Neurovascular coupling in severe aortic valve stenosis

Author:

Ovsenik Ana12ORCID,Podbregar Matej34,Lakič Nikola5,Brešar Martin67ORCID,Boškoski Pavle7ORCID,Verdenik Ivan8,Fabjan Andrej910ORCID

Affiliation:

1. Faculty of Medicine, Department of Biomedicine University of Ljubljana Ljubljana Slovenia

2. Department of Cardiology University Medical Centre Ljubljana Ljubljana Slovenia

3. Faculty of Medicine, Department of Internal Medicine University of Ljubljana Ljubljana Slovenia

4. Department of Intensive Care General Hospital Celje Celje Slovenia

5. Department of Cardiovascular Surgery University Medical Centre Ljubljana Ljubljana Slovenia

6. Jožef Stefan International Postgraduate School Ljubljana Slovenia

7. Department of Systems and Control Jožef Stefan Institute Ljubljana Slovenia

8. Department of Obstetrics and Gynaecology, Division for Research University Medical Centre Ljubljana Ljubljana Slovenia

9. Faculty of Medicine, Institute for Physiology University of Ljubljana Ljubljana Slovenia

10. Department of Vascular Neurology and Neurological Intensive Care University Medical Centre Ljubljana Ljubljana Slovenia

Abstract

AbstractObjectivesAortic stenosis (AS) is characterized by obstruction of blood outflow from the left ventricle, which can impair target organ perfusion such as the brain. We hypothesized that hemodynamic changes in AS may lead to dysfunction of cerebral blood flow regulatory mechanisms. The aim of our study was to evaluate neurovascular coupling in patients with AS by Transcranial Doppler ultrasonography.MethodsNeurovascular coupling was assessed using visually evoked cerebral blood flow velocity responses (VEFR) calculated as relative blood flow velocity changes in the posterior cerebral artery upon visual stimulation. We analyzed peak systolic, mean and end diastolic VEFR in 54 patients with severe AS and 43 controls in 10 consecutive cycles of visual stimulation. Repeated‐measures ANOVA test was used to compare cerebral hemodynamic data by group.ResultsPatients with AS had significantly higher peak systolic (12.9% ± 5.6% and 10.5% ± 4.5%; p = .009) and mean VEFR (14.4% ± 5.8% and 12.2% ± 4.9%; p = .021) compared to controls, whereas only a tendency for higher end diastolic VEFR was observed (16.7% ± 6.9% and 14.4% ± 6.2%; p = .061).ConclusionWe have shown for the first time that patients with severe AS exhibit higher VEFR than controls indicating dysregulation of neurovascular coupling, which can be one of the factors contributing to development of cognitive decline.

Publisher

Wiley

Subject

Behavioral Neuroscience

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