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Transcript
Original article
Cognitive disorders in elderly patients with permanent atrial
fibrillation
Beata Wożakowska-Kapłon1, 2, Grzegorz Opolski3, Dariusz Kosior3, Elżbieta Jaskulska -Niedziela1,
Ewa Maroszyńska -Dmoch1, Monika Włosowicz1
1 1st
Department of Cardiology, Centre of Cardiology, Kielce, Poland
Sciences Department, University of Jan Kochanowski, Kielce, Poland
3 1st Department of Cardiology, Medical University, Warsaw, Poland
2 Health
Abstract
Background: Atrial fibrillation (AF) is a risk factor for development of thromboembolic events with an annual stroke rate of 4.5%.
In subjects over 80 years AF is the single leading cause of major stroke. Moreover, about 25% of patients with AF in the absence of neurological
deficits have tomographic signs of one or more silent cerebral infarcts.
Aim: To investigate whether cognitive function in patients with permanent AF is significantly worse than in patients with sinus rhythm.
Methods: We included subjects aged > 65 years, without previous cerebrovascular events or dementia, with permanent arrhythmia
lasting > 12 months. The AF group comprised 51 patients, aged 75.8 years. The control group consisted of 43 patients with sinus rhythm.
The main points of the study protocol were: clinical history recording, physical examination, biochemical analyses, standard 12-lead ECG
and transthoracic echocardiography. Cognitive status was assessed by Mini Mental State Examination (MMSE).
Results: Patients had established AF with a median duration of 4.9 years (range 1-21 years). Of the 51 patients, 51% had hypertension, 37%
coronary artery disease, 12% presented sick sinus syndrome or atrioventricular advanced block with a VVI pacemaker implanted. There
were no significant differences between the two groups though AF patients presented left ventricular hypertrophy and history of myocardial
infarction more frequently. Patients in the sinus group had a lower-risk profile and received antithrombotic therapy less frequently than
the AF group. However, a significant proportion of patients, particularly in the AF group received less than optimal thromboembolic
prophylactic treatment with anticoagulants. Cognitive status was found to be significantly lower in the AF group, compared with the sinus
rhythm group: 24.8 ± 3.1 vs. 27.1 ± 2.6 (p < 0.05). There were 43% patients with cognitive impairment in the AF group and 14% in the sinus
rhythm group.
Conclusions: Permanent AF in patients aged over 65 years seems to be associated with lower MMSE score compared with subjects
with sinus rhythm. Cognitive impairment in older patients is a multifactorial disorder. One of the causes of low cognitive function in these
patients appears to be permanent AF. Further prospective clinical trials should help determine the possible role of inadequate anticoagulant
treatment, and its association with the deterioration of cognitive function in AF patients.
Key words: atrial fibrillation, elderly population, cognitive disorders
Kardiol Pol 2009; 67: 487-493
Introduction
Atrial fibrillation (AF) is the most common cardiac
arrhythmia encountered in clinical practice, with
the potential for serious consequences. It affects over 0.4%
of the population and is much more common in the elderly,
with the incidence of AF rising to ~10% in octogenarians
[1]. Atrial fibrillation is a risk factor for development
of thromboembolic disease with an annual rate of 4.5%
stroke incidence in AF patients [2]. In subjects over 80 years
AF is the single leading cause of major stroke [3].
Another manifestation of brain ischaemia are transient
ischaemic attacks. Nevertheless, patients with AF can
undergo silent cerebral infarctions, which means a loss
of brain tissue without specific recognised neurological
events [4]. Such a situation may lead to progressive
impairment of cognitive or motor function. Moreover,
about 25% of patients with AF in the absence
of neurological deficits have computed tomography (CT)
signs of one or more silent cerebral infarcts. Seventy percent
of these silent lesions were in the territory of the middle
cerebral artery in the Veterans Affairs SPINAF study [5].
Address for correspondence:
Beata Wożakowska-Kapłon MD, PhD, I Oddział Kardiologii, Świętokrzyskie Centrum Kardiologii, ul. Grunwaldzka 45, 25-736 Kielce,
tel.: +48 32 367 13 01, e-mail: [email protected]
Received: 20 July 2008. Accepted: 05 February 2009.
Kardiologia Polska 2009; 67: 5
488
Beata Wożakowska-Kapłon et al.
The aim of our study was to examine cognitive function
in older inpatients with permanent AF compared to
matched subjects with sinus rhythm.
Methods
Study group
In a cross-sectional prospective study we examined 51
inpatients with permanent AF out of 113 patients with AF,
and 43 ones without arrhythmia creating a control group,
selected from a population of 994 patients consecutively
admitted to the Cardiology Department between April 2003
and February 2004. Inclusion criteria were: age above 65
years, permanent non-rheumatic AF exceeding 12 months,
with underlying disease such as: controlled hypertension,
stable coronary artery disease, sick sinus syndrome (after
pacemaker implantation) or cardiomyopathy. Exclusion
criteria, the same for both the AF and the control group, were
history of TIA or stroke, diagnosis of dementia, Mini Mental
State Examination (MMSE) < 20 score, depression or
dysthymia, rheumatic valve disease, prosthetic heart valve,
congestive heart failure > NYHA class III, myocardial infarction
(< 3 months) or unstable angina, uncontrolled hypertension,
advanced atrioventricular block (when pacemaker not
implanted), diabetes mellitus, thyroid disease, severe liver or
renal insufficiency, alcohol abuse, carotid stenosis or
endarterectomy. Family predisposition towards dementia or
Alzheimer’s disease was not examined. Patients with
significant head trauma in the past were not included. The
main points of the study protocol were: clinical history
recording, physical examination, biochemical analyses,
standard 12-lead ECG and transthoracic echocardiography
(TTE). Neurological examination and CT examination were
performed to exclude non-vascular causes of cognitive
impairment. Left ventricular (LV) mass was calculated for
each echocardiographic study according to Devereaux’s
anatomically corrected regression equation [6]. Left atrial
dimension and LV mass were adjusted for body surface area.
The international normalised ratio (INR) taken into
consideration was that assessed at admission to the hospital
or the last value before anticoagulation withdrawal in
patients admitted for pacemaker reimplantation. Cognitive
status was assessed by MMSE [7] and depressed patients
were excluded by the Geriatric Depression Scale [8]. The
MMSE score is based on 20 clearly defined questions and
tasks, giving a maximal potential score of 30. Patients with
an MMSE score of < 25 were considered to have cognitive
impairment [9, 10].
The Katz activities of daily living scale (ADL) was used
to assess six basic activities, with the variables scored as
either 0 (no assistance required, independent in feeding,
continence, transferring, going to toilet, dressing, and
bathing) or 1 (independent in all but one of these functions)
up to 6 (dependent in all six functions, maximum assistance
needed, significant disability) [11]. The education level
criterion was the number of years of education.
Kardiologia Polska 2009; 67: 5
Forty three age-, gender-, and heart disease matched
subjects with sinus rhythm formed the control group. The
examination was performed in clinical stable patients. The
study was explained to each patient and written consent
was obtained. The study protocol was approved by
the local Ethical Committee.
Statistical analysis
The results are expressed as the mean ± standard
deviation in the case of a normal distribution, whereas
median values with ranges are given for non-normally
distributed variables. Statistical analyses were performed
with Student’s t test for continuous variables and the chi
square test for categorical variables, with a p value < 0.05
considered significant. Linear regression analysis was used
to study the relationship between cognitive decline and
other clinical variables. Variables with a p value ≤ 0.10 on
linear regression analysis were further examined by
multivariate regression analysis. The Pearson correlation
(r) coefficient was used to measure the strength
of the linear association between clinical and
echocardiographic variables and MMSE score. All analyses
were performed using the Statistical Analysis System
program (SAS Institute Inc., Cary, NC), version 8.2.
Results
Out of 113 patients with AF, 51 subjects (26 men and
25 women) met inclusion criteria (6 patients were excluded
due to dementia with MMSE score < 20 mean 18.2). The
average age of the 94 examined patients (51 with AF and
43 controls) was 75.3 (range 66-95 years) (47 men and
47 women). The most prevalent reasons for admission to
hospital among the AF group were symptoms of AF, heart
failure or coronary artery disease, ventricular arrhythmia
and single-chamber ventricular (VVI) pacemaker
reimplantation. The clinical characteristics of the AF and
control groups are shown in Table I. There were no
significant differences between the two groups though AF
patients presented LV hypertrophy more frequently. Controls
had a lower-risk profile received antithrombotic therapy
less frequently than the AF group. However, in both groups
and particularly in the AF group less than optimal
thromboembolic prophylactic treatment with anticoagulants
was found (71% of patients with AF were ineffectively
anticoagulated).
Cognitive status, as assessed by MMSE score, was
significantly decreased in the AF group compared with
the control group (24.8 ± 3.1 vs. 27.1 ± 2.6, p < 0.05) (Table II).
The lowest MMSE (21.6 ± 2.3) was noted in the oldest
(> 85 years) and less educated (≤ 8 years) patients with AF
vs. 26.0 ± 1.7 in the control group. In the group of AF patients
aged 66-75 years and better educated (> 8 years) MMSE
score was calculated as 25.9 ± 2.7 vs. 28.2 ± 2.1 in the control
group. In multivariate analysis the factors independently
associated with cognitive impairment were AF (r = –1.8,
489
Cognitive disorders in elderly patients with permanent atrial fibrillation
Table I. Patients’ baseline characteristics
Age [years]
Gender [male/female]
AF group
n = 51
Control group
n = 43
p
75.8 (66-95)*
74.9 (66-93)
NS
25/26
22/21
NS
Primary school or less (≤ 8 years of education)
33 (64%)
27 (63%)
NS
Duration of AF [years]
4.9 (1-21)
Previous MI
18 (35%)
14 (33%)
NS
Underlying heart disease
systemic hypertension
coronary artery disease
SSS/AV block (VVI pacemaker)
26 (51%)
19 (37%)
6 (12%)
23 (53%)
15 (35%)
5 (12%)
NS
NS
NS
NYHA class
I
II
III
6 (12%)
16 (31%)
29 (57%)
8 (18%)
11 (26%)
24 (56%)
NS
NS
NS
18 (36%)
39 (76%)
24 (47%)
23 (45%)
21 (31%)
4 (8%)
23 (45%)
28 (55%)
11 (22%) 9/2
15 (35%)
30 (70%)
22 (52%)
20 (48%)
17 (39%)
4 (9%)
17 (40%)
7 (17%)
22 (52%) 20/2
NS
NS
NS
NS
NS
NS
NS
< 0.05
< 0.05
Medication at enrolment
digoxin
ACE inhibitors
diuretics
beta-blockers
calcium antagonists
AT1-receptor blockade
statins
acenocoumarol
aspirin (75/150 mg)
INR (in patients treated with AC)
1.32 ± 0.6
1.46 ± 0.7
NS
8/28 (29%)
3/7 (43%)
#
Systolic BP [mmHg]
142 ± 23
137 ± 19
NS
HR [beats/min]
88 ± 11
71 ± 13
< 0.05
20 (39%)
9 (21%)
< 0.05
44 ± 11
46.3 ± 12
NS
Effective anticoagulation (INR 2-3)
LVH (LVMI ≥ 135 M, ≥ 110g/m2 F)
LVEF [%]
Abbreviations: AF – atrial fibrillation, NYHA – New York Heart Association, SSS – sick sinus syndrome, BP – blood pressure, HR – heart rate, MI – myocardial
infarction, AT1 – angiotensin II type 1, ACE – angiotensin-converting enzyme, LVH – left ventricular hypertrophy, LVMI – left ventricular mass index,
M – male, F – female, LVEF – left ventricular ejection fraction, INR – international normalized ratio, AC – acenocoumarol
* values are mean ± SD or median and range
# p value was not calculated
p < 0.0007) and limited activites of daily living (ADL)
(r = –0.52, p < 0.001) (Table III). Due to the low proportion and
small number of patients with therapeutic INR levels in both
groups, these data were not included in regression analysis.
Discussion
The present findings provide evidence that impairment
of cognitive functions may be associated with arrhythmia
in patients with AF. Permanent AF patients showed greater
cognitive decline compared with a very similar group
without arrhythmia. It could be hypothesised that
ischaemic lesions due to microembolisation may be
responsible for the cognitive dysfunction observed in
patients with chronic AF; however, it was not evaluated in
the present study. In previous studies, silent infarctions
were noted in 15-26% of patients with AF [5, 12]. In
addition, asymptomatic or silent cerebral infarctions, found
on CT scans, occur more commonly in the presence of AF
than in sinus rhythm [13].
Impaired cognitive function is the most sensitive
outcome measurement of cerebral target organ damage.
A decrease of cognitive function in patients with AF adds
support to the theory of a relation between vascular risk
factors in this condition. The prevalence of AF and
thromboembolic risk is associated with the arrhythmia
increase with advancing age, causing a particular problem
for the elderly. There may be another reason indicating
general atherosclerosis or AF as contributing to cognitive
impairment by atherothrombotic mechanisms. However,
in our control group compatible in age and vascular disease
we detected a significantly higher MMSE score than in
the AF group.
The beneficial role of oral anticoagulation therapy in
reducing stroke and thromboembolic events in patients
Kardiologia Polska 2009; 67: 5
490
Beata Wożakowska-Kapłon et al.
Table II. Comparison of activities of daily living and MMSE score between groups
AF group
n = 51
ADL score
Control group
n = 43
p
2.3 ± 0.6
2.1 ± 0.7
NS
MMSE score
24.8 ± 3.1
27.1 ± 2.6
< 0.05
Cognitive decline (MMSE < 25)
22 (43%)
6 (14%)
< 0.05
Abbreviations: ADL – activities of daily living
Table III. Correlation between clinical and echocardiographic variables and MMSE score
Variable
All patients (n = 94)
Univariate analysis
Multivariate analysis
R coefficient
p
R coefficient
Age
–0.21
< 0.05
–0.14
0.06
AF
–1.50
< 0.0001
–1.82
< 0.0007
AF duration
–0.08
0.67
-
-
0.47
< 0.01
0.23
0.37
Education [years]
p
HR
–0.36
0.07
–0.15
0.26
NYHA class
–0.04
0.05
0.20
0.51
ADL
–0.90
< 0.01
–0.52
< 0.001
LVEF
0.42
0.08
0.37
0.21
LV mass
0.11
0.58
-
-
Abbreviations: see Tables I and II, R coefficient – Pearson correlation between variables and MMSE score
with AF has been confirmed by recent large-scale studies
[14]. However, it is unknown whether there is
a concomitant reduction in silent cerebral infarcts and
the incidence of vascular dementia. In a substudy
of the prospective AFFIRM study concerning patients with
AF, functional status of patients, including MMSE, was
examined to determine whether some differences in
functional status outcome between rate-control and
rhythm-control strategy were present [15]. There were no
significant differences between the two arms. Adjusted
MMSE scores were about 28 and did not differ significantly
between treatment groups, in analyses based on actual
rhythm present at follow-up, or after adding warfarin use
to the analyses. College education was the only covariate
significantly associated with MMSE. Age was the only
significant covariate associated with change in MMSE
score over the course of 4 years. Patients ≥ 65 years old
experienced a decrease of 0.28 points per year more than
patients < 65 years of age [15]. The group of patients in
our study was older (75.8 vs. 69.8 years old), with more
serious LV impairment (EF 44-46 vs. 66-70%) and less often
anticoagulated (55 vs. 90-95% subjects) than patients in
the AFFIRM study.
In a previous study of elderly patients with non-valvular
chronic AF, in which the use or dose of anticoagulation
was low, age and the number of lacunar lesions were
associated with lower MMSE scores [16]. In the AFFIRM
Kardiologia Polska 2009; 67: 5
study, anticoagulation use was high with no significant
difference in stroke rates between groups, which may
explain the lack of detection of differences in cognitive
function in AF patients, if these differences depended upon
the relative incidences of cerebrovascular events. There is
a question whether better adherence to recommendations
for warfarin therapy in AF could improve cognitive function
in our group of patients. There is evidence that many
patients with AF do not receive recommended treatment.
In a study of 405 patients with AF, only 51% were
discharged from the hospital with a prescription for
warfarin, and fewer than half of patients over age 80
received warfarin [17]. It is well known that antithrombotic
therapy is underused in elderly patients with AF [18].
Though almost 80% used acenocoumarol or aspirin in our
study only a small number of them were treated with
a proper dose of these drugs. Probably cognitive
impairment is one of many reasons for antithrombotic
undertreatment in AF patients. Richards et al. [19] reported
that patients at risk of cardiovascular disease who received
primary preventive treatment with low-dose aspirin and/or
warfarin performed better in cognitive tests than
the placebo group.
Atrial fibrillation results not only in thromboembolism
but also in reduced cardiac output. The decrease in cardiac
output may be induced by heart failure. In our study
over 80% of patients had moderate heart failure (NYHA
491
Cognitive disorders in elderly patients with permanent atrial fibrillation
class II and III) in both groups. Cognitive impairment is
increasingly recognised as an important concomitant
condition of heart failure. A cross-sectional community study
of 1075 persons, aged more than 65 years, found a 1.96
(95% CI 1.07-3.58) times higher risk of cognitive impairment
in patients with heart failure than in those without [20].
Subjects with cardiac failure and AF often have multiple
vascular risk factors and may have multiple medical
comorbidities, including ischaemic heart disease,
hypertension, diabetes, renal disease, hepatic dysfunction,
depression, Alzheimer’s disease and sleep apnoea. Many
of these comorbidities are well-established risk factors for
cognitive impairment [21]. A major question regarding
the relationship between cognitive impairment and heart
failure is whether the change in cognitive status is caused
at least in part by cerebral hypoperfusion secondary to low
cardiac output due to LV dysfunction. The reduction
of cardiac output is greater at fast ventricular rates and may
lead to cerebral hypoperfusion episodes related to
beat-to-beat variability in length of cardiac cycles and finally
diffuse hypoxic brain damage. Chronic AF could lead to
long-standing cerebral hypoperfusion. Therefore, if
restoration of a regular sinus rhythm is impossible,
the control of ventricular rate in AF leads to a remarkable
improvement in cardiac performance and cerebral perfusion.
The results of our study are in accordance with several
previous reports but conflict with the study of Park et al.
[22]. An association between cognitive impairment and AF
was found in the Rotterdam prospective cohort study [23],
in a cross-sectional study of elderly Swedish men [24] and
in the Jóźwiak et al. study [25]. O’Connell JE et al. [26]
demonstrated that older people with non-valvular AF and
no clinical history of stroke had a poorer performance on
detailed neuropsychological testing than matched controls
in sinus rhythm. Similar results were published by Farina
et al. [27] and Sabatini [9]. However, Park et al. [22] did not
find an association between overall cognitive decline and
non-valvular AF after 3 years’ follow-up, or any apparent
effect of anti-thrombotic therapy. Patients in our study were
older, AF lasted longer and cognitive decline is probably
a multifactorial disorder. Although North American and
European meta-analyses showed that rhythm control was
not superior to rate control in a population of older patients
with recurrent persistent AF, it is not so clear regarding
cognitive functions in these patients [28-30]. There is no
evidence of whether proper anticoagulation substantially
reduces the cognitive decline at the same stage as
the incidence of clinical cerebral infarctions in AF [31].
The limitations of our study were the relatively small
number of patients and the use of only one method
of impaired cognitive function assessment. Therefore, this
is a pilot study. Further prospective studies should address
these unresolved issues.
In conclusion, cognitive impairment in older patients
is a multifactorial disorder. One of the causes of low
cognitive function in these patients appears to be
permanent AF. Further prospective clinical trials should
help determine the possible role of inadequate
anticoagulant treatment, and its association with
the deterioration of cognitive function in AF patients.
References
1. Kannel WB, Abbott RD, Savage DD, et al. Epidemiologic features
of chronic atrial fibrillation: the Framingham Study. N Engl
J Med 1982; 306: 1018-22.
2. Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an
independent risk factor for stroke: the Framingham Study.
Stroke 1991; 22: 983-8.
3. Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation: a major
contributor to stroke in the elderly. The Framingham Study. Arch
Intern Med 1987; 147: 1561-4.
4. EAFT Study Group. European Atrial Fibrillation Trial. Silent brain
infarction in nonrheumatic atrial fibrillation. Neurology 1996;
46: 159-65.
5. Ezekowitz MD, James KE, Nazarian SM, et al., for the Veterans
Affairs Stroke Prevention in Nonrheumatic Atrial Fibrillation
Investigators. Silent cerebral infarction in patients with
nonrheumatic atrial fibrillation. Circulation 1995; 92: 2178-82.
6. Devereaux RB, Reichek N. Echocardiographic determination of left
ventricular mass in man. Anatomic validation of the method.
Circulation 1977; 55: 613-8.
7. Folstein MF, Folstein S, McHugh PR. Mini-mental state. A practical
method for grading cognitive state of patients for the clinitian.
J Psychiatr Res 1975; 12: 189-98.
8. Brink TL, Yesavage JA, Lum O, et al. Screening tests for geriatric
depression. Clin Gerontol 1982; 1: 37-43.
9. Sabatini T, Frisoni GB, Barbisoni P, et al. Atrial fibrillation and
cognitive disorders in older people. J Am Geriatr Soc 2000; 48:
387-90.
10. Hansson L, Lithell H, Skoog I, et al. Study on COgnition and
Prognosis in the Elderly (SCOPE): baseline characteristics. Blood
Press 2000; 9: 146-51.
11. Katz S, Ford AB, Moskowitz RW, et al. Studies of illness in the aged.
The index of ADL: a standardized measure of biological and
psychosocial function. JAMA 1963; 185: 914-9.
12. Feinberg WM, Seeger JF, Carmody RF, et al. Epidemiologic features
of asymptomatic cerebral infarction in patients with nonvalvular
atrial fibrillation. Arch Intern Med 1990; 150: 2340-4.
13. Kempster PA, Gerraty RP, Gates PC. Asymptomatic cerebral
infarction in chronic atrial fibrillation. Stroke 1988; 19: 955-7.
14. Atrial Fibrilation Investigators. Risk factosr for stroke and efficacy
of antithrombotic treatment in atrial fibrillation: analysis of pooled
data from randomized controlled trials. Arch Intern Med
1994; 154: 1449-57.
15. Chung MK, Shemanski L, Sherman DG, et al. Functional status in
rate versus rhythm control strategies for atrial fibrillation. Results
of the Atrial Fibrillation Follow-up Investigation of Rhythm
Management (AFFIRM) functional status substudy. J Am Coll
Cardiol 2005; 46: 1891-9.
16. Zito M, Muscari A, Marini E, et al. Silent lacunar infarcts in elderly
patients with chronic nonvalvular atrial fibrillation. Aging
(Milano) 1996; 8: 341-6.
17. Hylek EM, D’Antonio J, Evans-Molina C, et al. Translating the results
of randomized trials into clinical practice: the challenge of warfarin
Kardiologia Polska 2009; 67: 5
492
candidacy among hospitalized elderly patients with atrial
fibrillation. Stroke 2006; 37: 1075-80.
18. Jacobs LG. The sin of omission: a systemic review of antithrombotic
therapy to prevent stroke in atrial fibrillation. J Am Geriatr
Soc 2001; 49: 91-4.
19. Richards M, Meade TW, Peart S, et al. Is there any evidence for
a protective effect of antithrombotic medication on cognitive
function in men at risk of cardiovascular disease? Some preliminary
findings. J Neurol Neurosurg Psychiatry 1997; 62: 269-72.
20. Pullicino PM, Wadley VG, McClure LA, et al. Factors contributing
to global cognitive impairment in heart failure: results from
a population-based cohort. J Card Fail 2008; 14: 290-5.
21. Knopman D, Boland LL, Mosley T, et al. Cardiovascular risk factors and
cognitive decline in middle-aged adults. Neurology 2001; 56: 42-8.
22. Park H, Hildreth A, Thomson R, et al. Non-valvular atrial fibrillation
and cognitive decline: a longitudinal cohort study. Age
Ageing 2007; 36: 157-63.
23. Ott A, Breteler MBM, de Bruyne MC, et al. Atrial fibrillation and
dementia in a population-based study. The Rotterdam Study.
Stroke 1997; 28: 316-21.
24. Kilander L, Andren B, Nyman H, et al. Atrial fibrillation is an
independent determinant of low cognitive function. A cross-sectional
study in elderly men. Stroke 1998; 29: 1816-20.
25. Jóźwiak A, Guzik P, Mathew A, et al. Association of atrial
fibrillation and focal neurologic deficits with impaired cognitive
Kardiologia Polska 2009; 67: 5
Beata Wożakowska-Kapłon et al.
function in hospitalized patients? 65 years of age. Am
J Cardiol 2006; 98: 1238-41.
26. O’Connell JE, Gray CS, French JM, et al. Atrial fibrillation and
cognitive function: case-control study. J Neurol Neurosurg
Psychiatry 1998; 65: 386-9.
27. Farina E, Magni E, Ambrosisni F, et al. Neuropsychological deficits
in asymptomatic atrial fibrillation. Acta Neurol Scand 1997; 96:
310-6.
28. The Atrial Fibrillation Follow-Up Investigation of Rhythm
Management (AFFIRM) Investigators. A comparison of rate
control and rhythm control in patients with atrial fibrillation.
N Engl J Med 2002; 347: 1825-33.
29. Hohnloser SF, Kuck KH, Lilienthal J. Rhythm or rate control in
atrial fibrillation- pharmacological intervention in atrial
fibrillation (PIAF): a randomised trial. Lancet 2000; 356:
1789-94.
30. Van Gelder IC, Hagens VE, Bosker HA, et al. A comparison
of rate control and rhythm control in patients with recurrent
persistent atrial fibrillation. New Engl J Med 2002; 347:
1834-40.
31. Rastas S, Verkkoniemi A, Polvikoski T, et al. Atrial fibrillation,
stroke, and cognition: a longitudinal population-based study
of people aged 85 and older. Stroke 2007; 38: 1454-60.
493
Upośledzenie funkcji poznawczych u chorych
z utrwalonym migotaniem przedsionków
Beata Wożakowska-Kapłon1, 2, Grzegorz Opolski3, Dariusz Kosior3, Elżbieta Jaskulska -Niedziela1,
Ewa Maroszyńska -Dmoch1, Monika Włosowicz1
1I
Oddział Kardiologii, Świętokrzyskie Centrum Kardiologii, Kielce
Nauk o Zdrowiu, Uniwersytet Humanistyczno-Przyrodniczy Jana Kochanowskiego, Kielce
3 I Katedra i Klinika Kardiologii, Warszawski Uniwersytet Medyczny
2 Wydział
Streszczenie
Wstęp: Migotanie przedsionków (ang. atrial fibrillation, AF) stanowi czynnik ryzyka powikłań zakrzepowo-zatorowych, które
występują rocznie u 4,5% chorych z AF. U osób z tą arytmią powyżej 80. roku życia AF jest główną przyczyną dużych udarów mózgu.
U ponad 25% chorych cierpiących na AF, pomimo braku zauważalnych ubytków neurologicznych, w badaniu tomograficznym stwierdza
się cechy jednego lub kilku (niemych klinicznie) ognisk udarowych.
Cel: Porównanie funkcji poznawczych u chorych z utrwalonym AF i w grupie osób o podobnym profilu klinicznym z rytmem
zatokowym.
Metody: Kryteria włączenia obejmowały wiek powyżej 65 lat, brak wcześniej stwierdzanej choroby naczyniowej mózgu lub
otępienia, utrwaloną arytmię trwającą powyżej 12 miesięcy. Do badania włączono 51 osób z AF w średnim wieku 75,8 roku. Grupa
kontrolna składała się z 43 chorych w podobnym wieku, o podobnym rozkładzie płci, z podobnymi chorobami towarzyszącymi, ale
z rytmem zatokowym. Protokół badania obejmował wywiad i badanie przedmiotowe, diagnostykę biochemiczną, standardowy
zapis 12-odprowadzeniowego EKG i badanie echokardiograficzne przezklatkowe.
Wyniki: Migotanie przedsionków trwało w badanej grupie średnio 4,9 roku (1–21 lat). Spośród 51 badanych osób nadciśnienie
tętnicze miało 51%, chorobę niedokrwienną serca 37%, u 12% stwierdzano niewydolność węzła zatokowego lub zaawansowany blok
przedsionkowo-komorowy i implantowany rozrusznik serca. Nie stwierdzano istotnych różnic między grupami, chociaż osoby z AF
częściej miały przerost mięśnia lewej komory i zawał serca w wywiadzie. Chorzy w grupie kontrolnej rzadziej otrzymywali terapię
przeciwkrzepliwą antagonistami witaminy K, chociaż w obu grupach, a zwłaszcza z AF, stwierdzano niewystarczającą terapię
przeciwkrzepliwą (nieuzyskanie terapeutycznych wartości INR) u osób ze wskazaniami do takiej terapii. Zdolności poznawcze oceniano
za pomocą testu MMSE (Mini Mental State Examination). U chorych z AF liczba punktów uzyskana w teście MMSE była istotnie
niższa w porównaniu z grupą kontrolną 24,8 ± 3,1 vs 27,1 ± 2,6 (p < 0,05). W grupie AF upośledzenie funkcji poznawczych rozpoznano
u 43% badanych, natomiast w grupie kontrolnej u 14%.
Wnioski: Wydaje się, że utrwalone AF u chorych powyżej 65. roku życia pogarsza funkcje poznawcze w porównaniu z osobami
z rytmem zatokowym.
Słowa kluczowe: migotanie przedsionków, chorzy starsi, upośledzenie funkcji poznawczych
Kardiol Pol 2009; 67: 487-493
Adres do korespondencji:
dr hab. n. med. Beata Wożakowska-Kapłon, I Oddział Kardiologii, Świętokrzyskie Centrum Kardiologii, ul. Grunwaldzka 45, 25-736 Kielce,
tel.: +48 41 367 13 01, e-mail: [email protected]
Praca wpłynęła: 20.07.2008. Zaakceptowana do druku: 05.02.2009.
Kardiologia Polska 2009; 67: 5