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Research Article| Volume 28, ISSUE 5, P1252-1260, May 2019

Aortic Pulsatility Propagates Intracranially and Correlates with Dilated Perivascular Spaces and Small Vessel Compliance

  • Author Footnotes
    1 orcid.org/0000-0003-2877-3075.
    Owen Thomas
    Correspondence
    Address correspondence to Owen M. Thomas, BM, BCh, DPhil, FRCR, Salford Royal NHS Foundation Trust, Stott Lane, Salford M68HD, United Kingdom.
    Footnotes
    1 orcid.org/0000-0003-2877-3075.
    Affiliations
    Salford Royal NHS Foundation Trust, Salford, United Kingdom
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  • Author Footnotes
    2 orcid.org/0000-0002-3974-0773.
    John Cain
    Footnotes
    2 orcid.org/0000-0002-3974-0773.
    Affiliations
    Salford Royal NHS Foundation Trust, Salford, United Kingdom

    Wolfson Molecular Imaging Centre, School of Medicine, University of Manchester, Greater Manchester, United Kingdom
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  • Author Footnotes
    3 orcid.org/0000-0003-1754-2191.
    Mehran Nasralla
    Footnotes
    3 orcid.org/0000-0003-1754-2191.
    Affiliations
    Wolfson Molecular Imaging Centre, School of Medicine, University of Manchester, Greater Manchester, United Kingdom
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  • Author Footnotes
    4 orcid.org/0000-0002-1623-0383.
    Alan Jackson
    Footnotes
    4 orcid.org/0000-0002-1623-0383.
    Affiliations
    Salford Royal NHS Foundation Trust, Salford, United Kingdom

    Wolfson Molecular Imaging Centre, School of Medicine, University of Manchester, Greater Manchester, United Kingdom
    Search for articles by this author
  • Author Footnotes
    1 orcid.org/0000-0003-2877-3075.
    2 orcid.org/0000-0002-3974-0773.
    3 orcid.org/0000-0003-1754-2191.
    4 orcid.org/0000-0002-1623-0383.

      Abstract

      Introduction: To test the hypotheses that changes in the aortic pulse-wave produced by arterial stiffening are (1) propagated into cerebral small vessels, (2) associated with reduced compliance of small cerebral arterial vessels, and (3) associated with the presence of dilated perivascular spaces (PVS). Methods: Fifteen volunteers and 19 patients with late-onset depression (LOD) were prospectively recruited, of which 6 fulfilled the criteria for treatment-resistant depression (TRD). Aortic pulse-wave velocity (PWV) was determined using Carotid-Femoral Doppler. Pulse-wave analysis (PWA) was performed using a SphygmoCor system. White-matter lesion load and PVS were scored on established MRI scales. Cerebral arterial and aqueductal cerebrospinal fluid (CSF) flow patterns were studied using quantitative phase-contrast angiography. Results: Depressed patients had more PVS (P < .05) and prolongation of the width of the arterial systolic pulse-wave in the carotid arteries (P < .01). There was no significant group difference for any PWV or PWA measurement. TRD patients showed more PVS than other LOD patients (P < .05). The fractional width of the arterial systolic peak correlated significantly with augmentation index (AIx) and heart rate-corrected augmentation index (AIx75; R2 = 0.302, P < .01and R2 = 0.363, P < .01 respectively). Arterial–aqueductal delay showed a negative correlation with estimated aortic systolic pressure (PWVsys; R2 =  0.293; P < .01), AIx (R2 = −0.491; P < .01) and AIx75 (R2 = −0.310; P < .01). PVS scores correlated with AIx (R2 = 0.485; P < .01) and AIx75 (R2 = −0.292; P < .01). Conclusion: Our findings support the hypothesis that increased arterial pulsatility resulting from central arterial stiffness propagates directly into cerebral vessels and is associated with the development of microvascular angiopathy, characterized by dilated PVS and decreased compliance of small arterial vessels.

      Key Words

      Abbreviations:

      AAD (arterial-aqueductal delay), AIx (augmentation index), AIx75 (heart rate-corrected augmentation index), LOD (late-onset depression), PWA (pulse-wave analysis), PCA (phase-contrast angiography), PVS (perivascular spaces / Virchow-Robin spaces), PWV (aortic pulse-wave velocity), SVD (small vessel disease), TRD (treatment-resistant depression)
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