Association between systemic microvascular dysfunction and resistant hypertension: Insights from a clinical...

Resistant arterial hypertension (RAH) is defined as failure to achieve adequate blood pressure control despite the use of at least three antihypertensive drug classes at maximally tolerated doses, including a diuretic. This phenotype confers markedly elevated cardiovascular risk. Systemic microvascular dysfunction is believed to contribute significantly to its pathophysiology. In non-resistant arterial hypertension (NRAH), early endothelial impairment and increased vasomotor tone are present but may remain partially reversible. However, direct comparisons of microvascular function across RAH, NRAH, and normotensive individuals are limited.

To compare systemic microvascular function among patients with RAH, patients with NRAH, and normotensive controls using laser speckle contrast imaging.

Microvascular reactivity was assessed at baseline and during acetylcholine (ACh) and sodium nitroprusside (SNP) iontophoresis, as well as post-occlusive reactive hyperemia (PORH). Baseline microvascular conductance, areas under the curve (AUCs) for ACh and SNP, and PORH peak and delta responses were compared using one-way ANOVA.

Baseline microvascular conductance was significantly higher in controls than in both hypertensive groups. Endothelium-dependent vasodilation (ACh AUC) showed progressive impairment from controls to NRAH to RAH. PORH responses demonstrated reduced peak microvascular conductance and smaller delta values in RAH compared with NRAH and controls. Endothelium-independent vasodilation (SNP AUC) was also diminished in RAH, suggesting structural arteriolar disorder.

RAH is associated with marked systemic microvascular impairment affecting both endothelial function and microvascular structure. These alterations occur alongside adverse metabolic and renal disorders, underscoring the complex interplay of vascular, metabolic, and renal mechanisms in treatment-resistant hypertension.