Cognitive disorders in elderly patients with permanent atrial fibrillation
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Beeaattaa WWoożżaakkoowwsskkaa--KKaappłłoonn11,, 22,, GGrrzzeeggoorrzz OOppoollsskkii33,, DDaarriiuusszz KKoossiioorr33,, EEllżżbbiieettaa JJaasskkuullsskkaa--NNiieeddzziieellaa11,, E
Ewwaa MMaarroosszzyyńńsskkaa--DDmmoocchh11,, MMoonniikkaa WWłłoossoowwiicczz11
11stDepartment of Cardiology, Centre of Cardiology, Kielce, Poland
2 Health Sciences Department, University of Jan Kochanowski, Kielce, Poland
31stDepartment of Cardiology, Medical University, Warsaw, Poland
A b s t r a c t B
Baacckkggrroouunndd:: 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.
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Aiimm:: To investigate whether cognitive function in patients with permanent AF is significantly worse than in patients with sinus rhythm.
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Meetthhooddss:: 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).
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Reessuullttss:: 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.
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Coonncclluussiioonnss:: 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.
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Keeyy wwoorrddss:: atrial fibrillation, elderly population, cognitive disorders
Kardiol Pol 2009; 67: 487-493
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: bw.kaplon@poczta.onet.pl
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Reecceeiivveedd:: 20 July 2008. AAcccceepptteedd:: 05 February 2009.
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].
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.
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,
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 A
AFF ggrroouupp CCoonnttrrooll ggrroouupp pp n
n == 5511 nn == 4433
Age [years] 75.8 (66-95)* 74.9 (66-93) NS
Gender [male/female] 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 26 (51%) 23 (53%) NS
coronary artery disease 19 (37%) 15 (35%) NS
SSS/AV block (VVI pacemaker) 6 (12%) 5 (12%) NS
NYHA class
I 6 (12%) 8 (18%) NS
II 16 (31%) 11 (26%) NS
III 29 (57%) 24 (56%) NS
Medication at enrolment
digoxin 18 (36%) 15 (35%) NS
ACE inhibitors 39 (76%) 30 (70%) NS
diuretics 24 (47%) 22 (52%) NS
beta-blockers 23 (45%) 20 (48%) NS
calcium antagonists 21 (31%) 17 (39%) NS
AT1-receptor blockade 4 (8%) 4 (9%) NS
statins 23 (45%) 17 (40%) NS
acenocoumarol 28 (55%) 7 (17%) < 0.05
aspirin (75/150 mg) 11 (22%) 9/2 22 (52%) 20/2 < 0.05
INR (in patients treated with AC) 1.32 ± 0.6 1.46 ± 0.7 NS
Effective anticoagulation (INR 2-3) 8/28 (29%) 3/7 (43%) #
Systolic BP [mmHg] 142 ± 23 137 ± 19 NS
HR [beats/min] 88 ± 11 71 ± 13 < 0.05
LVH (LVMI ≥ 135 M, ≥ 110g/m2F) 20 (39%) 9 (21%) < 0.05
LVEF [%] 44 ± 11 46.3 ± 12 NS
T
Taabbllee II.. Patients’ baseline characteristics
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
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
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 A
AFF ggrroouupp CCoonnttrrooll ggrroouupp pp n
n == 5511 nn == 4433
ADL score 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
T
Taabbllee IIII.. Comparison of activities of daily living and MMSE score between groups
Abbreviations: ADL – activities of daily living
V
Vaarriiaabbllee AAllll ppaattiieennttss ((nn == 9944)) U
Unniivvaarriiaattee aannaallyyssiiss MMuullttiivvaarriiaattee aannaallyyssiiss R
R ccooeeffffiicciieenntt pp RR ccooeeffffiicciieenntt pp
Age –0.21 < 0.05 –0.14 0.06
AF –1.50 < 0.0001 –1.82 < 0.0007
AF duration –0.08 0.67 - -
Education [years] 0.47 < 0.01 0.23 0.37
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 - -
T
Taabbllee IIIIII.. Correlation between clinical and echocardiographic variables and MMSE score
Abbreviations: see Tables I and II, R coefficient – Pearson correlation between variables and MMSE score
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.
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Upośledzenie funkcji poznawczych u chorych z utrwalonym migotaniem przedsionków
B
Beeaattaa WWoożżaakkoowwsskkaa--KKaappłłoonn11,, 22,, GGrrzzeeggoorrzz OOppoollsskkii33,, DDaarriiuusszz KKoossiioorr33,, EEllżżbbiieettaa JJaasskkuullsskkaa--NNiieeddzziieellaa11,, E
Ewwaa MMaarroosszzyyńńsskkaa--DDmmoocchh11,, MMoonniikkaa WWłłoossoowwiicczz11
1I Oddział Kardiologii, Świętokrzyskie Centrum Kardiologii, Kielce
2 Wydział Nauk o Zdrowiu, Uniwersytet Humanistyczno-Przyrodniczy Jana Kochanowskiego, Kielce
3I Katedra i Klinika Kardiologii, Warszawski Uniwersytet Medyczny
S t r e s z c z e n i e W
Wssttęępp:: 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.
C
Ceell:: Porównanie funkcji poznawczych u chorych z utrwalonym AF i w grupie osób o podobnym profilu klinicznym z rytmem zatokowym.
M
Meettooddyy:: 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.
W
Wyynniikkii:: 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%.
W
Wnniioosskkii:: Wydaje się, że utrwalone AF u chorych powyżej 65. roku życia pogarsza funkcje poznawcze w porównaniu z osobami z rytmem zatokowym.
S
Słłoowwaa kklluucczzoowwee: 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: bw.kaplon@poczta.onet.pl
P
Prraaccaa wwppłłyynnęęłłaa:: 20.07.2008. ZZaaaakkcceeppttoowwaannaa ddoo ddrruukkuu:: 05.02.2009.
