Download and Atrial Fibrillation - Chronic Obstructive Pulmonary Disease

Review Article
iMedPub Journals
Chronic Obstructive Pulmonary Diseases
http://www.imedpub.com/
2016
Vol.1 No.1:2
The Association between Chronic Obstructive Pulmonary Disease (COPD)
and Atrial Fibrillation: A Review
Varun Shah1, Trishla Desai1 and Abhinav Agrawal2,*
1Department
of Internal Medicine, University of Miami/JFK Medical Center Palm Beach Regional GME Consortium, Atlantis, Florida, USA
2Department
of Internal Medicine, Monmouth Medical Center, Long Branch, New Jersey, USA
*Corresponding author: Agrawal A, Chief Resident, Department of Medicine, Monmouth Medical Center, Long Branch, NJ, USA, Tel:
7328612184; E-mail: [email protected]
Rec date: Dec 21, 2015; Acc date: Dec 30, 2015; Pub date: Jan 6, 2016
Copyright: © 2016 Shah V, 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.
Abstract
COPD is one of the leading causes of Mortality &
Morbidity in the US and is associated with a wide variety
of cardiovascular diseases especially arrhythmias, angina,
myocardial infarction and congestive heart failure and is
directly associated with the severity of COPD described in
the GOLD initiative. COPD is an independent risk factor for
AF/AFL. Smoking, hypoxia and inflammation all contribute
to AF in COPD patients mainly via atrial remodeling while
hypercapnia contributes to it via increasing refractoriness
of the atrial musculature and a delay in the return of the
refractoriness to normal after resolution of the
hypercapnia. The most common EKG abnormality found in
patients with COPD is P pulmonale and the PQ interval is
the strongest predictor of developing AF. The P wave
Dispersion (PwD) was also an independent risk factor for
the development of AF and was found to be more in the
acute phase than in the stable phase.
The BODE index, an important prognostic score among
patients hospitalized with a COPD exacerbation has a
direct co relation with the prevalence of AF/AFL while the
DECAF score, which was found to be superior to the CURB
65 score as a mortality predictor for hospitalized patients,
includes AF as one of the criteria. Chronic hypoxemia is
one of the main reasons for altered pulmonary vein
anatomy and hence the presence of COPD was identified
as an independent risk factor for the recurrence of atrial
tachyarrhythmias after catheter ablation in patients with
COPD and the absence of COPD was also found to be an
independent predictor for a successful electrocardioversion. These patients were also found to have an
increased incidence of non-PV foci for the arrhythmias.
Oral glucocorticoids were associated with an increased
risk of developing AF especially high dose steroids. It is
recommended to correct the underlying respiratory
decompensation while treating patients with AF as they
render the treatment of AF ineffective. Nondihydropyridine calcium channel blockers should be used
as first line rate control agents for AF in patients with
concomitant COPD while the β-blockers, sotalol,
propafenone can be used in patients with obstructive lung
disease who do not have bronchospasm.
Keywords:
Chronic obstructive pulmonary disease;
Atrial fibrillation
Introduction
Chronic obstructive pulmonary disease (COPD) is a major
global public health problem. COPD is a common preventable
and treatable disease, which is characterized by persistent
airflow limitation that is usually progressive and associated
with an enhanced chronic inflammatory response in the
airways and the lung to noxious particles or gases. In 2020,
COPD is projected to rank fifth worldwide in terms of burden
of disease and third in terms of mortality [1] though presently
it is the 4th leading cause of Mortality and the 2nd leading
cause of Morbidity in the United States (US) [2].
Extra-pulmonary manifestations of COPD include
cardiovascular disease, skeletal muscle dysfunction,
osteoporosis, metabolic syndrome depression and lung cancer
[1]. COPD is associated with specific electrocardiographic (EKG)
abnormalities while an increased incidence of cardiac
arrhythmias has been reported which includes atrial fibrillation
(AF), atrial flutter (AFL), multifocal atrial tachycardia (MAT) and
non-sustained ventricular tachycardia (NSVT) [3]. It is
estimated that there were approximately 33.5 million people
with AF in 2010 worldwide (20.9 million men [95% uncertainty
interval (UI), 19.5-22.2 million] and 12.6 million women [95%
UI, 12.0-13.7 million]) [4] and it was also estimated that the
burden of AF in the United States alone would increase to atleast 5.6 million by 2050 [5].
COPD and Cardiovascular Disease
Patients with diagnosed and/or undergoing treatment for
COPD are at a substantially increased risk of hospitalizations
and mortality due to heart diseases. In one retrospective
cohort study, the prevalence of cardiovascular diseases (CVD)
was higher in the COPD group than the control group. After all
the cardiovascular risk factors were adjusted for odds ratios of
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prevalence were: arrhythmia 1.76 (confidence interval [CI]:
1.64-1.89), angina 1.61 (CI: 1.47-1.76), acute myocardial
infarction 1.61 (CI: 1.43-1.81), congestive heart failure 3.84 (CI:
3.56-4.14). There was also an increased risk of hospitalization
secondary to cardiovascular causes in the COPD group [6].
The Forced Vital Capacity (FVC), defined as the maximal
volume of air exhaled with maximally forced effort from a
maximal inspiration, Expressed in liters and the Forced
Expiratory Volume in one second (FEV1), defined as the
maximal volume of air exhaled in the first second of a forced
expiration from a position of full inspiration, expressed in liters
are the major determinants of the severity of COPD [1,7]. The
Global Initiative for Chronic Obstructive Lung Diseases (GOLD)
classifies the severity of airflow limitation as determined by
spirometry into 4 grades (GOLD 1, mild, FEV1 ≥80% predicted;
GOLD 2, moderate, FEV1 ≥50% but <80% predicted; GOLD 3,
severe, FEV1 ≥30% but <50% predicted; and GOLD 4, very
severe, FEV1 <30% predicted) using the fixed ratio, postbronchodilator FEV1/FVC <0.7 [1]. An association was also
established between the severity of airflow obstruction based
on the GOLD criteria and the prevalence of CVD which showed
that prevalence of CVD was higher among subjects with GOLD
2 (OR 2.9, 95% CI 2.4 to 3.6) and GOLD 3 or 4 COPD (OR 3.0,
95% CI 2.0 to 4.5), compared with normal subjects [8]. The
Atherosclerosis Risk in Communities (ARIC) cohort study
established an inverse co-relation between the FEV1 and rate
of incident AF which was independent of age, gender, BMI,
smoking and blood pressure [9].
A recent retrospective study showed that of COPD were
associated with an increased likelihood of AF/AFL (23.3% vs.
11.0%, respectively, p<0.0001), NSVT (13.0% vs. 5.9%,
respectively, p<0.0001), and sustained ventricular tachycardia
(SVT; 0.9% vs. 1.6%, respectively, p<0.0001) and that it
remained a significant predictor of AF/AFL and NSVT (p<0.0001
and p<0.0001, respectively) after adjusting for age, gender,
tobacco use, obesity, hypertension, coronary artery disease,
heart failure, diabetes, anemia, cancer, chronic kidney disease,
and rate/rhythm control medications [10]. This article provides
a succinct overview of the association of COPD with AF, the
arrythmogenic mechanisms and potential treatment
strategies.
COPD and Atrial Fibrillation: Potential
Causes of Arrhythmia and EKG
Changes
There seem to be a wide variety of reasons for arrhythmias
to occur in COPD beginning from risk factors, its effect in
altering cardiopulmonary physiology to the treatment of
COPD. Smoking, airway inflammation, hypoxia, hypercapnia,
pulmonary hypertension, β-adrenergic agonist and steroids all
contribute to ultimately causing or worsening AF [11-15].
Shan et al. attempted to postulate the reasoning for the
increased incidence of AF in smokers using a canine model.
They concluded that the pro fibrotic response of nicotine in
upregulation of expression of Transforming Growth Factor Beta
2
1(TGF-β1) and TGF-βRII at the protein level, and a 60-70%
decrease in the levels of miRNAs miR-133 and miR-590 was
critical in atrial remodeling in the canine atrium [16]. Smoking
was found to be an independent risk factor in the recurrence
of AF/AFL after cardioversion in women while an increased risk
of mortality and not arrhythmia was found in men [11].
It has been shown consistently that there exists an inverse
relationship between FEV1, FVC with AF. The Copenhagen City
Heart Study demonstrated that the Risk of new AF at reexamination was 1.8-times higher for FEV1 between 60-80% of
predicted compared with a FEV1 of ≥80% after adjustment for
sex, age, smoking, blood pressure, diabetes and body mass
index. They also showed that the risk of AF hospitalization was
1.3 times more with a FEV1 between 60-80% of predicted and
1.8 times with a FEV1 of ≤60% compared with a FEV1 of ≥80%,
proving that reduced lung function as an independent
predictor of AF [17]. It is well documented that oxidative stress
and inflammation are two of the major factors in the
pathophysiology of COPD and now postulations have also been
made of its impact in atrial remodeling and thus causing and
potentially worsening existing AF [12].
Hypoxia, commonly seen in patients with COPD, causes an
upregulation of Vascular Endothelial Growth Factor (VEGF)
secondary to an increase in Hypoxia-induced transcription
factor-1α (HIF-1α). Matrix metalloproteinase 9 (MMP9)
expression is increased in the atrium in a patient with AF and
potentially causes atrial remodeling. It was shown via
Immunofluorescence that there was excess production and colocalization of HIF-1α, VEGF and MMP-9 within the
endothelium of the atrial arteries in the AF group as compared
to patients without AF [13].
Patients with COPD are prone to have acute exacerbations
of the disease and common causes for this are usually viral
infections of the upper respiratory tract and infections of the
tracheobronchial tree [1]. Terzano et al. showed that
suboptimal pulmonary function, hypercapnia and high values
of pulmonary artery systolic pressure are independent
predictors of incident AF [18]. In their experimental sheep
model, Stevenson et al. showed the hypercapnia caused an
increase in the atrial musculature refractoriness and the
conduction time however, intriguingly, there was a delay in
only the conduction time to return to normal after the
resolution of hypercapnia prompting the theory that this
differential recovery time may be the reason for an increased
incidence of AF observed in the phase of eucapnia [19].
P pulmonale (P wave ≥0.25 mV in the inferior leads) is
usually omnipresent on EKG’s of patients with chronic lung
diseases. Hayashi et al, in a digital analysis of EKG’s in a 25 year
period showed P-wave duration and PQ interval were
significantly longer in the AF group than in the non-AF group
(115.4 ± 17.2 ms vs. 107.0 ± 17.2 ms, P=0.0003 and 166.3 ±
23.9 ms vs. 153.2 ± 25.4 ms, P=0.0001, respectively). They
concluded that the PQ interval is the strongest stratifier for AF
development in patients with P pulmonale [20]. The P wave
dispersion (PwD), which is the difference in the maximum and
minimum duration of the P wave, was also found to be an
independent risk factor associated in the development of AF
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Chronic Obstructive Pulmonary Diseases
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[21] and the PwD was found to be increased more in the acute
phase than in stable phase and is greater in patients with more
frequent exacerbations suggesting that the PwD could be a
target for prediction, prevention and therapy of acute
exacerbation of COPD [22].
The BODE index is a multidimensional 10-point scale which
integrates body mass index, degree of airflow obstruction and
dyspnea and exercise capacity measured in 6-min walk test
and the score is directly proportional with mortality. It was
shown that patient’s with higher BODE index scores had a
significantly greater prevalence of arrythmias including AF/AFL
and SVT [23]. The Dyspnea, Eosinopenia, Consolidation,
Acidemia and atrial Fibrillation (DECAF) score was introduced
by Steer et al, as a predictor of mortality in hospitalized
patients with COPD exacerbations. The DECAF score includes
the 5 strongest predictors of mortality i.e. MRC Dyspnea Score,
eosinopenia, consolidation, acidemia, and atrial fibrillation and
was found to be a stronger than the other predictors like the
CURB65 [24].
COPD and its Effect on Ablation
strategies of AF
COPD has a significant effect on cardiopulmonary physiology
but also has an impact in altering the anatomy of the same
system because of which it affects outcomes of catheter
ablations for AF, its progression and mortality. COPD is
associated with hypoxemia and acidosis, which leads to,
increased pulmonary vascular resistance. This causes an
increased level of inflammatory markers that promotes fibrosis
and thus causes structural remodeling of pulmonary vessels
[25]. A subgroup analysis of the European Heart Survey (EHS)
on AF by de Vos et al, gave rise to the HATCH score while
studying AF progression from paroxysmal to persistent. The
HATCH score was an abbreviation for heart failure, age,
previous episode of transient ischemic attack or stroke, COPD
and hypertension, which were all, found to be independent
predictors of AF progression [26]. In their study, Roh et al.
showed that significant alteration of pulmonary vein (PV)
anatomy was related to arrhythmogenicity. They also showed
that non-PV foci were more common in the chronic lung
disease group (26.7%) than in the control group (5.0%;
P=0.025) and all the non-PV foci were located in the right
atrium [27]. The impact of COPD on outcomes of catheter
ablation in patients with AF in terms of recurrence was
evaluated in a prospective study by Gu et al, which showed
that non-paroxysmal AF (P=0.013, OR=1.767, 95% CI:
1.129-2.765) as well as the presence of COPD (P=0.029,
OR=1.951, 95% CI: 1.070-3.557) were the independent
predictors for higher atrial tachyarrhythmia recurrence [28].
Absence of COPD was found to be an independent predictor
for a successful electro-cardioversion in patients with AF while
the absence of COPD was also an independent predictor of
sinus rhythm at a 1 yr follows up [29].
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COPD Treatment Causing AF
Inhaled bronchodilator medications continue to remain the
mainstay treatment for COPD patients. It includes beginning
therapy with a β-2 agonist, an anticholinergic or a combination
of the two. A meta-analysis of randomized placebo-controlled
trials of β-2-agonist treatment in patients with obstructive
airway disease performed concluded that the initiation of
treatment increases heart rate and reduces potassium
concentrations compared to placebo and it causes adverse
cardiovascular events like CHF, AF, etc. likely through these
mechanisms along with β-1 adrenergic stimulation [14]. At the
same time the side effect profile of tiotropium was studied in
the UPLIFT trial and found no difference in the incidence of AF
in patients receiving tiotropium vs placebo [30]. Long term
glucocorticoid use is well known to cause hypertension,
Diabetes Mellitus, Left atrial enlargement, HF and ischemic
heart disease all of which can directly or indirectly cause AF. In
a population based, case control study current glucocorticoid
use was associated with an increased risk of AF or AFL
compared with never use (adjusted OR, 1.92; 95% confidence
interval [CI], 1.79-2.06) while among new glucocorticoid users;
the adjusted OR was 3.62 (95% CI, 3.11-4.22) (15). In another
case control study by van der Hooft et al, findings strongly
showed that patients receiving high-dose corticosteroid
therapy, not uncommon in the treatment of COPD, are at
increased risk of developing atrial fibrillation [31]. Huerta et al.
showed that inhaled steroids were not associated with an
increased risk of AF or arrhythmias while theophylline and oral
steroids were associated with an increased risk of arrhythmias
especially AF [32]. In a Meta-Analysis from 2013 on
Roflumilast, an increased incidence of AF as compared to
placebo was seen however the writers pointed out that this is
likely due to chance as most of the studies in the analysis had
excluded patients with major cardiovascular events [33].
Treatment Strategies
Per the AHA/ACC/HRS (American Heart Association/
American College of Cardiology/ Heart Rhythm Society)
guidelines, optimizing therapy for the underlying lung disease
with correction of the hypoxia and acidosis in patients with
COPD developing AF is the cornerstone for management as the
antiarrhythmic drugs or cardioversion are likely to be
ineffective until the respiratory decompensation has been
corrected. Bronchodilator agents like Theophylline and β
agonists have the propensity to precipitate AF and hence
should be avoided in patients with AF. Non β-1 selective
blockers, sotalol, propafenone and adenosine are
contraindicated in patients with bronchospasm however the β
blockers, sotalol and propafenone can be considered in
patients with obstructive lung disease who do not have
bronchospasm. They also recommend a non-dihydropyridine
calcium channel blocker as the first line therapy for rate
control in these patients while Amiodarone and Digoxin can
also be used, the latter in patients with preserved left
ventricular ejection fraction. In hemodynamically unstable
patients, direct cardioversion is recommended while AV nodal
ablation or ventricular pacing may be needed to control the
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2016
Vol.1 No.1:2
ventricular rate with the cardioversion posing challenges of its
own as mentioned above [34]. Despite these challenges, there
were significant improvements in quality of life scores in
patients with COPD post catheter ablation [24]. Kuralay et al.
showed that early prophylactic amiodarone in patients with
COPD undergoing coronary artery bypass grafting significantly
reduced the incidence of post-operative SVT’s including AF/AFL
[35].
Conclusion
COPD is one of the leading causes of Mortality & Morbidity
in the US. COPD is an independent risk factor for Atrial
fibrillation. It is recommended to correct the underlying
respiratory decompensation while treating patients with AF as
they render the treatment of AF ineffective. The presence of
atrial fibrillation is also a predictor for increased mortality in
patients admitted to the hospital with COPD. It is thus
important to understand this relationship between these two
disorders and appropriately manage both these co-morbidities
for improved outcomes.
None
Miller MR, Hankinson J, Brusasco V, Burgos F, Casaburi R, et al.
(2005) Standardisation of spirometry. Eur Respir J 26: 319-338.
8.
Johnston AK, Mannino DM, Hagan GW, Davis KJ, Kiri VA (2008)
Relationship between lung function impairment and incidence
or recurrence of cardiovascular events in a middle-aged cohort.
Thorax 63: 599-605.
9.
Li J, Agarwal SK, Alonso A, Blecker S, Chamberlain AM, et al.
(2014) Airflow obstruction, lung function, and incidence of atrial
fibrillation: the Atherosclerosis Risk in Communities (ARIC)
study. Circulation 129: 971-980.
10. Konecny T, Park JY, Somers KR, Konecny D, Orban M, et al. (2014)
Relation of chronic obstructive pulmonary disease to atrial and
ventricular arrhythmias. Am J Cardiol 114: 272-277.
11. Kinoshita M, Herges RM, Hodge DO, Friedman L, Ammash NM,
et al. (2009) Role of smoking in the recurrence of atrial
arrhythmias after cardioversion. Am J Cardiol 104: 678-682.
12. Korantzopoulos P, Kolettis TM, Galaris D, Goudevenos JA (2007)
remodeling of fibrillated atria the consequence of tissue
hypoxia? Circulation journal: official journal of the Japanese
Circulation Society; 74: 1815-1821.
The authors report no conflict of interest.
14. Salpeter SR, Ormiston TM, Salpeter EE (2004) Cardiovascular
effects of beta-agonists in patients with asthma and COPD: a
meta-analysis. Chest 125: 2309-2321.
Authorship Statement
All authors have contributed equally to the manuscript.
Ethical Statement
This article is not under consideration in any other journal
and this manuscript has not been published elsewhere.
References
15. Christiansen CF, Christensen S, Mehnert F, Cummings SR,
Chapurlat RD, et al. (2009) Glucocorticoid use and risk of atrial
fibrillation or flutter: a population-based, case-control study.
Archives of internal medicine;169: 1677-1683.
16. Shan H, Zhang Y, Lu Y, Zhang Y, Pan Z, et al. (2009)
Downregulation of miR-133 and miR-590 contributes to
nicotine-induced atrial remodelling in canines. Cardiovascular
research; 83: 465-472.
17. Buch P, Friberg J, Scharling H, Lange P, Prescott E (2003) Reduced
Vestbo J, Hurd SS, Rodriguez-Roisin R, Committee GS (2012) [An
overview of Global Strategy for the Diagnosis, Management and
Prevention of Chronic Obstructive Pulmonary Disease (GOLD)
(revised 2011)]. Zhonghua yi xue za zhi; 92: 937-938.
2.
Decramer M, Janssens W, Miravitlles M (2012) Chronic
obstructive pulmonary disease. Lancet 379: 1341-1351.
3.
Bhatt SP, Dransfield MT (2013) Chronic obstructive pulmonary
disease and cardiovascular disease. Translational research: the
journal of laboratory and clinical medicine; 162: 237-251.
4.
Chugh SS, Havmoeller R, Narayanan K, Singh D, Rienstra M, et al.
(2014) Worldwide epidemiology of atrial fibrillation: a Global
Burden of Disease 2010 Study. Circulation 129: 837-847.
4
7.
13. Ogi H, Nakano Y, Niida S, Dote K, Hirai Y, et al. (2010) Is structural
Conflict of Interest
5.
Curkendall SM, Lanes S, de Luise C, Stang MR, Jones JK, et al.
(2006) Chronic obstructive pulmonary disease severity and
cardiovascular outcomes. European journal of epidemiology; 21:
803-813.
The role of oxidative stress in the pathogenesis and
perpetuation of atrial fibrillation. International journal of
cardiology;115:135-143.
Financial Disclosures
1.
6.
Go AS, Hylek EM, Phillips KA, Chang Y, Henault LE, et al. (2001)
Prevalence of diagnosed atrial fibrillation in adults: national
implications for rhythm management and stroke prevention: the
AnTicoagulation and Risk Factors in Atrial Fibrillation (ATRIA)
Study. JAMA 285: 2370-2375.
lung function and risk of atrial fibrillation in the Copenhagen
City Heart Study. Eur Respir J 21: 1012-1016.
18. Terzano C, Romani S, Conti V, Paone G, Oriolo F, et al. (2014)
Atrial fibrillation in the acute, hypercapnic exacerbations of
COPD. European review for medical and pharmacological
sciences;18: 2908-2917.
19. Stevenson IH, Roberts-Thomson KC, Kistler PM, Edwards GA,
Spence S, et al. (2010) Atrial electrophysiology is altered by
acute hypercapnia but not hypoxemia: implications for
promotion of atrial fibrillation in pulmonary disease and sleep
apnea. Heart rhythm: the official journal of the Heart Rhythm
Society; 7: 1263-1270.
20. Hayashi H, Miyamoto A, Kawaguchi T, Naiki N, Xue JQ, et al.
(2014) P-pulmonale and the development of atrial fibrillation.
Circulation journal: official journal of the Japanese Circulation
Society; 78: 329-337.
21. Tukek T, Yildiz P, Akkaya V, Karan MA, Atilgan D, Yilmaz V, et al.
(2002) Factors associated with the development of atrial
fibrillation in COPD patients: the role of P-wave dispersion.
This article is available from:http://chronic-obstructive-pulmonary-disease.imedpub.com/
Chronic Obstructive Pulmonary Diseases
2016
Vol.1 No.1:2
Annals of noninvasive electrocardiology: the official journal of
the International Society for Holter and Noninvasive
Electrocardiology, Inc; 7: 222-227.
22. Bhatt SP, Nanda S, Kintzer JS (2012) Arrhythmias as trigger for
acute exacerbations of chronic obstructive pulmonary disease.
Respir Med 106: 1134-1138.
23. Grabicki M, Parysek H, Batura-Gabryel H, Brodnicka I (2008)
Comorbidities as an element of multidimensional prognostic
assessment of patients with chronic obstructive pulmonary
disease. Journal of physiology and pharmacology: an official
journal of the Polish Physiological Society; 59: 297-301.
24. Steer J, Gibson J, Bourke SC (2012) The DECAF Score: predicting
hospital mortality in exacerbations of chronic obstructive
pulmonary disease. Thorax; 67: 970-976.
25. Scharf SM, Iqbal M, Keller C, Criner G, Lee S, et al. (2002)
Hemodynamic characterization of patients with severe
emphysema. American journal of respiratory and critical care
medicine;166: 314-322.
26. de Vos CB, Pisters R, Nieuwlaat R, Prins MH, Tieleman RG, et al.
(2010) Progression from paroxysmal to persistent atrial
fibrillation clinical correlates and prognosis. Journal of the
American College of Cardiology; 55: 725-731.
27. Roh SY, Choi JI, Lee JY, Kwak JJ, Park JS, et al. (2011) Catheter
ablation of atrial fibrillation in patients with chronic lung
disease. Circ Arrhythm Electrophysiol 4: 815-822.
28. Gu J, Liu X, Tan H, Zhou L, Jiang W, et al. (2013) Impact of chronic
obstructive pulmonary disease on procedural outcomes and
quality of life in patients with atrial fibrillation undergoing
catheter ablation. J Cardiovasc Electrophysiol 24: 148-154.
29. Pisters R, Nieuwlaat R, Prins MH, Le Heuzey JY, Maggioni AP, et
al. (2012) Clinical correlates of immediate success and outcome
© Copyright iMedPub
at 1-year follow-up of real-world cardioversion of atrial
fibrillation: the Euro Heart Survey. Europace: European pacing,
arrhythmias, and cardiac electrophysiology: journal of the
working groups on cardiac pacing, arrhythmias, and cardiac
cellular electrophysiology of the European Society of Cardiology;
14: 666-674.
30. Tashkin DP, Celli B, Senn S, Burkhart D, Kesten S, et al. (2008) A
4-year trial of tiotropium in chronic obstructive pulmonary
disease. N Engl J Med 359: 1543-1554.
31. van der Hooft CS, Heeringa J, Brusselle GG, Hofman A, Witteman
JC, et al. (2006) Corticosteroids and the risk of atrial fibrillation.
Arch Intern Med 166: 1016-1020.
32. Huerta C, Lanes SF, García Rodríguez LA (2005) Respiratory
medications and the risk of cardiac arrhythmias. Epidemiology
16: 360-366.
33. Oba Y, Lone NA (2013) Efficacy and safety of roflumilast in
patients with chronic obstructive pulmonary disease: a
systematic review and meta-analysis.Therapeutic advances in
respiratory disease; 7: 13-24.
34. January CT, Wann LS, Alpert JS, Calkins H, Cigarroa JE, et al.
(2014) AHA/ACC/HRS guideline for the management of patients
with atrial fibrillation: a report of the American College of
Cardiology/American Heart Association Task Force on Practice
Guidelines and the Heart Rhythm Society. Journal of the
American College of Cardiology; 64: e1-76.
35. Kuralay E, Cingoz F, Kilic S, Bolcal C, Gunay C, et al. (2004)
Supraventricular tachyarrythmia prophylaxis after coronary
artery surgery in chronic obstructive pulmonary disease patients
(early amiodarone prophylaxis trial). European journal of cardiothoracic surgery: official journal of the European Association for
Cardio-thoracic Surgery; 25: 224-230.
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