Christian D Erkelens1, Haye H van der Wal2, Bauke M de Jong1, Jan-Willem Elting3, Remco Renken4, Marleen Gerritsen5, Peter Jan van Laar4, Vincent M van Deursen2, Peter van der Meer2, Dirk J van Veldhuisen2, Adriaan A Voors2, Gert-Jan Luijckx1. 1. Department of Neurology, University Medical Centre Groningen, Hanzeplein 1, PO Box 30.001, 9700RB, Groningen, the Netherlands. 2. Department of Cardiology, University Medical Centre Groningen, Hanzeplein 1, PO Box 30.001, 9700RB, Groningen, the Netherlands. 3. Department of Clinical Neurophysiology, University Medical Centre Groningen, Hanzeplein 1, PO Box 30.001, 9700RB, Groningen, the Netherlands. 4. Department of Radiology and Neuro-Imaging Centre, University Medical Centre Groningen, Hanzeplein 1, PO Box 30.001, 9700RB, Groningen, the Netherlands. 5. Department of Neuropsychology, University Medical Centre Groningen, Hanzeplein 1, PO Box 30.001, 9700RB, Groningen, the Netherlands.
Abstract
AIMS: Heart failure (HF) is associated with tissue hypoperfusion and congestion leading to organ dysfunction. Although cerebral blood flow (CBF) is preserved over a wide range of perfusion pressures in healthy subjects, it is impaired in end-stage HF. We aimed to compare CBF, autoregulation, and cognitive function in patients with mild non-ischaemic HF with healthy controls. METHODS AND RESULTS: Fifteen patients with mild idiopathic dilated cardiomyopathy and 15 matched healthy controls were studied. Co-existing cerebrovascular disease was excluded. All subjects, except five patients with an implantable cardioverter defibrillator, underwent magnetic resonance imaging for measurements of both CBF by arterial spin labelling and quantitative volume flow entering the brain. Cardiocerebral vascular function was assessed with Doppler techniques testing cerebral dynamic autoregulation and vasomotor reactivity. Cognitive analysis was performed by neuropsychological testing. Global and regional CBF did not differ between HF patients (44.3 mL/100 g.min) and controls (42.1 mL/100 g.min). Basilar but not carotid artery inflow was reduced in patients (1.95 mL/s vs. 2.51 mL/s, P = 0.009). Testing autoregulation revealed fewer dampened blood flow fluctuations in HF patients vs. controls (0.96% vs. 0.67%, P < 0.001). Vasomotor reactivity in HF patients showed a reduced CBF velocity (48.4% vs. 61.0%, P = 0.05) and regional cerebral oxygen saturation (18.3% vs. 23.8%, P = 0.02). Cognitive function overall was not affected. CONCLUSION: Although global CBF was unaffected in patients with mild HF, significant changes in basilar inflow volume, cerebral autoregulation and vasomotor reactivity were observed. We describe a model of dynamic cerebral mechanisms required to compensate for the impaired haemodynamics in early-stage HF.
AIMS: Heart failure (HF) is associated with tissue hypoperfusion and congestion leading to organ dysfunction. Although cerebral blood flow (CBF) is preserved over a wide range of perfusion pressures in healthy subjects, it is impaired in end-stage HF. We aimed to compare CBF, autoregulation, and cognitive function in patients with mild non-ischaemic HF with healthy controls. METHODS AND RESULTS: Fifteen patients with mild idiopathic dilated cardiomyopathy and 15 matched healthy controls were studied. Co-existing cerebrovascular disease was excluded. All subjects, except five patients with an implantable cardioverter defibrillator, underwent magnetic resonance imaging for measurements of both CBF by arterial spin labelling and quantitative volume flow entering the brain. Cardiocerebral vascular function was assessed with Doppler techniques testing cerebral dynamic autoregulation and vasomotor reactivity. Cognitive analysis was performed by neuropsychological testing. Global and regional CBF did not differ between HF patients (44.3 mL/100 g.min) and controls (42.1 mL/100 g.min). Basilar but not carotid artery inflow was reduced in patients (1.95 mL/s vs. 2.51 mL/s, P = 0.009). Testing autoregulation revealed fewer dampened blood flow fluctuations in HF patients vs. controls (0.96% vs. 0.67%, P < 0.001). Vasomotor reactivity in HF patients showed a reduced CBF velocity (48.4% vs. 61.0%, P = 0.05) and regional cerebral oxygen saturation (18.3% vs. 23.8%, P = 0.02). Cognitive function overall was not affected. CONCLUSION: Although global CBF was unaffected in patients with mild HF, significant changes in basilar inflow volume, cerebral autoregulation and vasomotor reactivity were observed. We describe a model of dynamic cerebral mechanisms required to compensate for the impaired haemodynamics in early-stage HF.
Authors: Bhaswati Roy; Mary A Woo; Danny J J Wang; Gregg C Fonarow; Ronald M Harper; Rajesh Kumar Journal: Eur J Heart Fail Date: 2017-05-30 Impact factor: 15.534
Authors: Fang Qin Goh; William K F Kong; Raymond C C Wong; Yao Feng Chong; Nicholas W S Chew; Tiong-Cheng Yeo; Vijay Kumar Sharma; Kian Keong Poh; Ching-Hui Sia Journal: Biology (Basel) Date: 2022-01-23
Authors: Mateusz G Adamski; Magdalena Sternak; Tasnim Mohaissen; Dawid Kaczor; Joanna M Wierońska; Monika Malinowska; Iwona Czaban; Katarzyna Byk; Kristina S Lyngsø; Kamil Przyborowski; Pernille B L Hansen; Grzegorz Wilczyński; Stefan Chlopicki Journal: J Am Heart Assoc Date: 2018-03-26 Impact factor: 5.501