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Review Article

iMedPub Journals Chronic Obstructive Pulmonary Diseases 2016


Vol.1 No.1:2
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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: abhinav72@gmail.com


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.

propafenone can be used in patients with obstructive lung


disease who do not have bronchospasm.
Abstract
COPD is one of the leading causes of Mortality & Keywords: Chronic obstructive pulmonary disease;
Morbidity in the US and is associated with a wide variety Atrial fibrillation
of cardiovascular diseases especially arrhythmias, angina,
myocardial infarction and congestive heart failure and is
directly associated with the severity of COPD described in Introduction
the GOLD initiative. COPD is an independent risk factor for
AF/AFL. Smoking, hypoxia and inflammation all contribute Chronic obstructive pulmonary disease (COPD) is a major
to AF in COPD patients mainly via atrial remodeling while global public health problem. COPD is a common preventable
hypercapnia contributes to it via increasing refractoriness and treatable disease, which is characterized by persistent
of the atrial musculature and a delay in the return of the airflow limitation that is usually progressive and associated
refractoriness to normal after resolution of the with an enhanced chronic inflammatory response in the
hypercapnia. The most common EKG abnormality found in airways and the lung to noxious particles or gases. In 2020,
patients with COPD is P pulmonale and the PQ interval is COPD is projected to rank fifth worldwide in terms of burden
the strongest predictor of developing AF. The P wave of disease and third in terms of mortality [1] though presently
Dispersion (PwD) was also an independent risk factor for it is the 4th leading cause of Mortality and the 2nd leading
the development of AF and was found to be more in the cause of Morbidity in the United States (US) [2].
acute phase than in the stable phase.
Extra-pulmonary manifestations of COPD include
The BODE index, an important prognostic score among cardiovascular disease, skeletal muscle dysfunction,
patients hospitalized with a COPD exacerbation has a osteoporosis, metabolic syndrome depression and lung cancer
direct co relation with the prevalence of AF/AFL while the [1]. COPD is associated with specific electrocardiographic (EKG)
DECAF score, which was found to be superior to the CURB abnormalities while an increased incidence of cardiac
65 score as a mortality predictor for hospitalized patients, arrhythmias has been reported which includes atrial fibrillation
includes AF as one of the criteria. Chronic hypoxemia is (AF), atrial flutter (AFL), multifocal atrial tachycardia (MAT) and
one of the main reasons for altered pulmonary vein non-sustained ventricular tachycardia (NSVT) [3]. It is
anatomy and hence the presence of COPD was identified estimated that there were approximately 33.5 million people
as an independent risk factor for the recurrence of atrial with AF in 2010 worldwide (20.9 million men [95% uncertainty
tachyarrhythmias after catheter ablation in patients with interval (UI), 19.5-22.2 million] and 12.6 million women [95%
COPD and the absence of COPD was also found to be an UI, 12.0-13.7 million]) [4] and it was also estimated that the
independent predictor for a successful electro- burden of AF in the United States alone would increase to at-
cardioversion. These patients were also found to have an least 5.6 million by 2050 [5].
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 COPD and Cardiovascular Disease
recommended to correct the underlying respiratory
decompensation while treating patients with AF as they Patients with diagnosed and/or undergoing treatment for
render the treatment of AF ineffective. Non- COPD are at a substantially increased risk of hospitalizations
dihydropyridine calcium channel blockers should be used and mortality due to heart diseases. In one retrospective
as first line rate control agents for AF in patients with cohort study, the prevalence of cardiovascular diseases (CVD)
concomitant COPD while the -blockers, sotalol, 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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1
Chronic Obstructive Pulmonary Diseases 2016
Vol.1 No.1:2

prevalence were: arrhythmia 1.76 (confidence interval [CI]: 1(TGF-1) and TGF-RII at the protein level, and a 60-70%
1.64-1.89), angina 1.61 (CI: 1.47-1.76), acute myocardial decrease in the levels of miRNAs miR-133 and miR-590 was
infarction 1.61 (CI: 1.43-1.81), congestive heart failure 3.84 (CI: critical in atrial remodeling in the canine atrium [16]. Smoking
3.56-4.14). There was also an increased risk of hospitalization was found to be an independent risk factor in the recurrence
secondary to cardiovascular causes in the COPD group [6]. of AF/AFL after cardioversion in women while an increased risk
of mortality and not arrhythmia was found in men [11].
The Forced Vital Capacity (FVC), defined as the maximal
volume of air exhaled with maximally forced effort from a It has been shown consistently that there exists an inverse
maximal inspiration, Expressed in liters and the Forced relationship between FEV1, FVC with AF. The Copenhagen City
Expiratory Volume in one second (FEV1), defined as the Heart Study demonstrated that the Risk of new AF at re-
maximal volume of air exhaled in the first second of a forced examination was 1.8-times higher for FEV1 between 60-80% of
expiration from a position of full inspiration, expressed in liters predicted compared with a FEV1 of 80% after adjustment for
are the major determinants of the severity of COPD [1,7]. The sex, age, smoking, blood pressure, diabetes and body mass
Global Initiative for Chronic Obstructive Lung Diseases (GOLD) index. They also showed that the risk of AF hospitalization was
classifies the severity of airflow limitation as determined by 1.3 times more with a FEV1 between 60-80% of predicted and
spirometry into 4 grades (GOLD 1, mild, FEV1 80% predicted; 1.8 times with a FEV1 of 60% compared with a FEV1 of 80%,
GOLD 2, moderate, FEV1 50% but <80% predicted; GOLD 3, proving that reduced lung function as an independent
severe, FEV1 30% but <50% predicted; and GOLD 4, very predictor of AF [17]. It is well documented that oxidative stress
severe, FEV1 <30% predicted) using the fixed ratio, post- and inflammation are two of the major factors in the
bronchodilator FEV1/FVC <0.7 [1]. An association was also pathophysiology of COPD and now postulations have also been
established between the severity of airflow obstruction based made of its impact in atrial remodeling and thus causing and
on the GOLD criteria and the prevalence of CVD which showed potentially worsening existing AF [12].
that prevalence of CVD was higher among subjects with GOLD
Hypoxia, commonly seen in patients with COPD, causes an
2 (OR 2.9, 95% CI 2.4 to 3.6) and GOLD 3 or 4 COPD (OR 3.0,
upregulation of Vascular Endothelial Growth Factor (VEGF)
95% CI 2.0 to 4.5), compared with normal subjects [8]. The
secondary to an increase in Hypoxia-induced transcription
Atherosclerosis Risk in Communities (ARIC) cohort study
factor-1 (HIF-1). Matrix metalloproteinase 9 (MMP9)
established an inverse co-relation between the FEV1 and rate
expression is increased in the atrium in a patient with AF and
of incident AF which was independent of age, gender, BMI,
potentially causes atrial remodeling. It was shown via
smoking and blood pressure [9].
Immunofluorescence that there was excess production and co-
A recent retrospective study showed that of COPD were localization of HIF-1, VEGF and MMP-9 within the
associated with an increased likelihood of AF/AFL (23.3% vs. endothelium of the atrial arteries in the AF group as compared
11.0%, respectively, p<0.0001), NSVT (13.0% vs. 5.9%, to patients without AF [13].
respectively, p<0.0001), and sustained ventricular tachycardia
Patients with COPD are prone to have acute exacerbations
(SVT; 0.9% vs. 1.6%, respectively, p<0.0001) and that it
of the disease and common causes for this are usually viral
remained a significant predictor of AF/AFL and NSVT (p<0.0001
infections of the upper respiratory tract and infections of the
and p<0.0001, respectively) after adjusting for age, gender,
tracheobronchial tree [1]. Terzano et al. showed that
tobacco use, obesity, hypertension, coronary artery disease,
suboptimal pulmonary function, hypercapnia and high values
heart failure, diabetes, anemia, cancer, chronic kidney disease,
of pulmonary artery systolic pressure are independent
and rate/rhythm control medications [10]. This article provides
predictors of incident AF [18]. In their experimental sheep
a succinct overview of the association of COPD with AF, the
model, Stevenson et al. showed the hypercapnia caused an
arrythmogenic mechanisms and potential treatment
increase in the atrial musculature refractoriness and the
strategies.
conduction time however, intriguingly, there was a delay in
only the conduction time to return to normal after the
COPD and Atrial Fibrillation: Potential resolution of hypercapnia prompting the theory that this
differential recovery time may be the reason for an increased
Causes of Arrhythmia and EKG incidence of AF observed in the phase of eucapnia [19].
Changes P pulmonale (P wave 0.25 mV in the inferior leads) is
There seem to be a wide variety of reasons for arrhythmias usually omnipresent on EKGs of patients with chronic lung
to occur in COPD beginning from risk factors, its effect in diseases. Hayashi et al, in a digital analysis of EKGs in a 25 year
altering cardiopulmonary physiology to the treatment of period showed P-wave duration and PQ interval were
COPD. Smoking, airway inflammation, hypoxia, hypercapnia, significantly longer in the AF group than in the non-AF group
pulmonary hypertension, -adrenergic agonist and steroids all (115.4 17.2 ms vs. 107.0 17.2 ms, P=0.0003 and 166.3
contribute to ultimately causing or worsening AF [11-15]. 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
Shan et al. attempted to postulate the reasoning for the development in patients with P pulmonale [20]. The P wave
increased incidence of AF in smokers using a canine model. dispersion (PwD), which is the difference in the maximum and
They concluded that the pro fibrotic response of nicotine in minimum duration of the P wave, was also found to be an
upregulation of expression of Transforming Growth Factor Beta independent risk factor associated in the development of AF

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Chronic Obstructive Pulmonary Diseases 2016
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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
COPD Treatment Causing AF
frequent exacerbations suggesting that the PwD could be a Inhaled bronchodilator medications continue to remain the
target for prediction, prevention and therapy of acute mainstay treatment for COPD patients. It includes beginning
exacerbation of COPD [22]. therapy with a -2 agonist, an anticholinergic or a combination
The BODE index is a multidimensional 10-point scale which of the two. A meta-analysis of randomized placebo-controlled
integrates body mass index, degree of airflow obstruction and trials of -2-agonist treatment in patients with obstructive
dyspnea and exercise capacity measured in 6-min walk test airway disease performed concluded that the initiation of
and the score is directly proportional with mortality. It was treatment increases heart rate and reduces potassium
shown that patients with higher BODE index scores had a concentrations compared to placebo and it causes adverse
significantly greater prevalence of arrythmias including AF/AFL cardiovascular events like CHF, AF, etc. likely through these
and SVT [23]. The Dyspnea, Eosinopenia, Consolidation, mechanisms along with -1 adrenergic stimulation [14]. At the
Acidemia and atrial Fibrillation (DECAF) score was introduced same time the side effect profile of tiotropium was studied in
by Steer et al, as a predictor of mortality in hospitalized the UPLIFT trial and found no difference in the incidence of AF
patients with COPD exacerbations. The DECAF score includes in patients receiving tiotropium vs placebo [30]. Long term
the 5 strongest predictors of mortality i.e. MRC Dyspnea Score, glucocorticoid use is well known to cause hypertension,
eosinopenia, consolidation, acidemia, and atrial fibrillation and Diabetes Mellitus, Left atrial enlargement, HF and ischemic
was found to be a stronger than the other predictors like the heart disease all of which can directly or indirectly cause AF. In
CURB65 [24]. 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
COPD and its Effect on Ablation interval [CI], 1.79-2.06) while among new glucocorticoid users;
strategies of AF 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
COPD has a significant effect on cardiopulmonary physiology showed that patients receiving high-dose corticosteroid
but also has an impact in altering the anatomy of the same therapy, not uncommon in the treatment of COPD, are at
system because of which it affects outcomes of catheter increased risk of developing atrial fibrillation [31]. Huerta et al.
ablations for AF, its progression and mortality. COPD is showed that inhaled steroids were not associated with an
associated with hypoxemia and acidosis, which leads to, increased risk of AF or arrhythmias while theophylline and oral
increased pulmonary vascular resistance. This causes an steroids were associated with an increased risk of arrhythmias
increased level of inflammatory markers that promotes fibrosis especially AF [32]. In a Meta-Analysis from 2013 on
and thus causes structural remodeling of pulmonary vessels Roflumilast, an increased incidence of AF as compared to
[25]. A subgroup analysis of the European Heart Survey (EHS) placebo was seen however the writers pointed out that this is
on AF by de Vos et al, gave rise to the HATCH score while likely due to chance as most of the studies in the analysis had
studying AF progression from paroxysmal to persistent. The excluded patients with major cardiovascular events [33].
HATCH score was an abbreviation for heart failure, age,
previous episode of transient ischemic attack or stroke, COPD Treatment Strategies
and hypertension, which were all, found to be independent
predictors of AF progression [26]. In their study, Roh et al. Per the AHA/ACC/HRS (American Heart Association/
showed that significant alteration of pulmonary vein (PV) American College of Cardiology/ Heart Rhythm Society)
anatomy was related to arrhythmogenicity. They also showed guidelines, optimizing therapy for the underlying lung disease
that non-PV foci were more common in the chronic lung with correction of the hypoxia and acidosis in patients with
disease group (26.7%) than in the control group (5.0%; COPD developing AF is the cornerstone for management as the
P=0.025) and all the non-PV foci were located in the right antiarrhythmic drugs or cardioversion are likely to be
atrium [27]. The impact of COPD on outcomes of catheter ineffective until the respiratory decompensation has been
ablation in patients with AF in terms of recurrence was corrected. Bronchodilator agents like Theophylline and
evaluated in a prospective study by Gu et al, which showed agonists have the propensity to precipitate AF and hence
that non-paroxysmal AF (P=0.013, OR=1.767, 95% CI: should be avoided in patients with AF. Non -1 selective
1.129-2.765) as well as the presence of COPD (P=0.029, blockers, sotalol, propafenone and adenosine are
OR=1.951, 95% CI: 1.070-3.557) were the independent contraindicated in patients with bronchospasm however the
predictors for higher atrial tachyarrhythmia recurrence [28]. blockers, sotalol and propafenone can be considered in
Absence of COPD was found to be an independent predictor patients with obstructive lung disease who do not have
for a successful electro-cardioversion in patients with AF while bronchospasm. They also recommend a non-dihydropyridine
the absence of COPD was also an independent predictor of calcium channel blocker as the first line therapy for rate
sinus rhythm at a 1 yr follows up [29]. 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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Chronic Obstructive Pulmonary Diseases 2016
Vol.1 No.1:2

ventricular rate with the cardioversion posing challenges of its 6. Curkendall SM, Lanes S, de Luise C, Stang MR, Jones JK, et al.
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cardiology;115:135-143.
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This article is not under consideration in any other journal Downregulation of miR-133 and miR-590 contributes to
and this manuscript has not been published elsewhere. nicotine-induced atrial remodelling in canines. Cardiovascular
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