期刊
JOURNAL OF PHYSIOLOGY-LONDON
卷 600, 期 10, 页码 2311-2325出版社
WILEY
DOI: 10.1113/JP283112
关键词
arrhythmia; cerebral haemodynamics; cerebral perfusion; heart failure with reduced ejection fraction; ischaemic heart disease
资金
- Saskatchewan Health Research Foundation [4522, 3468]
- NSERC [05323]
- Canadian Resuscitation Outcomes Consortium
- Heart and Stroke Foundation [G-16-00014255]
- CIHR [201503MOP-342412-MOVCEEA]
Ventricular arrhythmias are associated with cerebral hypoperfusion and neurological impairment. This study found that irregular heartbeats, both single and multiple, influence cerebral haemodynamics in a population-specific, arrhythmia-type and organ-dependent manner. The magnitude of these haemodynamic perturbations is greatest in heart failure patients with reduced ejection fraction and is inversely related to cognitive performance. Chronic arrhythmias may exacerbate existing cerebral hypoperfusion in these patients.
Ventricular arrhythmias are associated with neurological impairment and could represent a source of cerebral hypoperfusion. In the present study, data from healthy individuals (n = 11), patients with ischaemic heart disease (IHD; ejection fraction >40%; n = 9) and patients with heart failure with reduced ejection fraction (HFrEF; EF = 31 (5)%, n = 11), as well as data from swine surgeries, where spontaneous ventricular arrhythmias were observed during cerebrovascular examination (transcranial Doppler ultrasound in humans and laser Doppler in swine) were analysed retrospectively to investigate the effect of arrhythmia on cerebral microvascular haemodynamics. A subset of participants also completed the Montreal Cognitive Assessment (MoCA). Middle cerebral artery mean blood velocity (MCA(Vmean)) decreased during premature ventricular contraction (PVC) in all groups, and data from swine indicate PVCs reduced cerebral microvascular perfusion. Overall MCA(Vmean) was decreased in the HFrEF vs. control group. Further, % increment MCA(Vmean)/% increment mean arterial pressure during the PVC was greater in the HFrEF vs. control group and was correlated with decreased MoCA scores. Subanalysis of HFrEF data revealed that during bigeminy MCA(Vmean) decreased owing to reductions during irregular beats only. During non-sustained ventricular tachycardia, MCA(Vmean) decreased but recovered above baseline upon return to sinus rhythm. Also, haemodynamic perturbations during and following the PVC were greater in the brachial artery vs. the MCA. Therefore, ventricular arrhythmias decreased indices of cerebral perfusion irrespective of IHD or HFrEF. The relative magnitude of arrhythmia-induced haemodynamic perturbations appears to be population specific and arrhythmia type and organ dependent. The cumulative burden of arrhythmia-induced deficits may exacerbate existing cerebral hypoperfusion in HFrEF and contribute to neurological abnormalities in this population. Key points Irregular heartbeats are often considered benign in isolation, but individuals who experience them frequently have a higher prevalence of cerebrovascular and/or cognitive associated disorders. How irregular heartbeats affect blood pressure and cerebral haemodynamics in healthy and cardiovascular disease patients, those with and without reduced ejection fraction, remains unknown. Here it was found that in the absence of symptoms associated with irregular heartbeats, such as dizziness or hypotension, single, multiple non-sustained and sustained irregular heartbeats influence cerebral haemodynamics in a population-specific, arrhythmia-type and organ-dependent manner. Relative deficits in the index of cerebral blood flow normalized to relative deficits in blood pressure were greatest in patients with heart failure with reduced ejection and inversely related with cognitive performance. Chronic arrhythmias may exacerbate existing cerebral hypoperfusion in heart failure with reduced ejection fraction, thereby providing a mechanistic link between otherwise benign irregular heartbeats and cognitive dysfunction, independent of embolism.
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