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Prevention of cognitive dysfunction in patients with atrial fibrillation

Since the precise mechanism(s) of cognitive disorders in patients with atrial fibrillation ( AF ) is not fully known, the optimal way to prevent cognitive dysfunction for a given patient remains to be established.
Both disease states share common risk factors that include aging, smoking, hypertension, diabetes, sleep apnoea, physical inactivity, vascular disease, inflammation, and heart failure.
Many of these risk factors represent modifiable targets for preventative therapies and if treated early may lower the risk of both diseases.

Stroke prevention is the principal priority in the management of atrial fibrillation and integrated approaches such as the Atrial fibrillation Better Care ( ABC ) pathway ( Avoid stroke, Better symptom management, Cardiovascular and comorbidity risk reduction ) may improve atrial fibrillation management.

Stroke prevention therapy, particularly oral anticoagulation, applied to the appropriate patients according to risk stratification proposed in scientific guidelines may reduce the risk of dementia.

Fridberg and Rosenqvist studied 444 106 AF patients over 1.5 million years at risk. Anticoagulation use was in 202 946 ( 46% ) of the patients with the primary anticoagulant used Warfarin ( 94% ). In AF patients not treated with anticoagulation, 60% were on Aspirin.
In multivariate analysis, the strongest predictors of dementia were in order: age ( hazard ratio, HR per decade 2.19, 95% CI 2.16–2.22 ), Parkinson’s disease ( HR 2.46, 95% CI 2.25–2.69 ), absence of oral anticoagulation treatment ( HR 2.08, 95% CI 1.73–2.53 ), and alcohol abuse ( HR 1.53, 95% CI 1.41–1.66 ).

In patients managed long term with vitamin K antagonists ( VKAs ), for example, TTR ( Time in Therapeuc Range ) is inversely associated with new-onset dementia.
Risk of dementia is augmented in AF patients who are frequently over anticoagulated or receiving antiplatelet therapy. However, dementia can have a confounding effect on maintenance of TTR, and oral anticoagulation in AF patients has not been consistently associated with either improved cognitive function or less hippocampal atrophy.
Anticoagulation with Warfarin neither influenced the reduction of total brain volume nor cognitive function in individuals with atrial fibrillation.
Non-vitamin K antagonist oral anticoagulant therapy may reduce the incidence of brain micro-haemorrhage compared with VKAs, but whether NOACs improve long-term cognitive function is currently unknown.

A recent community-based study provided some optimism in this regard and found that NOAC therapies were associated with lower stroke and dementia rates compared with Warfarin.
Considering the incidence of dementia in atrial fibrillation, only trials with large numbers of patients and extended long-term follow-up would be able to firmly estab
lish the possible benefit of oral anticoagulation on the subsequent risk of cognitive decline.
Preventing early onset of atrial fibrillation through lifestyle or risk factor modification could delay the onset and progression of cognitive decline.
Prevention and early management of smoking, excess alcohol consumption, hypertension, obesity, diabetes, and sleep apnoea may reduce the onset and/or progression of atrial fibrillation with concomitant reductions in stroke and possibly cognitive function. However, such risk factor modifications may have independent positive effects on cognitive function regardless of the development of atrial fibrillation.

It is also unclear if aggressive modification should start at the time of onset of atrial fibrillation. Lifestyle modification may also reduce the risk of cognitive decline in AF patients.
Prevention of cognitive dysfunction may include general measures proposed in the treatment and management of vascular dementia or Alzheimer’s disease.
Several trials have tested the effects of physical activity and cognitive training in Alzheimer’s disease and have shown some evidence of efficacy on cognitive endpoints.
Most of the trials, however, had short follow-up periods.
Further evidence is needed to confirm the optimal design and dose of interventions, the appropriate target population, and the efficacy of such interventions.
Innovations such as the development of multi-domain interventions and the use of biomarkers or genetic profiles to better target higher-risk patients are being assessed in ongoing trials.
However, differentiating the AF-dependent or AF-independent effects of lifestyle and risk factor modifications remains a major challenge.

There are no robust data to affirm that therapy for rhythm control with medication or successful atrial fibrillation catheter ablation can prevent cognition disorders in AF patients.
Atrial fibrillation catheter ablation may not eliminate atrial fibrillation in the majority of patients, but rather attenuate overall AF burden.
Follow-up data beyond 5 or 10 years are limited, and suggest that 2–5% of successfully ablated patients will have recurrences annually.
Furthermore, many of these recurrences may be asymptomatic and the prognostic implication of asymptomatic episodes on both stroke risk and cognitive function is unknown.

In patients with persistent atrial fibrillation for whom which rhythm control is not pursued, atrioventricular ( AV ) node ablation with pacemaker implantation that restores a predictable R-R interval and heart rate has been shown, in a small study, to improve frontal and temporal blood flow and improve memory and learning. ( Xagena )

Source: Dagres N et al, Europace, 2018