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. 2021 Jul;106(7):1643-1653.
doi: 10.1113/EP089319. Epub 2021 May 25.

Impact of acute changes in blood pressure and arterial stiffness on cerebral pulsatile haemodynamics in young and middle-aged adults

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Impact of acute changes in blood pressure and arterial stiffness on cerebral pulsatile haemodynamics in young and middle-aged adults

Wesley K Lefferts et al. Exp Physiol. 2021 Jul.

Abstract

New findings: What is the central question of this study? Does cerebrovascular pulsatility respond differently to acute increases in arterial stiffness in middle-aged compared with young adults? What is the main finding and its importance? Compared with young adults, middle-aged adults exhibited similar changes in cerebral pulsatile damping despite attenuated changes in carotid diameter and cerebrovascular pulsatility during blood pressure-dependent, but not blood pressure-independent, increases in large artery stiffness.

Abstract: Acute manipulation of arterial stiffness through interventions that increase sympathetic activity might provoke cerebral pulsatility and damping and reveal whether cerebrovascular haemodynamics respond differently to transient elevations in arterial stiffness in middle-aged compared with young adults. We compared cerebral pulsatility and damping in middle-aged versus young adults during two different sympathetic interventions [cold pressor test (CP) and lower-body negative pressure (LBNP)] that increase arterial stiffness acutely. Cerebrovascular haemodynamics were assessed in 15 middle-aged (54 ± 7 years old; 11 female) and 15 sex-matched young adults (25 ± 4 years old) at rest and during the CP test (4 min, 6.4 ± 0.8°C) and LBNP (6 min, -20 mmHg). Mean blood pressure was measured continuously via finger photoplethysmography. Carotid-femoral pulse wave velocity (cfPWV) and carotid stiffness were measured via tonometry and ultrasound. Blood velocity pulsatility index (PI) was measured at the middle cerebral (MCA) and common carotid artery (CCA) using Doppler, with pulsatile damping calculated as CCA PI divided by MCA PI. Increases in cfPWV were driven by changes in mean pressure during CP but not during LBNP in both groups (P < 0.05). Pulsatile damping decreased in both groups (P < 0.05) despite reductions in MCA PI and greater carotid dilatation during CP in young compared with middle-aged adults (P < 0.05). Pressure-independent increases in cfPWV during LBNP did not alter pulsatile damping but decreased MCA PI in both young and middle-aged adults (P < 0.05). These data suggest that changes in carotid diameter and cerebrovascular pulsatility differ between young and middle-aged adults despite similar changes in cerebral pulsatile damping during blood pressure-dependent, but not blood pressure-independent, increases in large artery stiffness.

Keywords: arterial stiffness; cerebral haemodynamics; pulsatility.

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Conflict of interest statement

We have no conflicts of interest to disclose.

Figures

Figure 1:
Figure 1:
Study design and data measurement timeline. **Mental stress data presented in Appendix. Solid line denotes continuous measurement, striped bar denotes analysis period from continuous data. CA, carotid artery; FA, femoral artery; BA, brachial artery; BP, blood pressure; HR, heart rate; ETCO2, end-tidal CO2, PI, pulsatility index; D, diameter; V, blood velocity; WIA, wave intensity analysis.
Figure 2:
Figure 2:
Changes in mean pressure, cfPWV, and MCA pulsatile damping at rest and during each intervention in young and middle-aged adults. *p<0.05 vs Rest; †p<0.05 vs Young. A) Age p<0.001(0.71), Intervention p<0.001(0.39), Interaction p=0.65(0.01); B) Age p=0.002(0.30), Intervention p<0.001(0.46), Interaction p=0.62(0.01); C) Age p=0.93(0.00), Intervention p<0.001(0.77), Interaction p=0.92(0.00); D) Age p<0.001(0.70), Intervention p=0.38(0.03), Interaction p=0.35(0.04); E) Age p<0.001(0.36), Intervention p=0.03(0.17), Interaction p=0.51(0.02); F) Age p=0.51(0.02), Intervention p=0.16(0.07), Interaction p=0.60(0.01)

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