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Jun 17, 2018 - ition of “classical” OH (ESC, 2009), study participants were recruited into four groups: Asymptomatic No OH (control, ANo), Symptomatic No OH ...
Age and Ageing 2017; 46: i25–i26 doi: 10.1093/ageing/afx059.100

© The Author 2017. Published by Oxford University Press on behalf of the British Geriatrics Society. All rights reserved. For permissions, please email: [email protected]

Scientific Research – Cardiovascular 100

DOES IMPAIRMENT OF DYNAMIC CEREBRAL AUTOREGULATION EXPLAIN THE SYMPTOMS ASSOCIATED WITH CLASSICAL ORTHOSTATIC HYPOTENSION?

A C L Ong1, P K Myint2, J F Potter3,4 The Ipswich Hospital, Ipswich 2 University of Aberdeen 3 University of East Anglia 4 Norfolk and Norwich University Hospital

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Introduction: In older adults orthostatic hypotension (OH) is common, has increased morbidity and mortality, but is not always symptomatic. However some people have classical orthostatic symptoms without a postural fall in systemic BP. This study tested the hypothesis that impairment of dynamic cerebral auto-regulation (dCA) might explain the symptoms associated with OH. Methods: Based on reproducible clinical symptoms ( < 3 minutes of standing) and definition of “classical” OH (ESC, 2009), study participants were recruited into four groups:

Asymptomatic No OH (control, ANo), Symptomatic No OH (SNo), Asymptomatic OH (AOH), and Symptomatic OH (SOH). Baseline and head-up-tilt (HUT) measurements were recorded (HUT for 30 minutes or to symptom onset). Transcranial Doppler ultrasound, beat-to-beat BP, ECG and CO2 monitored at baseline and during tilt. Baseline autonomic function, arterial stiffness, cardiac baroreceptor sensitivity (BRS) calculated. dCA (as the auto-regulatory index ARI) assessed before and during tilt. Results: Groups: ANo (n = 24), SNo(n = 18), AOH (n = 20), SOH (n = 23), mean age 73.9 ± 7.1 years. Baseline: No significant differences between the 4 groups for cardiac BRS, arterial stiffness, cerebral blood flow velocity (CBFV) or dCA in either study. HUT: falls in BP, CO2 and CBFV, increases in HR, and fall in ARI amongst symptomatic subjects prior to the end of HUT (maximum duration or symptom onset) compared to preHUT ARI values which were: ANo 5.2 ± 0.2, SNo 3.2 ± 0.1, AOH 3.7 ± 0.1, SOH 4.8 ± 0.3. When comparing those who were symptomatic (n = 23) versus those who were asymptomatic (n = 46) during HUT, regardless of initial classification there was a significant difference in the ARI (−1.2 ± 1.1 vs 0.7 ± 0.9, p < 0.001). Conclusions: Symptoms during HUT were related to a fall in CBFV associated with impaired dynamic cerebral auto-regulation. This is the first description of abnormalities in dCA in relation to symptoms and haemodynamic changes associated with OH, although these changes can only be detected during HUT.

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