Researchers have shown that the tendency of atrial fibrillation to impair cognitive function stems, at least in part, from a reduction in blood flow to the brain.
New research indicates that the tendency of atrial fibrillation (AF) to impair cognitive function stems, at least in part, from a reduction in blood flow to the brain.
Data from the first 26 patients to finish an ongoing study of atrial fibrillation in Iceland demonstrated via 2 different measures that successful cardioversion increased cerebral blood flow and brain perfusion, both over baseline and in comparison to patients whose hearts were not shocked back into rhythm.
The patients underwent phase-contrast magnetic resonance imaging to measure cerebral blood flow and arterial spin labeling to measure brain perfusion on 2 occasions: before cardioversion and 10 weeks after treatment.
Mean cerebral blood flow increased from 557.4 ml/min at baseline to 627.1 ml/min in the 17 patients whose electrocardiograms indicated normal heart rhythm at the 10-week follow-up (p=0.01). Their whole-brain perfusion, moreover, increased from 35.6 ml/100 g/min to 40.8 ml/100 g/min (p<0.01) while their gray-matter brain perfusion rose from 39.3 ml/100 g/min to 45.7 ml/100 g/min (p<0.001).
Among patients who still suffered AF at the 10-week follow-up, mean cerebral blood flow and brain perfusion actually declined over the course of the study — cerebral blood flow from 599.8 ml/min to 574.2 ml/min and brain perfusion from 34.5 ml/100g/min to 32.5 ml/100g/min — but the declines were not large or consistent enough to reach the point of statistical significance.
Spearman correlation for the 2 methods of measuring cerebral blood was 0.86 (p<0.0001).
Research team members, who presented their findings at the European Heart Rhythm Europace-Cardiostim meeting in Milan, acknowledged the relatively small number of patients in the sample and noted that the paper on the completed study will include data on a larger number of people.
Still, they said, the results were so consistent in patients measured to date that they achieved high levels of significance and justified a bold hypothesis about the potential meaning of the finding: “Altered cerebral blood flow might play a role in the decline in cognitive function and brain volume seen in patients with AF.”
The association between AF and cognitive decline stems, in large part, from the tendency of AF to cause strokes that, in turn, impair brain function.
That said, the 6,500-patient Rotterdam Study, along with a number of smaller studies, has demonstrated that AF patients who never suffer a stroke still experience unusual rates of cognitive decline.
Determining the cause of this association has been difficult, in part because of the significant overlap in the known risk factors for both conditions: age, hypertension, diabetes, cardiac failure, and, of course, stroke.
Prior efforts to determine the cause of the association focused on determining whether particular types of AF patients faced greater risk of cognitive decline while other types of AF patients faced less risk or no risk at all.
Researchers have found, for example, a particularly high risk of brain impairment among AF patients who are under 70 years old or those who have already progressed to the early stages of dementia when they are first diagnosed with AF.
Another factor that appears to increase the risk of cognitive decline, a factor that would seem to contradict the findings of the study from Iceland, is the use of various types of ablation to restore the heart to normal sinus rhythm (and, presumably, increase blood flow to the brain).
The use of oral anticoagulants — be they traditional vitamin K antagonists or newer compounds such as dabigatran, rivaroxaban, or apixaban — has long been thought to protect brain function by reducing ischemic strokes but they can also endanger the brain by increasing the risk of hemorrhagic strokes and brain micro-hemorrhages.