Pathophysiology and Clinical Relevance of Microvascular Remodeling in Arterial Hypertension

Long-term exposure to high blood pressure leads to systemic structural and functional changes of microcirculation, a condition named microvascular remodeling. Microvascular remodeling can be assessed in subcutaneous small resistance arteries or non-invasively at the retinal level using Scanning Laser Doppler Flowmetry and Adaptive Optics. Capillary rarefaction is also a marker of hypertensive vascular impairment resulting in a lack of nutrient and oxygen supply. In hypertension, microvascular remodeling and large artery damage are part of a vicious cycle that eventually leads to target organ damage and worsen cardio-renal-cerebrovascular outcomes. This review describes the inflammatory nature of microvascular remodeling and aims to unravel the association of microvascular remodeling with hypertension-mediated organ damage, also providing an overview on its clinical relevance. Summary of macro- and microvascular crosstalk in hypertension and its clinical consequences. Top right: different effects of drug classes. Bottom left: pathobiological drivers. Bottom right: knowledge gap. ACE-is = ACE-inhibitors. ARBs= angiotensin 2 receptor blockers. BBs= beta blockers. CAD=coronary artery disease. CCBs= calcium channel blockers. HFpEF= heart failure with preserved ejection fraction. CKD= chronic kidney disease. HFrEF= heart failure with reduced ejection fraction. LV= left ventricle. PVAT= perivascular adipose tissue. PWV= pulse wave velocity. RAAS= renin-angiotensin-aldosterone system. VSMCs= vascular smooth muscle cells. WLR= wall to lumen ratio