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Improved Turnaround Times | Median time to first decision: 12 days

Research ArticleExtracranial Vascular
Open Access

Vitamin D and Vulnerable Carotid Plaque

J.S. McNally, T.M. Burton, B.W. Aldred, S.-E. Kim, M.S. McLaughlin, L.B. Eisenmenger, G.J. Stoddard, J.J. Majersik, D.V. Miller, G.S. Treiman and D.L. Parker
American Journal of Neuroradiology November 2016, 37 (11) 2092-2099; DOI: https://doi.org/10.3174/ajnr.A4849
J.S. McNally
aFrom the Department of Radiology and Imaging Sciences, Utah Center for Advanced Imaging Research (J.S.M., B.W.A., S.-E.K., M.S.M., L.B.E., D.L.P.)
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T.M. Burton
bDepartment of Neurology (T.M.B., J.J.M.)
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B.W. Aldred
aFrom the Department of Radiology and Imaging Sciences, Utah Center for Advanced Imaging Research (J.S.M., B.W.A., S.-E.K., M.S.M., L.B.E., D.L.P.)
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S.-E. Kim
aFrom the Department of Radiology and Imaging Sciences, Utah Center for Advanced Imaging Research (J.S.M., B.W.A., S.-E.K., M.S.M., L.B.E., D.L.P.)
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M.S. McLaughlin
aFrom the Department of Radiology and Imaging Sciences, Utah Center for Advanced Imaging Research (J.S.M., B.W.A., S.-E.K., M.S.M., L.B.E., D.L.P.)
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L.B. Eisenmenger
aFrom the Department of Radiology and Imaging Sciences, Utah Center for Advanced Imaging Research (J.S.M., B.W.A., S.-E.K., M.S.M., L.B.E., D.L.P.)
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G.J. Stoddard
cDepartment of Orthopedics, Study Design and Biostatistics Center (G.J.S)
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J.J. Majersik
bDepartment of Neurology (T.M.B., J.J.M.)
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D.V. Miller
dDepartment of Pathology (D.V.M.)
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G.S. Treiman
eDepartment of Surgery at the University of Utah and VA Salt Lake City Health Care System, Salt Lake City, Utah (G.S.T.).
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D.L. Parker
aFrom the Department of Radiology and Imaging Sciences, Utah Center for Advanced Imaging Research (J.S.M., B.W.A., S.-E.K., M.S.M., L.B.E., D.L.P.)
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    Fig 1.

    Carotid and brain MR imaging. Carotid IPH and maximum plaque thickness were detected by using the MPRAGE sequence as shown in this representative image with right-sided carotid IPH (A). 3D TOF MRA was used alongside duplex sonography in all patients to determine lumen findings, as in this subject with 26% stenosis by NASCET criteria (B). Stroke was determined by using the American Heart Association criteria supplemented with DWI, as in this example with recent right MCA distribution infarcts (C and D).

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    Fig 2.

    Linear regression of MR imaging–detected IPH volume, plaque thickness, and vitamin D status. Pooled data demonstrate the IPH volume negative correlation with vitamin D level (A) and correlation with maximal plaque thickness (partial r = 0.45, P < .001, thin dashed line) and low-versus-normal vitamin D levels (partial r = 0.26, P = .003; low vitamin D level: empty squares and thick dashed line; normal vitamin D levels: solid circles and thick solid line, B).

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    Fig 3.

    Linear regression of IPH area on histology, plaque area, and vitamin D status. Representative MPRAGE-positive plaque (upper image) and IPH area outlined on the corresponding hematoxylin-eosin stain (lower image) (A). Pooled data demonstrate the IPH area negatively correlating with vitamin D levels (B) and positively correlating with plaque area (partial r = 0.46, P < .001, thin dashed line) and low-versus-normal vitamin D levels (partial r = 0.22, P = .03, low vitamin D level: empty squares and thick dashed line; normal vitamin D level: solid circles and thick solid line) (C).

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    Fig 4.

    Association of IPH volume, vitamin D levels, and ischemic stroke. IPH volume was negatively correlated with vitamin D levels as in Fig 2A (thin dashed line). When stratified by ischemic stroke status, IPH volume was more negatively correlated with vitamin D levels (hollow squares, thick dashed line, partial r = −0.21, P = .27) in ischemic stroke compared to without it (solid circles, thick solid line, partial r = −0.06, P = .53) (A). Vitamin D levels were also lower in groups positive-versus-negative for stroke in the setting of IPH-negative plaque (mean, 33.5 ± 13.2 ng/mL in 73 carotids versus 26.2 ± 17.4 ng/mL in 7 carotids, P = .17) and less so in the setting of IPH-positive plaque (27.8 ± 12.6 ng/mL in 25 carotid arteries versus 25.6 ± 11.1 ng/mL in 23 carotid arteries, P = .51) (B). S indicates carotid territory ischemic stroke status (positive or negative).

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    Fig 5.

    Vitamin D supplementation and follow-up. A, Patient 1: Baseline (upper arrow) versus 1-year follow-up (lower arrow) with vitamin D supplementation and medical therapy, including statins and antiplatelet and antihypertensive medications, demonstrates decreased IPH volume in a patient with no interval stroke (vitamin D baseline/1 year: 18.1/26.8 ng/mL; carotid IPH baseline/1 year: 0.151/0.115 cm3, or 24.1% decreased IPH volume). The patient remained asymptomatic in the year between the 2 scans. B, Patient 2: Baseline (upper arrow) versus 1-year follow-up (lower arrow) without vitamin D supplementation but with medical therapy, including statins and antiplatelet and antihypertensive medications, demonstrates minimally changed IPH volume (vitamin D baseline/1 year: 20.9/10.7 ng/mL; carotid IPH baseline/1 year: 1.041/0.996 cm3, or 4.3% decreased IPH volume). In addition, this patient had bilateral strokes in the year between the 2 scans.

Tables

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    Table 1:

    Final MRI-IPH prediction modela

    Carotid IPH PredictorPRP Value95% CI
    Maximum plaque thickness, per 1-mm increase1.40<.0011.18–1.67
    Low vitamin D level of <30 ng/mL, low versus high2.05.031.06–3.96
    • ↵a The final prediction model for the presence of MRI-detected carotid IPH depended on 2 factors: maximum plaque thickness and low vitamin D levels.

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    Table 2:

    IPH prediction model with angiotensin system confoundersa

    Carotid IPH PredictorPRP Value95% CI
    Maximum plaque thickness, per 1-mm increase1.40<.0011.18–1.67
    Low vitamin D level, <30 ng/mL, low versus high2.07.041.05–4.09
    Angiotensin II level (ng/L), per 1-U increase1.00.800.99–1.01
    ACE inhibitor use1.05.870.56–1.99
    ARB use0.93.900.31–2.77
    • Note:—ARB indicates angiotensin receptor blockers.

    • ↵a To illustrate the lack of confounding, we included markers of systemic angiotensin activity, including angiotensin II, ACE inhibitor use, and ARB use in addition to our final model of maximum plaque thickness and low vitamin D levels.

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American Journal of Neuroradiology: 37 (11)
American Journal of Neuroradiology
Vol. 37, Issue 11
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Cite this article
J.S. McNally, T.M. Burton, B.W. Aldred, S.-E. Kim, M.S. McLaughlin, L.B. Eisenmenger, G.J. Stoddard, J.J. Majersik, D.V. Miller, G.S. Treiman, D.L. Parker
Vitamin D and Vulnerable Carotid Plaque
American Journal of Neuroradiology Nov 2016, 37 (11) 2092-2099; DOI: 10.3174/ajnr.A4849

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Vitamin D and Vulnerable Carotid Plaque
J.S. McNally, T.M. Burton, B.W. Aldred, S.-E. Kim, M.S. McLaughlin, L.B. Eisenmenger, G.J. Stoddard, J.J. Majersik, D.V. Miller, G.S. Treiman, D.L. Parker
American Journal of Neuroradiology Nov 2016, 37 (11) 2092-2099; DOI: 10.3174/ajnr.A4849
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