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How often is non-valvular atrial fibrillation the cause of brain infarction?
G van Merwijk1, J Lodder, J Bamford
1Department of Neurology, University Hospital, Maastricht, The Netherlands.
Insights
Non-valvular atrial fibrillation is unlikely to cause lacunar infarcts but may contribute to cortical infarcts. This finding impacts anticoagulant therapy trials for stroke patients.
Area of Science:
- Neurology
- Cardiology
- Stroke Medicine
Background:
- Non-valvular atrial fibrillation (NVAF) is a known risk factor for ischemic stroke.
- Determining if NVAF is the cause or an incidental finding in stroke patients is crucial for treatment.
Purpose of the Study:
- To assess the frequency of NVAF as a cause of ischemic stroke compared to primary intracerebral hemorrhage.
- To differentiate the role of NVAF in cortical versus lacunar infarcts.
Main Methods:
- Retrospective analysis of NVAF frequency in patients with primary intracerebral hemorrhage, cortical infarcts, and lacunar infarcts.
- Comparison of NVAF prevalence across different stroke types using odds ratios and confidence intervals.
Main Results:
- NVAF frequency in lacunar infarcts was similar to primary intracerebral hemorrhage (OR: 1.28, P=1.0).
- NVAF frequency was significantly higher in cortical infarcts compared to primary intracerebral hemorrhage (OR: 5.57, P=0.0001).
- Suggests NVAF is unlikely to cause lacunar infarcts but may be a significant factor in approximately 30% of cortical infarcts.
Conclusions:
- NVAF is likely incidental in lacunar infarcts and primary intracerebral hemorrhage.
- NVAF may be a causative factor in a substantial proportion of cortical infarcts.
- These findings are vital for designing and evaluating anticoagulant trials in stroke patients with NVAF.
Abstract:
To calculate how often non-valvular atrial fibrillation should be considered as the cause of ischaemic stroke rather than an incidental finding as in primary cerebral haemorrhage, the frequency of non-valvular atrial fibrillation in 75 consecutive patients with primary intracerebral haemorrhage was compared with that in 63 patients with cortical infarcts and 44 patients with lacunar infarcts who were taken at random from 1487 consecutive patients with cerebral infarcts admitted during the same period. The frequency of non-valvular atrial fibrillation in lacunar infarcts did not differ from that in primary intracerebral haemorrhage (odds ratio: 1.28; 95% confidence interval: 0.32-5.1) (P = 1.0), whereas it was significantly higher in cortical infarcts (odds ratio: 5.57; 95% confidence interval 2.00-15.4) (P = 0.0001). Our findings suggest that non-valvular atrial fibrillation in lacunar infarcts, as in primary intracerebral haemorrhage, is unlikely to be the cause of this type of stroke, whereas perhaps 30% of all cortical infarcts are not caused by non-valvular atrial fibrillation when present. These data are important for the planning and explanatory evaluation of trials on the preventive effect of anticoagulants in stroke patients with non-valvular atrial fibrillation.