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      Impact of Circadian Blood Pressure Pattern on Silent Cerebral Small Vessel Disease: A Systematic Review and Meta‐Analysis

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          Abstract

          Background

          Abnormal circadian blood pressure ( BP) variations during sleep, specifically the non‐dipping (<10% fall in nocturnal BP) and reverse‐dipping patterns (rise in nocturnal BP), have been associated with an increased risk of cardiovascular events and target organ damage. However, the relationship between abnormal sleep BP variations and cerebral small vessel disease markers is poorly established. This study aims to assess the association between non‐dipping and reverse‐dipping BP patterns with markers of silent cerebral small vessel disease.

          Methods and Results

          MEDLINE, Embase, and Cochrane Databases were searched from inception through November 2019. Studies that reported the odds ratios (ORs) for cerebral small vessel disease markers in patients with non‐dipping or reverse‐dipping BP patterns were included. Effect estimates from the individual studies were extracted and combined using the random‐effect, generic inverse variance method of DerSimonian and Laird. Twelve observational studies composed of 3497 patients were included in this analysis. The reverse‐dipping compared with normal dipping BP pattern was associated with a higher prevalence of white matter hyperintensity with a pooled adjusted OR of 2.00 (95% CI, 1.13–2.37; I 2=36%). Non‐dipping BP pattern compared with normal dipping BP pattern was associated with higher prevalence of white matter hyperintensity and asymptomatic lacunar infarction, with pooled ORs of 1.38 (95% CI, 0.95–2.02; I 2=52%) and 2.33 (95% CI, 1.30–4.18; I 2=73%), respectively. Limiting to only studies with confounder‐adjusted analysis resulted in a pooled OR of 1.38 (95% CI, 0.95–2.02; I 2=52%) for white matter hyperintensity and 1.44 (95% CI, 0.97–2.13; I 2=0%) for asymptomatic lacunar infarction.

          Conclusions

          The non‐dipping and reverse‐dipping BP patterns are associated with neuroimaging cerebral small vessel disease markers.

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          Most cited references38

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          CNS small vessel disease

          CNS small vessel disease (CSVD) causes 25% of strokes and contributes to 45% of dementia cases. Prevalence increases with age, affecting about 5% of people aged 50 years to almost 100% of people older than 90 years. Known causes and risk factors include age, hypertension, branch atheromatous disease, cerebral amyloid angiopathy, radiation exposure, immune-mediated vasculitides, certain infections, and several genetic diseases. CSVD can be asymptomatic; however, depending on location, lesions can cause mild cognitive dysfunction, dementia, mood disorders, motor and gait dysfunction, and urinary incontinence. CSVD is diagnosed on the basis of brain imaging biomarkers, including recent small subcortical infarcts, white matter hyperintensities, lacunes, cerebral microbleeds, enlarged perivascular spaces, and cerebral atrophy. Advanced imaging modalities can detect signs of disease even earlier than current standard imaging techniques. Diffusion tensor imaging can identify altered white matter connectivity, and blood oxygenation level-dependent imaging can identify decreased vascular reactivity. Pathogenesis is thought to begin with an etiologically specific insult, with or without genetic predisposition, which results in dysfunction of the neurovascular unit. Uncertainties regarding pathogenesis have delayed development of effective treatment. The most widely accepted approach to treatment is to intensively control well-established vascular risk factors, of which hypertension is the most important. With better understanding of pathogenesis, specific therapies may emerge. Early identification of pathologic characteristics with advanced imaging provides an opportunity to forestall progression before emergence of symptoms.
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            Circadian rhythms and the molecular clock in cardiovascular biology and disease

            The Earth turns on its axis every 24 h; almost all life on the planet has a mechanism - circadian rhythmicity - to anticipate the daily changes caused by this rotation. The molecular clocks that control circadian rhythms are being revealed as important regulators of physiology and disease. In humans, circadian rhythms have been studied extensively in the cardiovascular system. Many cardiovascular functions, such as endothelial function, thrombus formation, blood pressure and heart rate, are now known to be regulated by the circadian clock. Additionally, the onset of acute myocardial infarction, stroke, arrhythmias and other adverse cardiovascular events show circadian rhythmicity. In this Review, we summarize the role of the circadian clock in all major cardiovascular cell types and organs. Second, we discuss the role of circadian rhythms in cardiovascular physiology and disease. Finally, we postulate how circadian rhythms can serve as a therapeutic target by exploiting or altering molecular time to improve existing therapies and develop novel ones.
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              Blood pressure and clinical outcomes in the International Stroke Trial.

              Among patients with acute stroke, high blood pressure is often associated with poor outcome, although the reason is unclear. We analyzed data from the International Stroke Trial (IST) to explore the relationship between systolic blood pressure (SBP), subsequent clinical events over the next 2 weeks, and functional outcome at 6 months in patients with acute stroke. We included in the analysis 17 398 patients from IST with confirmed ischemic stroke. A single measurement of SBP was made immediately before randomization. Clinical events within 14 days of randomization were recorded: recurrent ischemic stroke, symptomatic intracranial hemorrhage, death resulting from presumed cerebral edema, fatal coronary heart disease, and death. Survival and dependency were assessed at 6 months. Outcomes were adjusted for age, sex, clinical stroke syndrome, time to randomization, consciousness level, atrial fibrillation, and treatment allocation (aspirin, unfractionated heparin, both, or neither). A U-shaped relationship was found between baseline SBP and both early death and late death or dependency: early death increased by 17.9% for every 10 mm Hg below 150 mm Hg (P<0.0001) and by 3.8% for every 10 mm Hg above 150 mm Hg (P=0.016). The rate of recurrent ischemic stroke within 14 days increased by 4.2% for every 10-mm Hg increase in SBP (P=0.023); this association was present in both fatal and nonfatal recurrence. Death resulting from presumed cerebral edema was independently associated with high SBP (P=0.004). No relationship between symptomatic intracranial hemorrhage and SBP was seen. Low SBP was associated with a severe clinical stroke (total anterior circulation syndrome) and an excess of deaths from coronary heart disease (P=0.002). Both high blood pressure and low blood pressure were independent prognostic factors for poor outcome, relationships that appear to be mediated in part by increased rates of early recurrence and death resulting from presumed cerebral edema in patients with high blood pressure and increased coronary heart disease events in those with low blood pressure. The occurrence of symptomatic intracranial hemorrhage within 14 days was independent of SBP.
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                Author and article information

                Contributors
                drronpichaic@gmail.com
                Journal
                J Am Heart Assoc
                J Am Heart Assoc
                10.1002/(ISSN)2047-9980
                JAH3
                ahaoa
                Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
                John Wiley and Sons Inc. (Hoboken )
                2047-9980
                01 June 2020
                16 June 2020
                : 9
                : 12 ( doiID: 10.1002/jah3.v9.12 )
                : e016299
                Affiliations
                [ 1 ] Division of Neurology Faculty of Medicine Chulalongkorn University and King Chulalongkorn Memorial Hospital Bangkok Thailand
                [ 2 ] King Chulalongkorn Memorial Hospital Thai Red Cross Society Bangkok Thailand
                [ 3 ] Department of Medicine University of Mississippi Medical Center Jackson MS
                [ 4 ] Division of Nephrology Department of Medicine Mayo Clinic Rochester MN
                [ 5 ] Department of Cardiovascular Medicine Mayo Clinic Rochester MN
                [ 6 ] Department of Internal Medicine University of Arizona Tucson AZ
                [ 7 ] Department of Internal Medicine Mayo Clinic Jacksonville FL
                [ 8 ] University Hospitals Birmingham NHS Foundation Trust Birmingham United Kingdom
                [ 9 ] Department of Medicine Faculty of Medicine Chulalongkorn University and King Chulalongkorn Memorial Hospital Bangkok Thailand
                Author notes
                [*] [* ]Correspondence to: Ronpichai Chokesuwattanaskul, MD, King Chulalongkorn Memorial Hospital, Bangkok, Thailand. E‐mail: drronpichaic@ 123456gmail.com
                Author information
                https://orcid.org/0000-0001-7973-8267
                https://orcid.org/0000-0002-4463-7447
                Article
                JAH35213
                10.1161/JAHA.119.016299
                7429026
                32476573
                61f2713e-e2c6-4779-a2bd-7359d0326c3f
                © 2020 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                : 27 February 2020
                : 30 April 2020
                Page count
                Figures: 3, Tables: 1, Pages: 17, Words: 5781
                Categories
                Systematic Review and Meta‐analysis
                Systematic Review and Meta‐analysis
                Custom metadata
                2.0
                16 June 2020
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.5 mode:remove_FC converted:19.07.2020

                Cardiovascular Medicine
                blood pressure variability,circadian,meta‐analysis,microbleed,white matter,cerebrovascular disease/stroke,high blood pressure,magnetic resonance imaging (mri)

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