Asymptomatic Atrial Fibrillation Affects Cognition
April 1, 1998 3 minutes read
Asymptomatic Atrial Fibrillation Affects Cognition
ABSTRACT & COMMENTARY
Source: Farina E, et al. Neuropsychological deficits in asymptomatic atrial fibrillation. Acta Neurol Scand 1997;96:310-316.
Non-rheumatic atrial fibrillation (nraf) has a prevalence of 2-4% in the population more than 60 years of age.1 Chronic NRAF increases stroke risk five- to seven-fold, and up to 35% of NRAF patients have a stroke during their lifetime.2 In some studies,3 but not all,4 paroxysmal AF has been associated with a smaller risk of embolic stroke than chronic AF. Patients with chronic NRAF, but not those with paroxysmal NRAF have an additional risk for asymptomatic (silent) cerebral infarcts.5
Farina and associates evaluated the cognitive status of NRAF patients with a negative history for cerebrovascular disease and compared them with age-matched controls with normal sinus rhythm (NSR). Their hypothesis was that silent cerebral infarcts and chronic or temporary reduction in cerebral perfusion might influence the cognitive performance of NRAF patients.
The study included 37 consecutive patients with chronic (n = 16; mean age, 65.3 ± 6.6 years) or paroxysmal (n = 21; mean age, 58.3 ± 9.5 years) NRAF. An equal number of control subjects in NSR were matched for age, education, the presence of hypertension, and smoking habits. The Hamilton Depression Rating Scale was administered to both groups, and the scores did not differ significantly between NRAF patients and controls.
Only mild neurological abnormalities were detected in patients and controls. Abnormal deep tendon reflexes and primitive reflexes were significantly more frequent in paroxysmal AF patients than in controls (P < 0.05). Cerebellar signs were significantly more frequent in chronic NRAF patients than in controls (P < 0.01). Brain CT scans detected one or more hypotense lesions in five of 16 chronic NRAF patients (31%) and in two of 21 paroxysmal NRAF patients (10%).
Patients with chronic NRAF showed poorer performance in tasks exploring attention and verbal memory functions. The paroxysmal NRAF group was significantly impaired only in long-term memory tasks. (See Table.) The neuropsychological findings were confirmed even after excluding patients from both groups with CT evidence of infarcts. The authors conclude that neurologically asymptomatic NRAF is associated with a significant impairment in attention and memory.
Table: Selected Neuropsycholgical Test Results: Median Score and Range
Test |
Chronic NRAF (n = 16) |
Controls (n = 16) |
Paroxysmal NRAF (n = 21) |
Controls (n = 21) |
| Mini-mental state exam | 29 (26-30) | 30 (28-30) | 29 (26-30) | 30 (28-30) |
| Raven 36 p.m. (color) | 29 (20-35) | 31 (28-35) | 30 (23-30) | 33 (22-36) |
| Attentional matrices | 46 (17-57)* | 57 (42-60) | 54 (35-60) | 58 (42-60) |
| Wais subset digit symbol | 32 (15-60) | 34 (19-80) | 41 (20-72) | 44 (19-78) |
| Wais subset digit span | 5 (4-6)* | 7 (5-8) | 6 (5-9) | 7 (5-9) |
| Logical memory test | 14 (8-19)§ | 18 (12-23) | 16 (10-22)~ | 20 (12-23) |
* P < 0.0001; § P = 0.001; ~P < 0.05
COMMENTARY
The authors found that deterioration of some cognitive functions is associated with AF even in patients without a history of stroke. In this series, the greater impairment of memory and attention in chronic rather than paroxysmal AF patients could reflect either the effects of long-standing cerebral hypoperfusion or of multiple microembolic infarcts. Further studies are needed to determine which is the more important cause of cerebral damage and also whether these changes herald future dementia.
The present findings suggest that asymptomatic AF is a misnomer and that NRAF patients are at risk for the development of cognitive impairment. Therefore, physicians should consider aggressive intervention even before there is evidence of embolism. Intervention includes attempting to revert and then maintaining patients in NSR and, if that is not possible, employing prophylactic anticoagulation. (See also editor's comment after the following abstract.) -jjc
References
1. Kannel WB, et al. N Engl J Med 1982;306:1018-1122.
2. Cerebral Embolism Task Force. Arch Neurol 1986;43:71-84.
3. Wiener I, et al. Am J Cardiol 1987;59:177-179.
4. The Stroke Prevention in AF Investigators. Arch Intern Med 1994;154:1449-1457.
5. Ezekowitz MD, et al. Circulation 1995;92:2178-2182.
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