JACC in a Flash: Atrial Fibrillation: Damaging to the Brain in More Ways Than One
Large registries have reported an increased risk for thromboembolism and mortality with atrial fibrillation (AF), independently from the presence of other comorbidities. Does type of AF—either persistent or paroxysmal—impact the prevalence and outcomes of cerebrovascular events in these patients? In a recent JACC article, Fiorenzo Gaita, MD, and colleagues investigated the prevalence of silent cerebral ischemia (SCI) in AF patients, as well as the potential for cognitive decline in these patients.
Two hundred-seventy subjects were enrolled in the study: 180 patients with AF (50% paroxysmal and 50% persistent) and 90 controls. All participants received clinical assessment, neurological examination, cerebral MR, and underwent the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS).
At least one SCI was present in 80 (89%) patients with paroxysmal AF, 83 (92%) with persistent AF, and in 41 (46%) of controls. Patients with persistent AF also had a significantly higher number of episodes of SCI per person than paroxysmal AF patients (41.1±28.0 vs. 33.2±22.8; p = 0.04); and, as expected, the number of SCI episodes per person with either type of AF was higher than controls. Overall, either type of arrhythmia contributed to an 11 times higher risk for SCI compared to people in sinus rhythm (OR = 11.2; 95% CI 6-21; p < 0.01), while there was no difference with respect to the different forms of arrhythmia (OR=1.5; 95% CI 0.5-4.1; p = 0.61).
AF also had a negative effect on cognitive performance, as assessed by RBANS: 82.9±11.5 for persistent AF, 86.2±13.8 for paroxysmal AF, and 92.4±15.4 points for controls. Lower scores in the persistent AF type were mainly due to poorer performance on visual-spatial ability tests. When looking at evidence of lesions on magnetic resonance (MR), the authors determined that the “spotted pattern” lesions could have damaged the frontal subcortical cerebral circuits that play a role in the visual-spatial cognitive functions. “The anatomical brain damage visible by MR did not remain, from a functional point of view, really ‘silent,’” they wrote. “The present data suggest that an initially limited cerebral damage may become overt as the number of cerebral lesions increases due to persistence of the arrhythmia.”
While current research about persistent and paroxysmal AF assumes that both arrythmias present similar stroke risk, Dr. Gaita and colleagues found that persistent AF showed a higher number of lesions—possibly due to the longer presence and duration of AF in the persistent form, causing greater exposure time to AF-related thromboembolic etiology—and should perhaps be managed differently. “Studies on symptomatic cerebral damage rarely differentiate between the two clinical forms of the arrhythmia,” they noted. “Considering the high clinical impact that this finding may provide it surely warrants further confirmation.”
“When analyzing the relationship between atrial fibrillation and silent brain ischemia, the most important question is whether prophylactic antithrombotic treatment may be able to reduce the incidence of silent brain lesions as it has been proven to do for clinical strokes,” Steven Shea, MD, and Marco Di Tullio, MD, wrote in an accompanying editorial. Answering this question will require appropriately designed and powered prospective studies, but the current study provides crucial information to guide future research in the detection, monitoring, and characterization of AF. They concluded, “Devising feasible and cost-effective strategies for detecting asymptomatic atrial fibrillation in subgroups, such as the elderly, that are at high risk for the arrhythmia may become crucial to dealing with a condition that, as the article by Gaita et al. reminds us, can damage the brain in more ways than one.”
Gaita F, Corsinovi L, Anselmino M, et al. J Am Coll Cardiol. 2013 June 29. [Epub ahead of print]
Shea S, Di Tullio M. J Am Coll Cardiol. 2013 June 29. [Epub ahead of print]
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