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 sex-matched healthy controls underwent simultaneous recordings of middle cerebral artery blood flow velocity (CBFV), BP, and end-tidal CO2 concentration. Thirty-four controls and 28 patients underwent additional near-infrared spectroscopy recordings (oxygenated [O2Hb] 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).
Highlights
The mechanisms of high blood pressure (HBP) -related brain pathology progression remain relatively unclear
A frequently-used approach to describe these dynamics is the estimation of phase shift and gain derived from transfer function analysis (TFA)[15,16,17,18,19,20,21]: at a given cycle of BP and cerebral artery blood flow velocity (CBFV) changes, e.g. BP and CBF changes with a cycle duration of 10 seconds (=0.1 Hz) gain describes the power transformation from BP to CBFV, and phase shift indicates how much earlier or later in time the BP cycle will be found in the CBFV
We used this dynamic approach in treated chronic HBP patients and hypothesize that the regulatory effects of the resistance vessels as indicated by phase and gain are normalized in the macrocirculatory system BP - CBFV
Summary
The mechanisms of high blood pressure (HBP) -related brain pathology progression remain relatively unclear. Treated chronic HBP results in normal brain capillary hemodynamics while the resistance vessel state is disturbed (phase decrease, gain increase). 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)[14,15,16]. This reversibility might not be present in patients with chronic HBP25 We used this dynamic approach in treated chronic HBP patients and hypothesize that the regulatory effects of the resistance vessels as indicated by phase and gain are normalized in the macrocirculatory system BP - CBFV (assessed in the middle cerebral artery). Our second hypothesis is that the TFA parameters and/or the capillary transit time between CBFV and the concentrations of oxygenated Hb or deoxygenated Hb demonstrate pathological results which ideally should demonstrate a relationship with the amount of WMLs as classified by the Fazekes scale[26] score
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