Cerebral macro- and microcirculatory blood flow dynamics in successfully treated chronic hypertensive patients with and without white mater lesions

Abstract

the mechanisms of high blood pressure (HBp)-related brain pathology progression remain relatively unclear. We investigated whether lowering BP in chronic HBP patients normalizes cerebral perfusion dynamics at resistance vessel and capillary levels. Sixty-seven patients with HBP and 49 age-and sexmatched healthy controls underwent simultaneous recordings of middle cerebral artery blood flow velocity (cBfV), Bp, and end-tidal co 2 concentration. Thirty-four controls and 28 patients underwent additional near-infrared spectroscopy recordings (oxygenated [o 2 Hb] and deoxygenated [HHb] hemoglobin). Degree of microcirculatory white matter lesions was graded by Fazekas scale. Dynamic cerebral autoregulation (dCA) was assessed by transfer function analysis. BP was successfully lowered (patients = 89 ± 15 mm Hg, controls = 87 ± 17), but cerebrovascular resistance was higher in BP patients (p < 0.05). BP-CBFV phase was lower in very low frequency (VLF) (left/right: 48 ± 20°/44 ± 17; controls: 61 ± 20/60 ± 21; p < 0.001) and low frequency (LF) (34 ± 14/35 ± 14; controls: 48 ± 20/44 ± 17; p < 0.05) ranges. Gain was higher in VLF range (in %/ mm Hg 0.56 ± 0.44/0.59 ± 0.49; controls: 0.32 ± 0.29/0.34 ± 0.32; p ≤ 0.005). BP-CBFV phase and gain did not differ across Fazekas groups. Across all patients, the capillary phases and gains (CBFV-[O2Hb], CBFV-[HHb]) were comparable to controls. Successfully treated chronic HBP results in normal brain capillary hemodynamics while the resistance vessel state is disturbed (phase decrease, gain increase). The cerebral consequences of chronic high blood pressure (HBP) are manifold: the most frequent are hemorrhagic and nonhemorrhagic stroke, cerebral small vessel disease with white matter lesions (WML), microbleeds, or brain atrophy which can lead to cognitive decline and dementia 1. Small vessel disease has also been reported to contribute to the pathogenesis of Alzheimer's disease 2,3. The pathological mechanisms of HBP-related brain pathology progression, however, are unclear. Among others, a constant elevated level of mean systolic or diastolic BP and their variabilities 4,5 , autonomic BP regulation disturbances 6 , increased pulse pressure amplitudes 7 , ischemic effects on the brain due to cerebral autoregulation (CA) failure 8-11 , and capillary dysfunction 12 are proposed mechanisms of continuous cerebral tissue damage. More recently, aging is assumed to accelerate the HBP-driven pathologies 3,13. Cerebral blood flow is determined by BP-dependent regulatory effects and by metabolic influences on the resistance vessels via feedback mechanisms. These regulatory mechanisms can be observed noninvasively by cerebral blood flow velocity (CBFV) and its wave form, and by changes in the microcirculatory concentrations of oxygenated and deoxygenated hemoglobin (Hb) via near-infrared spectroscopy (NIRS) 14-16. Anatomically, CBFV mirrors the regulatory effects in front of the resistance vessel in the large (macrocirculatory) brain supplying arteries such as the middle cerebral artery, while the...

Associations Between White Matter Hyperintensity Burden, Cerebral Blood Flow and Transit Time in Small Vessel Disease: An Updated Meta-Analysis

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Hemodynamics of Leptomeningeal Collaterals after Large Vessel Occlusion and Blood Pressure Management with Endovascular Treatment

“…A long history of hypertension may indicate impaired autoregulatory function. 105 Additionally, as the blood flow inversely corresponds to the fourth-order of the vascular luminal diameter, the LMC perfusion will not suffice to replace the normal physiologic CBF through anatomically intact large vessels.…”

Association of Intensive vs Standard Blood Pressure Control With Regional Changes in Cerebral Small Vessel Disease Biomarkers

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