Key result
Impaired cerebrovascular reactivity strongly tracks white matter lesions in hypertensive rheumatoid arthritis.
Why the study?
The role of cerebral autoregulation as a risk factor for structural brain changes in patients with arterial hypertension comorbid with rheumatoid arthritis remains uncertain.
Cross-Sectional (n=33)
Open-label
No
Effect estimate: r=0.84
p-value: p=0.0003
Structural brain changes in patients with hypertension and rheumatoid arthritis are strongly associated with impaired cerebrovascular reactivity and inversely correlated with methotrexate dose, suggesting potential targets for neuroprotection.
Introduction. Arterial hypertension (AH) and rheumatoid arthritis (RA) are both associated with an increased risk of cardiovascular diseases and their complications, including symptomatic and asymptomatic brain damage. Both diseases exert a synergistic effect on the vascular wall, leading to impaired vascular compensatory capacity. Cerebral autoregulation adjusts cerebral arterial tone to fluctuations in blood pressure, but its role as a risk factor for structural brain changes remains uncertain. Aim: To study the clinical and immune-inflammatory features of RA in patients with AH, to analyze parameters of endothelial dysfunction, vascular stiffness, cerebrovascular reactivity (CVR), and to identify associations of these parameters with structural brain changes on magnetic resonance imaging (MRI). Material and Methods. The open observational cross-sectional study included 33 patients with grade 1–2 AH comorbid with RA, without neurological deficit, aged 61.0 [56.0; 65.0] years. All patients underwent brain MRI, transcranial Doppler ultrasonography of the middle cerebral arteries to assess CVR during hyperoxic and hypercapnic tests, sphygmography to evaluate arterial stiffness. Endothelial function was assessed using ultrasound evaluation of flow-mediated dilation (FMD) of the brachial artery. Results. Patients with AH comorbid with RA had a high frequency of impaired CVR in hyperoxic and hypercapnic tests (72.7% and 87.5% of patients, respectively), impaired FMD (81.8%), and increased arterial stiffness (39.4%). Brain MRI revealed enlarged perivascular spaces in 100% of patients with no signs of cortical atrophy. The majority of patients (63.6%) had focal white matter lesions. The number of white matter lesions was inversely correlated with the methotrexate dose (r =−0.84; p=0.0026), with the CVR parameter – the autoregulation response normalized by arterial blood pressure (NAR O2 ) in the hyperoxic test (r=−0.57; p=0.0297). The number of white matter lesions was directly correlated with the relative change coefficient of the resistive index in the middle cerebral artery during the hypercapnic test (CCrelRI CO2 ; r=0.84; p=0.0003). Conclusion. The brain structural changes in patients AH and RA are associated with impaired CVR, increased arterial stiffness, endothelial dysfunction, and are inversely related to the intensity of anti-inflammatory therapy. The obtained results allow identifying key therapeutic targets when developing neuroprotection stretegies in patients with AH comorbid with RA.
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Rebrova et al. (2026) conducted a cross-sectional in Arterial hypertension comorbid with rheumatoid arthritis (n=33). Arterial hypertension comorbid with rheumatoid arthritis was evaluated on Correlation between number of white matter lesions and relative change coefficient of resistive index during hypercapnic test (r=0.84, p=0.0003). Brain white matter lesions in patients with hypertension and rheumatoid arthritis correlated directly with impaired cerebrovascular reactivity (r=0.84) and inversely with methotrexate dose (r=-0.84).
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