This is Your Brain, and This is Your Brain on Atrial Fibrillation: The Roles of Cardiac Malperfusion Events and Vascular Dysfunction in Cognitive Impairment

Abstract

AF is an independent and strong predictor of long-term cognitive decline. However, the mechanism for this cognitive decline is difficult to define and likely multifactorial, leading to many different hypotheses. Examples include macro- or microvascular stroke events, biochemical changes to the blood–brain barrier related to anticoagulation, or hypo-hyperperfusion events. This review explores and discusses the hypothesis that AF contributes to cognitive decline and dementia through hypo-hyperperfusion events occurring during cardiac arrhythmias. We briefly explain several brain perfusion imaging techniques and further examine the novel findings associated with changes in brain perfusion in patients with AF. Finally, we discuss the implications and areas requiring more research to further understand and treat patients with cognitive decline related to AF.

Revitalizing brain perfusion: Unveiling advancements through rhythm control strategies in atrial fibrillation—A systematic review

“…Indirect techniques, including NIRS, transcranial Doppler, and phase‐contrast MRI, measure physiological parameters reflecting cerebral perfusion 14,35 . AF significantly impacts perfusion by disrupting the regularity of diastolic and systolic timing, leading to beat‐to‐beat variability in cardiac output and decreased CBF 36,37 . This impairment in CBF, despite normal stroke volume, may result in cerebral hypoperfusion, particularly as AF progresses 36 .…”

“… 14 , 35 AF significantly impacts perfusion by disrupting the regularity of diastolic and systolic timing, leading to beat‐to‐beat variability in cardiac output and decreased CBF. 36 , 37 This impairment in CBF, despite normal stroke volume, may result in cerebral hypoperfusion, particularly as AF progresses. 36 Notably, flow‐mediated dilation improves after cardioversion and catheter ablation, indicating some reversibility of arrhythmia‐induced dysfunction.…”

“… 36 , 37 This impairment in CBF, despite normal stroke volume, may result in cerebral hypoperfusion, particularly as AF progresses. 36 Notably, flow‐mediated dilation improves after cardioversion and catheter ablation, indicating some reversibility of arrhythmia‐induced dysfunction. 36 , 38 Our analysis indicates that rhythm control may enhance brain perfusion, supported by 7 studies 11 , 19 , 23 , 24 , 25 , 26 , 27 with direct measurement and 3 studies with indirect measurement.…”

“… 36 Notably, flow‐mediated dilation improves after cardioversion and catheter ablation, indicating some reversibility of arrhythmia‐induced dysfunction. 36 , 38 Our analysis indicates that rhythm control may enhance brain perfusion, supported by 7 studies 11 , 19 , 23 , 24 , 25 , 26 , 27 with direct measurement and 3 studies with indirect measurement. 21 , 28 , 29 The indirect methods encompass SctO2 and THI.…”

Mortality benefit with AF ablation: Impact of normal sinus rhythm seen in CABANA and EAST AFnet

“…For this review, we will assume the latter aspect of this argument that AF contributes directly towards these cardiovascular diseases and mortality‐associated outcomes and its treatment represents a means to improve outcomes. In this regard, some of potential direct mechanisms of mortality include macro‐ and micro‐thrombosis and embolic events, macro‐ and micro‐bleeding from vascular injury and anticoagulant exposure, altered organ perfusion from beat‐by‐beat variance in cardiac output, loss of A–V synchrony, incomplete or impaired diastolic filling, acute or chronic reactive stress responses that increase sympathetic nervous system activity, decrease parasympathetic nervous system activity, and augment the renin‐angiotensin‐aldosterone system, and maladaptive consequences from a proinflammatory state, oxidative stress, a hypercoagulable state, with insulin and immune resistance amongst other factors 8 . Many of these mechanisms may serve as targets to lower risk such as the use, timing or use, and efficacy of use of anticoagulant therapy to mitigate stroke risk.…”