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      Relations of arterial stiffness with postural change in mean arterial pressure in middle-aged adults: The Framingham Heart Study

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          Abstract

          Impaired regulation of blood pressure upon standing can lead to adverse outcomes, including falls, syncope, and disorientation. Mean arterial pressure typically increases upon standing; however, an insufficient increase or a decline in mean arterial pressure upon standing may result in decreased cerebral perfusion. Orthostatic hypotension has been reported in older people with increased arterial stiffness, whereas the association between orthostatic change in mean arterial pressure and arterial stiffness in young-to-middle aged individuals has not been examined. We analyzed orthostatic blood pressure response and comprehensive hemodynamic data in 3205 participants (1693 [53%] women) in the Framingham Heart Study Third Generation cohort. Participants were predominantly middle-aged (mean age: 46±9 years). Arterial stiffness was assessed using carotid-femoral pulse wave velocity, forward pressure wave amplitude, and characteristic impedance of the aorta. Adjusting for standard cardiovascular disease risk factors, orthostatic change in mean arterial pressure (6.9±7.7 mm Hg) was inversely associated with carotid-femoral pulse wave velocity (partial correlation, r p = −0.084, P<0.0001), forward wave amplitude (r p = −0.129, P<0.0001), and characteristic impedance (r p = −0.094, P<0.0001). The negative relation between forward wave amplitude and change in mean arterial pressure on standing was accentuated in women (P=0.002 for sex interaction). Thus, higher aortic stiffness was associated with a blunted orthostatic increase in mean arterial pressure, even in middle age. The clinical implications of these findings warrant further study.

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          Author and article information

          Journal
          7906255
          4217
          Hypertension
          Hypertension
          Hypertension (Dallas, Tex. : 1979)
          0194-911X
          1524-4563
          3 February 2017
          April 2017
          01 April 2018
          : 69
          : 4
          : 685-690
          Affiliations
          [1 ]Cardiovascular Engineering, Inc., Norwood, MA
          [2 ]Cardiovascular Research Center, Rhode Island Hospital, W. Alpert Medical School of Brown University, Providence, RI
          [3 ]National Heart Lung and Blood Institute's and Boston University's Framingham Heart Study, Framingham, MA
          [4 ]Department of Biostatistics, Boston University School of Public Health, Boston, MA
          [5 ]Evans Department of Medicine, Boston University School of Medicine, Boston, MA
          [6 ]Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA
          [7 ]National Heart, Lung, and Blood Institute, Bethesda, MD
          [8 ]Preventive Medicine and Cardiology Sections, Boston University School of Medicine, Boston, MA
          Author notes
          Address correspondence to: Gary F. Mitchell, MD, Cardiovascular Engineering, Inc., 1 Edgewater Drive, Suite 201, Norwood, MA 02062, Phone: 781-788-4900, Fax: 781-788-4901, GaryFMitchell@ 123456mindspring.com
          Article
          PMC5382873 PMC5382873 5382873 nihpa847769
          10.1161/HYPERTENSIONAHA.116.08116
          5382873
          28264924
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