Key result
Resistant hypertension in T2D is linked to ~15-point lower cerebrovascular vasodilatory response to hypercapnia.
Why the study?
The characteristics of cerebrovascular reactivity in hypertension depending on blood pressure control and type 2 diabetes presence, and their relationship with subclinical brain changes, were not well defined.
Cross-Sectional (n=90)
No
Absolute Event Rate: 4.1% vs 18.9%
p-value: p=0.002
The combination of resistant hypertension and type 2 diabetes results in pronounced cerebrovascular reactivity disturbances, which are closely linked to subclinical structural brain alterations such as white matter damage and impaired cerebrospinal fluid dynamics.
Impaired cerebrovascular reactivity in resistant hypertension with diabetes should not yet change practice; leaves open prospective validation of its link to brain injury risk.
Aim. To study the characteristics of cerebrovascular reactivity (CVR) in patients with hypertension (HTN) depending on blood pressure control and the presence of type 2 diabetes (T2D), as well as the relationship between CVR impairment and subclinical structural brain changes based on magnetic resonance imaging in patients with resistant hypertension (RHT) combined with T2D. Material and methods. The analysis included data from 27 patients with RH and T2D, 33 patients with controlled hypertension (CHT) and T2D, and 30 patients with CHT without T2D, who underwent a standard clinical examination. Middle cerebral artery (MCA) CVR was assessed using transcranial Doppler as follows: a breath-holding test to calculate the hypercapnia coefficient (C(+)), a hyperventilation test to calculate the hypocapnia coefficient (C(–)), and total cerebrovascular reserve (CR). In the RHT+T2D group, brain MRI (1,5 T) was additionally performed. Results. Patients in the RHT+T2D group demonstrated a reduced vasodilation response to hypercapnia (C(+), p=0,002) and a reduced vasoconstrictor response to hypocapnia (C(–), p=0,04) compared with the CHT+T2D group. The C(+) did not differ between the two CHT groups (p=0,44). The C(–) was higher in the CHT+T2D group than in both the RHT+T2D group (p=0,04) and the CHT group without T2D (p=0,02). Impaired C(+) in the RHT+T2D group occurred more frequently due to a more frequent paradoxical vasoconstrictor response (p<0,001). Among patients with T2D, inadequate BP control was associated with a reduction in CR (p=0,003), whereas no differences in CR were observed between CHT patients with and without T2D (p=0,07). In the RHT+T2D group, reduced MCA vasodilatory response to hypercapnia (the C(+)) correlated with MRI findings suggestive of impaired cerebrospinal fluid dynamics and white matter damage. An exaggerated C(–) response to hyperventilation was associated with dilation of the chiasmatic cistern. Conclusion. The combination of RHT and T2D is characterized by the most pronounced disturbances in cerebrovascular reactivity compared with CHT+T2D and CHT without T2D. The clinical relevance of these disturbances in patients with RHT and T2D is underscored by their close association with subclinical brain alterations, including impaired cerebrospinal fluid flow and white matter damage.
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Falkovskaya et al. (2026) conducted a cross-sectional in Hypertension and Type 2 Diabetes (n=90). Resistant hypertension with Type 2 Diabetes vs. Controlled hypertension with Type 2 Diabetes was evaluated on Vasodilatory response to hypercapnia (C(+)) (p=0.002). Patients with resistant hypertension and type 2 diabetes demonstrated a significantly reduced cerebrovascular vasodilatory response to hypercapnia (4.1% vs 18.9%) compared to patients with controlled hypertension and type 2 diabetes.
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