Neurovascular coupling and cerebral autoregulation in atrial fibrillation

Author:

Junejo Rehan T12ORCID,Braz Igor D3,Lucas Samuel JE14,van Lieshout Johannes J567,Phillips Aaron A8,Lip Gregory YH2,Fisher James P19

Affiliation:

1. School of Sport, Exercise & Rehabilitation Sciences, College of Life & Environmental Sciences, University of Birmingham, Birmingham, UK

2. Liverpool Centre for Cardiovascular Science, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, UK

3. Medical School, University Center of Volta Redonda, Volta Redonda, Brazil

4. Centre for Human Brain Health, College of Life & Environmental Sciences, University of Birmingham, Birmingham, UK

5. Department of Internal Medicine, University of Amsterdam, Amsterdam, The Netherlands

6. Laboratory for Clinical Cardiovascular Physiology, AMC Center for Heart Failure Research, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

7. MRC/Arthritis Research UK Centre for Musculoskeletal Ageing Research, School of Life Sciences, University of Nottingham Medical School, Queen's Medical Centre, Nottingham, UK

8. Departments of Physiology, Pharmacology & Clinical Neurosciences, Libin Cardiovascular Institute, Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Alberta, Canada

9. Department of Physiology, Faculty of Medical & Health Sciences, University of Auckland, Auckland, New Zealand

Abstract

The risk of cognitive decline and stroke is increased by atrial fibrillation (AF). We sought to determine whether neurovascular coupling and cerebral autoregulation are blunted in people with AF in comparison with age-matched, patients with hypertension and healthy controls. Neurovascular coupling was assessed using five cycles of visual stimulation for 30 s followed by 30 s with both eyes-closed. Cerebral autoregulation was examined using a sit–stand test, and a repeated squat-to-stand (0.1 Hz) manoeuvre with transfer function analysis of mean arterial pressure (MAP; input) and middle cerebral artery mean blood flow velocity (MCA Vm; output) relationships at 0.1 Hz. Visual stimulation increased posterior cerebral artery conductance, but the magnitude of the response was blunted in patients with AF (18 [8] %; mean [SD]) and hypertension (17 [8] %), in comparison with healthy controls (26 [9] %) ( P < 0.05). In contrast, transmission of MAP to MCA Vm was greater in AF patients compared to hypertension and healthy controls, indicating diminished cerebral autoregulation. We have shown for the first time that AF patients have impaired neurovascular coupling responses to visual stimulation and diminished cerebral autoregulation. Such deficits in cerebrovascular regulation may contribute to the increased risk of cerebral dysfunction in people with AF.

Publisher

SAGE Publications

Subject

Cardiology and Cardiovascular Medicine,Neurology (clinical),Neurology

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