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. 2019 Oct;7(20):e14212.
doi: 10.14814/phy2.14212.

Exploring Cerebrovascular Function in Osteoarthritis: "Heads-up"

Affiliations

Exploring Cerebrovascular Function in Osteoarthritis: "Heads-up"

Baraa K Al-Khazraji et al. Physiol Rep. 2019 Oct.

Abstract

Individuals with osteoarthritis (OA) are at greater risk of cardiovascular and cerebrovascular incidents; yet, cerebrovascular control remains uncharacterized. Our primary outcome was to acquire cerebrovascular control metrics in patients with OA and compare measures to healthy control adults (CTL) without OA or cardiovascular complications. Our primary covariate was a 10-year risk factor for cardiovascular and stroke incidents, and secondary covariates were other cardiovascular disease risk factors (i.e., body mass index, carotid intima media thickness, and brachial flow-mediated dilation). Our secondary outcomes were to assess anatomical and functional changes that may be related to cerebrovascular reactivity were also acquired such as white matter lesion volume and brief cognitive assessments. In 25 adults (n = 13 CTL, n = 12 OA), under hypercapnia, magnetic resonance imaging (3T) was used to acquire a "Global Cerebrovascular Reactivity" index across the larger intracranial cerebral arteries and white matter lesions, and transcranial Doppler was used for both middle cerebral artery hemodynamic responses to hypercapnia and to assess autoregulation via a sit-to-stand task. Compared to CTL, OA had lower "Global Cerebrovascular Reactivity" index responses to hypercapnia, autoregulatory responses, and greater white matter lesions (P < 0.05). These differences persisted after covarying for the outlined primary and secondary covariates. Patients with OA, in the absence of known cardiovascular disease, can exhibit pre-clinical and impaired (compared to CTL) peripheral and cerebrovascular control metrics.

Keywords: Cerebrovascular control; cardiovascular disease risk factors; magnetic resonance imaging; osteoarthritis; transcranial Doppler ultrasound; white matter lesions.

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Conflict of interest statement

The authors have no competing interests to disclose.

Figures

Figure 1
Figure 1
Unadjusted baseline cross‐sectional area (CSA), percent change from baseline in response to hypercapnia (%CSA), and reactivity (CSA Reactivity; %/mmHg) are shown for the bilateral (right, R; left; L) middle (MCA), posterior (PCA), anterior (ACA) cerebral arteries, and the internal carotid (ICA) and basilar intracranial arteries across control (CTL) and osteoarthritis (OA) individuals. Values presented as mean ± S.D. Between‐group raw mean differences are indicated with * to indicate OA different from CTL after covarying for the primary covariate of 10‐year risk factor for CVD/stroke.
Figure 2
Figure 2
Unadjusted between‐group (control, CTL; osteoarthritis, OA) cross‐sectional area reactivity (from baseline) during hypercapnia averaged across the nine larger intracranial cerebral arteries. Both individual participant data (circles) and mean ± S.D. are shown. Between‐group raw mean differences are indicated with * to indicate OA different from CTL, with specific between‐group differences after primary and secondary covariate analyses detailed in Table 2.

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