absence of a rise in blood pressure?In other vascular beds, endurance exercise interventions consistently demonstrate improved macrovascular and/or microvascular function in middle-aged and older adults.7,8 These findings clearly provide a rationale for examining the effect of endurance exercise training on cerebral perfusion, particularly in diabetics and/or hypertensive individuals with microvascular complications. The diabetic patients would be further served by the powerful antidiabetic effects of exercise.9 If endurance exercise training improves microvascular function in middle-aged and older adults, the effect is likely systemic and will, therefore, improve cerebral perfusion. Maintaining or increasing cerebral perfusion (in addition to cerebral responsiveness to CO2 and autoregulatory mechanisms) is also of critical importance in aging humans who are at risk for both cognitive decline and vascular dysfunction. Cognitive function is closely associated with cerebral blood flow and brain atrophy, and a reduction in either may precipitate the age-related decline in cognitive function.10 The association between brain volume and blood flow is particularly striking in individuals with either mild cognitive impairment or mild Alzheimer disease.11 In this context, physical activity has been shown to prevent the age-related decline in cognitive function and may be associated with a greater brain volume. Although Kim et al1 showed that cognitive function did not change over the 6 months of treatment, longer-term follow-up may be necessary for interventional studies.In conclusion, the epidemiological evidence clearly shows reduced mortality and incidence of cardiovascular events with blood pressure–lowering medications. However, it is unclear what the impact of this treatment has on long-term cognitive function and how it is physiologically linked to changes in brain blood flow. Finally, will exercise training in fact triple the reward in hypertensive diabetics by improving their blood pressure, improving glycemic control, and improving brain blood flow?DisclosuresNone.FootnotesThe opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.Correspondence to Michael J. Joyner, 200 1st St SW, Mayo Clinic, Rochester, MN 55905. E-mail joyner.michael@mayo.eduReferences1. Kim Y-S, Davis SCAT, Truijen J, Stok WJ, Secher NH, van Lieshout JJ. Intensive blood pressure control affects cerebral blood flow in type 2 diabetes mellitus patients. Hypertension. 2011: 57:738–745.LinkGoogle Scholar2. Kivipelto M, Helkala EL, Hanninen T, Laakso MP, Hallikainen M, Alhainen K, Soininen H, Tuomilehto J, Nissinen A. Midlife vascular risk factors and late-life mild cognitive impairment: a population-based study. Neurology. 2001; 56:1683–1689.CrossrefMedlineGoogle Scholar3. Roberts RO, Geda YE, Knopman DS, Christianson TJ, Pankratz VS, Boeve BF, Vella A, Rocca WA, Petersen RC. Association of duration and severity of diabetes mellitus with mild cognitive impairment. Arch Neurol. 2008; 65:1066–1073.CrossrefMedlineGoogle Scholar4. Jack CR, Shiung MM, Gunter JL, O'Brien PC, Weigand SD, Knopman DS, Boeve BF, Ivnik RJ, Smith GE, Cha RH, Tangalos EG, Petersen RC. Comparison of different MRI brain atrophy rate measures with clinical disease progression in AD. Neurology. 2004; 62:591–600.CrossrefMedlineGoogle Scholar5. Ainslie PN, Cotter JD, George KP, Lucas S, Murrell C, Shave R, Thomas KN, Williams MJ, Atkinson G. Elevation in cerebral blood flow velocity with aerobic fitness throughout healthy human ageing. J Physiol. 2008; 586:4005–4010.CrossrefMedlineGoogle Scholar6. Lautenschlager NT, Cox KL, Flicker L, Foster JK, van Bockxmeer FM, Xiao J, Greenop KR, Almeida OP. Effect of physical activity on cognitive function in older adults at risk for Alzheimer disease: a randomized trial. JAMA. 2008; 300:1027–1037.CrossrefMedlineGoogle Scholar7. Black MA, Green DJ, Cable NT. Exercise prevents age-related decline in nitric-oxide-mediated vasodilator function in cutaneous microvessels. J Physiol. 2008; 586:3511–3524.CrossrefMedlineGoogle Scholar8. DeSouza CA, Shapiro LF, Clevenger CM, Dinenno FA, Monahan KD, Tanaka H, Seals DR. Regular aerobic exercise prevents and restores age-related declines in endothelium-dependent vasodilation in healthy men. Circulation. 2000; 102:1351–1357.LinkGoogle Scholar9. Stewart KJ. Exercise training and the cardiovascular consequences of type 2 diabetes and hypertension: plausible mechanisms for improving cardiovascular health. JAMA. 2002; 288:1622–1631.CrossrefMedlineGoogle Scholar10. Poels MM, Ikram MA, Vernooij MW, Krestin GP, Hofman A, Niessen WJ, van der Lugt A, Breteler MM. Total cerebral blood flow in relation to cognitive function: the Rotterdam Scan Study. J Cereb Blood Flow Metab. 2008; 28:1652–1655.CrossrefMedlineGoogle Scholar11. Luckhaus C, Cohnen M, Fluss MO, Janner M, Grass-Kapanke B, Teipel SJ, Grothe M, Hampel H, Peters O, Kornhuber J, Maier W, Supprian T, Gaebel W, Modder U, Wittsack HJ. The relation of regional cerebral perfusion and atrophy in mild cognitive impairment (MCI) and early Alzheimer's dementia. Psychiatry Res. 2010; 183:44–51.CrossrefMedlineGoogle 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 Alexanderson H and Boström C (2020) Exercise therapy in patients with idiopathic inflammatory myopathies and systemic lupus erythematosus – A systematic literature review, Best Practice & Research Clinical Rheumatology, 10.1016/j.berh.2020.101547, 34:2, (101547), Online publication date: 1-Apr-2020. April 2011Vol 57, Issue 4 Advertisement Article InformationMetrics © 2011 American Heart Association, Inc.https://doi.org/10.1161/HYPERTENSIONAHA.110.168070PMID: 21357273 Originally publishedFebruary 28, 2011 PDF download Advertisement" @default.
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