Research Article - (2015) Volume 3, Issue 1

Non Valvular Atrial Fibrillation Related Ischaemic Stroke at the Teaching Hospital of Yalgado Ouedraogo, Burkina Faso

Mandi D Germain1, Samadoulougou K André1,2, Yaméogo R Aristide1*, Millogo RC Georges1,2, Naïbé D Temoua1, Kaboré PK Hervé1, Kologo K Jonas1 and Zabsonré Patrice1,2
1Service de Cardiologie du Centre Hospitalier Universitaire Yalgado Ouédraogo (CHU-YO), Burkina Faso
2Unité de Formation et de Recherche en Sciences de la Santé/ Université de Ouagadougou, Burkina Faso
*Corresponding Author: Yaméogo R Aristide, Service de Cardiologie du Centre Hospitalier Universitaire Yalgado Ouédraogo (CHU-YO), P.O: 11 BP 804 CMS Ouagadougou 11, Burkina Faso, Tel: 00226-66 48 58 58 Email:

Abstract

Objectives: We aim to describe the epidemiological and prognostic characteristics of non valvular atrial fibrillation related stroke.
Patients and methods: We retrospectively analyzed data of hospitalized patients from January 1st 2010 to June 30th 2012 in the two contiguous departments of cardiology and neurology, at the teaching hospital of Yalgado Ouédraogo, Burkina Faso.
Results: We recorded 391 cases of ischaemic stroke. Cardioembolic stroke was observed in 159 patients out of who, non valvular atrial fibrillation accounted for 43.5%. Atrial fibrillation was persistent/permanent in 60 cases (87%). The mean age ± SD was 63.3 ± 14.2 years (extremes: 26-91 years). Hypertension was observed in 85.5% of the cases. The mean CHA2 DS2 -VASc score was 4.72 ± 1.16. The mean HAS-BLED score was 2.35 ± 0.92 with a low to intermediate bleeding risk score (≤ 2) in 60.9 % of patients. The rate of vitamin K antagonists use was 52%. They were introduced at least a week after stroke onset in 34 cases. A mean follow up of two weeks in hospital noticed haemorrhagic transformation and ischaemic recurrence in respectively 8.7% and 2.9% of the cases. Mortality rate of 21.7% during hospitalization was predicted by large sized cerebral infarction and congestive heart failure (p<0.05).
Conclusion: Non valvular atrial fibrillation stroke is associated with in-hospital high mortality and is subject to early recurrence.

Keywords: Ischaemic stroke; Non valvular atrial fibrillation; Anticoagulation; Hemorrhagic transformation; Mortality; Burkina Faso

Introduction

Ischaemic stroke is a leading cause of acquired disability and death in adults [1]. Cardioembolic stroke accounts for 14-30% of all ischaemic strokes and appears to be associated with higher mortality and early recurrence [2,3]. Atrial fibrillation (AF) is the most common cardiac source of cerebral embolism with many associated risk factors [4,5]. Managing AF alone or with stroke is challenging and costly [6-8]. Data regarding AF related stroke are scarce in Sub-Saharan African including Burkina Faso. We aim to describe the epidemiological and prognostic characteristics of Non Valvular Atrial Fibrillation (NVAF) related stroke during hospitalization period.

Patients and Methods

We retrospectively analyzed data of hospitalized patients from January 1st 2010 to June 30th 2012 in the two contiguous departments of cardiology and neurology, at the teaching hospital of Yalgado Ouédraogo, Burkina Faso, west Africa. Those were included in the study, patients with ischaemic stroke diagnosed by cranial Computed Tomographic (CT) scan and/or by clinical stroke (persistence of focal neurological symptoms for over 24 hours period) who presented AF confirmed by a standard 12-lead electrocardiogram (ECG) or 24-hours Holter ECG. Transthoracic echocardiography (TTE) was used to screen patients with non valvular AF in the absence of rheumatic or degenerative cardiac valvular disease and valvular prosthesis.

TTE and transoesophageal echocardiography (TOE) were performed to look for other concomitant cardiac sources of cerebral embolism [9]. Doppler ultrasonography was used to eliminate cervical large-artery atherosclerotic sources of embolism (obstructive carotid and vertebro-basilar artery disease).

Lone AF was defined as a condition without associated concomitant cardiac source of embolism. The cerebral infarction was assumed largesized in case of infarct diameter above 30 mm at baseline. Congestive heart failure included shortness of breath weakness, edema, rales, rhonchi, or wheezes, presence of a third or fourth heart sound. Left ventricular ejection fraction (LVEF) was assessed by TTE in all patients. Urban area was defined by both Ouagadougou and Bobo- Dioulasso, the two biggest cities of Burkina Faso where International Normalized Ratio (INR) could be performed. Thromboembolic risk was evaluated according to CHA2DS2Vasc score [10]. Bleeding risk stratification was based on HAS-BLED score [11]. Cardiovascular vascular risk factors were evaluated according to the 2013 European Society of Hypertension/European Society of Cardiology [12].

For statistical analysis, EPI info TM software (version 7.0.9.34) was used. The categorical variables were expressed as percentages. Continuous variables were expressed in terms of means ± SD. Chi square test or Fisher’s exact test were used for proportions comparison as appropriate. A logistic regression model was used to identify risk factors independently associated with death. For each analysis, a significant difference was defined as p<0.05.

Results

During the study period, 2010 patients were hospitalized at both departments. We recorded 391 cases of ischaemic stroke. Cardioembolic stroke was observed in 159 patients out of who, NVAF accounted for 43.5% (43 females and 26 males). Atrial fibrillation was persistent/ permanent in 60 cases (87%) and paroxystic in nine cases (13%). The mean age was 63.3 ± 14.2 years (extremes: 26-91 years). Forty five patients (65.2%) were ≥ 60 years old. Cardiovascular risk factors included hypertension in 85.5% (n=59), dyslipidemia in 24.6% (n=17) and diabetes in 21.7% (n=15) of patients. Alcohol abuse was observed in 25 cases (36.2%). Neurological deficit occurred in 63 cases and congestive heart failure was noticed in nine patients. The sociodemographic and clinical characteristics of the study patients at admission are shown in Table 1.

Characteristic Number (n) Percentage (%)
Mean age (years) 63.3 ± 14.2 -
Age rage
<60 11 16
60-74 45 65.2
≥75 13 18.8
Sex Females/Males 43/26 62.3/37.7
Type of atrial fibrillation
Paroxystic 9 13
Persistent 17 24.6
Long-standing persistent 19 27.5
Permanent 24 34.8
Cardiovascularriskfactors
Hypertension 59 85.5
Dyslipidemia 17 24.6
Smoking 17 24.6
Diabetesmellitus 15 21.7
Obesity 10 14.5
Prior ischaemic stroke 12 17.4
Clinicalfeatures
Congestive heartfailure 9 13
Pure motorweakness 63 91.3
Impaired verbal processing 42 60.9
Weakness of face 26 37.7
Association of the three types of deficit 43 62.3
Syncope 21 30.4
Alteredconsciousness 11 16
Palpitations 19 27.5
Ongoingantiplatelettherapy 19 27.5

Table 1: Socio-demographic and clinical characteristics of study patients at baseline.

Cranial CT scan was normal in four cases (5.8%) and found a hypodensity in 65 cases (94.2%). The localization of such lesion was unique in 61.5% and had multiple foci in 38.5% of patients. The cerebral infarct was large-sized in 18 patients (27.7%).

Concomitant potential cardiac sources of ischaemic stroke were noticed in 45 cases (65.2%). These underlying sources included hypertensive dilated cardiomyopathy in 15 cases and left sided thrombus in 10 cases (Table 2). Mean LVEF was 61.6% ± 14.6 (28- 80). Eight patients had a LVEF<40% and eleven had a LVEF between 40 and 54%. Cervical arterial Doppler ultrasonography performed in 28 patients has shown plaque in 23 cases without significant atherothrombotic stenosis (< 50%).

Concomitant potentialcardiac sources of embolism Number (n) Percentage (%)
 High-risk sources of embolism
Hypertensive dilatedcardiomyopathy 15 21.7
Cardiothyreosis† 2 2.9
Leftsided thrombus 10 14.5
Restrictive cardiomyopathy 4 5.8
Medium-risk sources of embolism
Spontaneousechocontrast 16 23.2
Hypertrophic hypertensive cardiomyopathy 2 2.9
Ischaemiccardiomyopathy (>4 weeks) 5 7.3
Patent foramen ovale 2 2.9
Communicant interatrial septal aneurysm 1 1.4

Table 2: Concomitant potential cardiac sources of cerebral embolism in 69 patients (†with dilated left cavities).

The mean CHA2DS2-VASc score was 4.72 ± 1.16 (extremes 2 and 7) and all patients had high thromboembolic risk. The mean HAS-BLED score was 2.35 ± 0.92 (extremes: 1 and 5) with a low to intermediate bleeding risk score (≤ 2) in 60.9 % of patients (Figure 1). Characteristics comprising both CHA2DS2-Vasc stroke risk score and HAS-BLED bleeding risk are shown in Table 3.

vascular-medicine-surgery-distribution-patients-atrial

Figure 1: Distribution of all 69 patients with non valvular atrial fibrillation according to CHA2DS2-Vasc and HAS-BLED scores.

Risk factor Number Percentage
Thromboembolic risk factors (CHA2DS2-Vasc)
Congestive heartfailure/ LVEF<0,40 14 20.3
Hypertension 59 85.5
Age ≥ 75 years 13 18.8
Diabetesmellitus 15 21.7
Ischaemic stroke 69 100.0
Vasculardisease 5 7.2
Age 65-74 years 23 33.3
Femalesex 43 62.3
Bleedingriskfactors(HAS-BLED)
Hypertension (SBP >160 mmHg) 5 7.2
Alteredkidneyfunction 12 17.4
Hepaticfunctionimpairment 0 0.0
Stroke 69 100.0
Bleeding 0 0.0
Labile INRs 0 0.0
Age>65 years 36 52.2
Antiplatelettherapy 19 27.5
Alcohol 25 36.2

Table 3: Distribution of CHA2DS2-Vasc and HAS-BLED scores risk factors in study patients (LVEF: left ventricular ejection fraction; SBP: systolic blood pressure; INR: International Normalized Ratio).

Low molecular weight heparin (LMWH), enoxaparin in our context was used for secondary prevention of stroke recurrence in 55 patients before switching to vitamin K antagonist (VKA) in 36 cases (52%). VKA were introduced at least a week after stroke onset in 34 cases and sooner in two cases. VKA were prescribed in 60.9% (n=31) of 51 patients without large sized cerebral infarction versus 27.8% (n=5) of those with larger cerebral infarction (RR=2.19; CI95%=[1.01-4.76]; p=0.02). VKA treatment was observed in 66.7% of the 42 patients from urban area versus 29.6% of 27 patients from other areas (RR=2.25; CI95%=[1.21-4.18]; p=0.003). Antiplatelet therapy was prescribed in 94.2% of the study patients. It was associated with VKA in 35 cases and used alone in 14 patients. Ventricular rate control was obtained using antiarrhythmic drug in 55% of the cases comprising amiodarone (n=14), β-blockers (n=19) and digoxine (n=5). Table 4 indicates therapy received by study population during hospitalization period.

Treatment Number Percentage (%)
Anticoagulants 55 79,7
LMWH alone 19 27,5
LMWH VKA 36 52,0
None 14 20,3
Antiplatelettherapy 65 94,2
Alone 14 20,3
With VKA 35 50,7
With LMWH 16 23,2
None   4   5,8
Antiarrhythmicdrugs
Digoxin   5   7,3
Amiodarone 14 20,3
β-blockers 19 27,5
Otherdrugs
ACE/ARBs 55 79,7
Statins 51 74,0
Earlyrehabilitation 55 79,7

Table 4: Distribution of study treatment in 69 patients during hospitalization period (LMWH: low molecular weight heparin (enoxaparin), VKA: vitamin K antagonist; ACE: angiotensin-converting enzyme inhibitors; ARBs: angiotensin receptor blockers).

A mean follow up of 12.8 days ± 7.8 (extremes: two and 45 days) in hospital noticed complete regression of neurological deficit in 18 patients (26.1%). Complications were observed in 17 patients including haemorrhagic transformation in 8.7% (n=6), seizures in 8.7% (n=6) and ischaemic stroke recurrence in 2.9% (n=3). Five out of 18 patients with larger cerebral infarct developed haemorrhagic transformation (RR=14.17; CI95%=[1.77-113.25]; p=0.003). Only three patients among those under VKA (n=36) developed haemorrhagic transformation (RR=0.41; CI95%=[0.09 – 2.34]; p=0.46). Mortality rate during hospitalization period was 21.7% (n=15). It was associated on univariate analysis with older age ≥ 75 years, large sized cerebral infarct, haemorrhagic transformation and congestive heart failure. On multivariate analysis, large sized cerebral infarct and congestive heart failure were independent and significant predictor death (Table 5). Immediate cause of death was of cardiac (n=4) and neurological (n=7) origin. Table 6 showed distribution of complications and causes of death in study population.

Factor Death Univariateanalysis Multivariate analysis*
n/N RR (CI 95%) p OR (CI 95%) p
Age (years) <75 9/56 1.00   1.00  
≥ 75 6/13 2.87 (1.24- 6.64) 0.018 4.06 (0.83 – 19.68) 0.082
Congestive heart failure Non 10/60 1.00   1.00  
Oui 5/9 3.33 (1.48- 7.52) 0.019 6.32 (1.04 – 38.37) 0.045
Haemorrhagic transformation Non 11/63 1.00   1.00  
Oui 4/6 3.82 (1.75- 8.33) 0.018 3.77 (0.39 – 36.53) 0.252
Infarct size (cm) <3 6/51 1.00   1.00  
≥ 3 9/18 4.25 (1.76-10.27) <0.001 4.40 (1.01 – 19.26) 0.049

Table 5: Factors associated with death on univariate and multivariate analysis in the 69 study patients during hospitalization period (RR: Risk ratio; OR: Odds Ratio; CI 95%: confident Interval at 95% of association measure; *Adjustment for variables listed on the table).

  Number (n) Percentage (%)
Complications
Haemorrhagic transformation 6 8.7
Stroke recurrence 2 2.9
Seizures 6 8.7
Mesentericinfarction 1 1.5
Venousthromboembolicdisease 1 1.5
Pressure ulcers 1 1.5
Causes of death
Congestive heartfailure 4 -
Cerebralherniation 3 -
Haemorrhagic transformation 2 -
Stroke recurrence 2 -
Sepsis 3 -
Mesentericinfarction 1 -

Table 6: Complications occurred during hospitalization period and immediate causes of death in all 69 patients with atrial fibrillation.

Discussion

The retrospective pattern of the study and lack of ambulatory follow up data may have underestimated the assessment of some parameters. Nevertheless current results gave an overview of the problem in our setting. All study patients did not benefit from large-artery atherosclerosis research based on the fact that it was a retrospective study and we just reported data of those who underwent this Doppler ultrasonography. Moreover Doppler ultrasonography was not performed in patients with an obvious cardiac cause of ischaemic stroke and/or in those who could not afford such exam (knowing Burkina Faso belongs to low income countries with no share care system). Arterial angiography was not available at that time.

NVAF, the most common source of cardioembolic stroke was observed in 43.5% of all cardiac causes of cerebral embolism in our study. Damorou et al. [13] in Togo and Paciaroni et al. [14] in Italia have reported lower rates in patients presenting their first episode of ischaemic stroke with respectively 19.8% and 20.3% of the cases. Conversely, Yip et al. [15] at Taiwan observed 69% of AF in a subgroup of cardioembolic stroke. Discrepancies in rates may be explained by patients’ selection criteria and quality of AF screening methods used after stroke onset. A possible underuse of VKA for primary prevention of thromboembolism in AF may have played a role in low income regions such as Burkina Faso.

NVAF is frequently associated with other cardiac sources of stroke which were similarly found in Kim et al. series [16] and ours with respectively 65.2% and 68% of the cases.

In a Japanese study [17] including 234 patients suffering from NVAF related stroke, AF was classified as paroxystic and permanent in respectively 42.3% and 57.7% of the cases. Our data have supported results from Marini et al. [18] study in Italia with a persistent to permanent AF rate being above 80%. These marked differences in types of AF between studies are probably related to weight carried by 24-hours Holter ECG in detecting paroxystic AF after ischaemic stroke onset. Regardless of the type of AF (paroxystic or permanent), the annual risk of cerebral embolism in the absence antithrombotic treatment is identical and assessed to range from 3 to 5% but widely depends on CHA2DS2-VASc score [6]. The mean CHA2DS2-VASc score in our study was 4.72 and all patients had a score ≥ 2 indicating a very high risk of embolism and a need of antithrombotic treatment except contraindications. Moreover, bleeding risk was low to intermediate (HAS-BLED score: 1-2) in 60.9% of our study patients suggesting safer initiation of anticoagulation therapy. This bleeding risk was high (HASBLED score ≥ 3) in 39.1% of patients indicating cautious introduction of anticoagulation therapy with a close follow-up [19]. Secondary prevention of cerebral embolism in NVAF is widely addressed in series worldwide. Accordingly, it is recommended to quickly start treatment with heparinoïds in patients at very high risk of thromboembolism after an individual assessment of risk/benefit ratios [14,20,21]. For long term secondary prevention of ischaemic stroke in AF, VKA remain the gold standard treatment in reducing the risk of recurrence by 70 % [22]. In a survey of practice patterns of anticoagulation therapy in acute ischaemic stroke in Korea among physicians, the most common method of immediate treatment initiation was heparin followed by warfarin (68%) and then warfarin alone or warfarin with aspirin in the absence of large-sized infarct and haemorrhagic transformation [23]. In the PREFER in AF study, the rate of oral anticoagulation use in 2012 was >80% in Europe including patients at high risk of bleeding since publication of 2010 ESC Guidelines on atrial fibrillation [24]. Only 52% of our study patients benefit from VKA treatment. This relatively low rate of VKA use in our setting is partly due to physician’s worry about bleeding risk and also geographic and financial constraints on accessing frequent International Normalized Ratio (INR) follow-up. However, new oral anticoagulants a great progress in therapeutics could be an alternative to VKA in a near future and modify our practice [3], due to their simpler way of use and comparative reduction of major bleeding risk [25,26].

Early haemorrhagic transformation risk in AF related stroke accounts for 2.7% at one week [3]. Our results supported data from a prospective multicentric study of 1125 patients nevertheless suffering from ischaemic stroke of all origin with a rate of 8.7% and this haemorrhagic transformation is significantly associated with large-sized infarct [27]. Ischaemic stroke recurrence in AF is assessed to be 2.5% and 5% at one week and one month respectively [2,3]. We reported recurrence rate of 2.9% at two weeks period.

Atrial fibrillation related ischaemic stroke is classically severe with high mortality rate during the acute phase in comparison to other sources of cerebral embolism. We found in hospital rate of death (21.7%) that supported data from literature [2,13,28]. Mortality was predicted by large sized cerebral infarct and congestive heart failure (p<0.05). Death in cardioembolic stroke is mainly due to neurological complications and cardiac comorbidities [2].

Conclusion

NVAF related stroke is associated with higher mortality during hospitalization and subject to early recurrence. A better use of international guidelines on primary and secondary prevention of cerebral embolism in AF may contribute to reduce the burden of the problem. Introduction of INR self-measurement equipment in remote areas or new oral anticoagulants could be an alternative way of treatment follow-up in rural and semi-urban areas with poorly equipped hospitals.

Author’s Contribution

All authors did fully participate in the study. Paper writing process was a team work.

Acknowledgements

We are grateful to Professor Jean Kaboré and team for the close collaboration in managing patients between cardiologists and neurologists. Thank you for giving us permission to collect data at neurology department.

References

  1. Mukherjee D, Patil CG (2011) Epidemiology and the global burden of stroke. World Neurosurg 76: 85-90.
  2. Arboix A, Alió J (2010) Cardioembolic stroke: clinical features, specific cardiac disorders and prognosis. CurrCardiol Rev 6: 150-161.
  3. Muresan IP, Alamowitch S (2011) Préventionsecondaire des infarctuscérébrauxliés á l’arythmiecomplète par fibrillation auriculaire :quel(s) traitement(s) et dansquel(s) délai(s)? PratNeurol - FMC 2:6-20.
  4. Lloyd-Jones D, Adams R, Carnethon M, Simone G D, Ferguson T B, et al. (2009) Heart disease and stroke statistics--2009 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 119: 21-181.
  5. Lloyd-Jones DM, Wang TJ, Leip EP, Larson M G, Levy D, et al. (2004) Lifetime risk for development of atrial fibrillation: the Framingham Heart Study. Circulation 110: 1042-1046.
  6. Davy J-M, Roubille F, Tri Cung T (2010) La fibrillation atriale en 2010: unpoids croissant sur la morbidité et la mortalitécardiovasculaires. Ann CardiolAngéiologie 59: 4-13.
  7. Donnan GA, Fisher M, Macleod M, Davis SM (2008) Stroke. Lancet 371: 1612-1623.
  8. De los Ríos la Rosa F, Broderick JP (2013) Toward a modern delivery of stroke care in emerging economies. J Stroke Cerebrovasc Dis Off J Natl Stroke Assoc 22: 1-3.
  9. Adams HP Jr, Bendixen BH, Kappelle LJ, Biller J, Love BB, et al. (1993) Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment. Stroke J CerebCirc 24: 35-41.
  10. Lip GYH, Nieuwlaat R, Pisters R,Lane DA, Crijns H J G M (2010) Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the euro heart survey on atrial fibrillation. Chest 137: 263–272.
  11. Pisters R, Lane DA, Nieuwlaat R, Cees B de Vos, Harry JGM Crijns, et al. (2010) A novel user-friendly score (HAS-BLED) to assess 1-year risk of major bleeding in patients with atrial fibrillation: the Euro Heart Survey. Chest 138: 1093-1100.
  12. Mancia G, Fagard R, Narkiewicz K, Redon J, Zanchetti A, et al. (2013) 2013 ESH/ESC Guidelines for the management of arterial hypertension. Eur Heart J 34: 2159-2219.
  13. Damorou F, Togbossi E, Pessinaba S (2008) Accidents vasculairescérébraux (AVC) et affections cardio-vasculairesemboligènes. Mali Méd 23:31-33.
  14. Paciaroni M, Agnelli G, Micheli S, Caso V (2007) Efficacy and safety of anticoagulant treatment in acute cardioembolic stroke: a meta-analysis of randomized controlled trials. Stroke J CerebCirc 38:423-430.
  15. Yip PK, Jeng JS, Lee TK (1997) Subtypes of ischemic stroke. A hospital-based stroke registry in Taiwan (SCAN-IV). Stroke J CerebCirc 28:2507-2512.
  16. Kim YD, Park B, Cha MJ (2010) Stroke severity in concomitant cardiac sources of embolism in patients with atrial fibrillation. J NeurolSci 298: 23-27.
  17. Deguchi I, Ogawa H, Ohe Y (2013) Rate of antithrombotic drug use and clinical outcomes according to CHADS2 scores in patients with an initial cardioembolic stroke who had nonvalvular atrial fibrillation. J Stroke Cerebrovasc Dis Off J Natl Stroke Assoc 22:846–850.
  18. Marini C, De Santis F, Sacco S (2005) Contribution of atrial fibrillation to incidence and outcome of ischemic stroke: results from a population-based study. Stroke J CerebCirc 36: 1115-1119.
  19. Camm AJ, Kirchhof P, Lip GYH (2010) Guidelines for the management of atrial fibrillation: the Task Force for the Management of Atrial Fibrillation of the European Society of Cardiology (ESC). Eur Heart J 31: 2369-2429.
  20. European Stroke Organisation (ESO) Executive Committee, ESO Writing Committee (2008) Guidelines for management of ischaemic stroke and transient ischaemic attack 2008. Cerebrovasc Dis Basel Switz 25:457-507.
  21. Singer DE, Albers GW, Dalen JE (2008) Antithrombotic therapy in atrial fibrillation: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest 133: 546-592.
  22. Saxena R, Koudstaal PJ (2004) Anticoagulants for preventing stroke in patients with nonrheumatic atrial fibrillation and a history of stroke or transient ischaemic attack. Cochrane Database Syst Rev CD000185.
  23. Lee JH, Park KY, Heo JH, Kwon SU (2011) Immediate Anticoagulation for Acute Cardioembolic Stroke is Still Popular in Selective Cases in Korea. Korean J Stroke 13: 120.
  24. Kirchhof P, Ammentorp B, Darius H, Caterina RD, Heuzey JL, et al. (2013) Management of atrial fibrillation in seven European countries after the publication of the 2010 ESC Guidelines on atrial fibrillation: primary results of the PREventionoFthromboemolic events--European Registry in Atrial Fibrillation (PREFER in AF). Europace 16: 6-14.
  25. Bruins Slot K, Berge E (2013) Factor Xa inhibitors versus vitamin K antagonists for preventing cerebral or systemic embolism in patients with atrial fibrillation. Cochrane Database Syst Rev 8: CD008980.
  26. Sardar P, Chatterjee S, Wu WC, Lichstein E, Ghosh J, et al. (2013) New oral anticoagulants are not superior to warfarin in secondary prevention of stroke or transient ischemic attacks, but lower the risk of intracranial bleeding: insights from a meta-analysis and indirect treatment comparisons. PloS One 8: 77694.
  27. Paciaroni M, Agnelli G, Corea F(2008) Early hemorrhagic transformation of brain infarction: rate, predictive factors, and influence on clinical outcome: results of a prospective multicenter study. Stroke J CerebCirc 39:2249-2256.
  28. Arboix A, García-Eroles L, Massons JB, et al. (2000) Atrial fibrillation and stroke: clinical presentation of cardioembolic versus atherothrombotic infarction. Int J Cardiol 73:33-42.
Citation: Germain MD, André SK, Aristide YR, Georges MRC, Temoua ND, et al. (2015) Non Valvular Atrial Fibrillation Related Ischaemic Stroke at the Teaching Hospital of Yalgado Ouédraogo, Burkina Faso. J Vasc Med Surg 3:171.

Copyright: © 2015 Germain MD, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.