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DOI: http://dx.doi.org/10.15403/jgld.2014.1121.dac
Paroxysmal Postprandial Atrial Fibrilation Suppressed by
Laparoscopic Repair of a Giant Paraesophageal Hernia
Compressing the Left Atrium
Daniel A. Cristian1,3, Alin S. Constantin1, Mariana Barbu2, Dan Spătaru2,3, Traean Burcoș1,3, Florin A. Grama1,3
1) General Surgery
Department;
2) Department of Cardiology,
Colțea Clinical Hospital;
3) Carol Davila University
of Medicine and Pharmacy,
Bucharest
Romania
Abstract
We present the case of a patient with a giant paraesophageal hernia associated with paroxysmal postprandial
atrial fibrillation that was suppressed after surgery. The imaging investigations showed the intrathoracic
displacement of a large part of the stomach, which pushed the left atrial wall causing atrial fibrillation. The
laparoscopic surgical repair acted as sole treatment for this condition.
Key words: giant hiatal hernia – paroxysmal postprandial atrial fibrillation – laparoscopic hiatal hernia repair.
Abbreviations: AF: atrial fibrillation; GEJ: gastroesophageal junction; GERD: gastroesophageal reflux disease;
HH: hiatal hernia; PEH: paraesophageal hernia; PPI: proton pump inhibitor.
Address for correspondence:
Dr. Florin Andrei Grama
Colţea Hospital, General
Surgery Department 1,
I.C. Brătianu Street,
District 3, 030171,
Bucharest
Romania
[email protected]
Received: 14.11.2014
Accepted: 08.12.2014
Introduction
The current anatomical
classification of hiatal hernia
(HH) includes four types. Type I
are sliding HHs with the gastroesophageal junction (GEJ)
migrated above the diaphragm
while the stomach is in its normal
anatomical position. Type II are
pure paraesophageal hernias
(PEHs) with the GEJ in its normal
anatomical position while the
fundus is herniated through
the hiatus. Type III hernias are
a combination of type I and II
and type IV are defined by the
herniation of other structures
than the stomach. Types II – IV
hernias as a group are referred
to as PEHs and represent 5-15%
of the total HHs, with more than
90% of the PEHs being Type III
[1].
No standard definition exists
for the term “giant” PEH, some
authors defining it as a herniation
of more than 30% of the stomach,
while others of more than 50%
[2]. Two potential mechanisms could explain the etiology of a
giant HH: gastroesophageal reflux disease (GERD) that leads
to esophageal scarring and shortening, and chronic positive
pressure on the diaphragmatic hiatus with a predisposition to
herniation [2].
Atrial fibrillation (AF), GERD and HHs are often seen in
clinical practice and it has been suggested that GERD and
HH represent risk factors for AF [3, 4]. Hiatal hernia appears
to be associated with increased frequency of AF both in men
and women of all age groups [5]. Hiatal hernia can directly
impinge on the left atrium in a similar way as atrial masses.
Since atrial masses are associated with various arrhythmias
due to cardiac compression, HHs could potentially result in a
similar effect [6, 7]. The link between the upper gastrointestinal
tract and the AF is suggested also by the reported reduced
number of recurrences of AF with the use of PPI or Nissen
fundoplication [8].
Case report
We report the case of a 77-year-old female who presented
at the Cardiology Department complaining of minimal effort
dyspnea. The patient also mentioned daily acid regurgitation
and postprandial palpitations. Her medical history included
chronic heart failure, arterial hypertension, anxiety disorder,
chronic obstructive pulmonary disease (COPD) stage III GOLD
and a recent left humeral neck fracture, surgically treated.
Her heart rate was of 110 bpm and the blood pressure
measured 130/80 mmHg with no antihypertensive medication.
J Gastrointestin Liver Dis, March 2015 Vol. 24 No 1: 113-116
114
Cristian et al
The 12-lead electrocardiogram indicated AF. The 24 hours
Holter monitoring demonstrated AF to be paroxysmal and
associated with eating. Hormone levels, the clinical and
echographic assessments of the thyroid function and structure
showed no abnormalities.
Chest radiography showed widening of the mediastinum
and a large abnormal shadow overlapping the heart (Fig. 1).
The transthoracic echocardiography demonstrated a mass
compressing the left atrium, a mild mitral regurgitation and no
signs of hypertensive cardiopathy (Fig. 2). Left ventricular size
and the contractile function were preserved and there was no
significant valvular disease. Upper endoscopy was performed
as well and revealed reflux esophagitis (grade A) and a giant
PEH with 2/3 of the superior part of the stomach being situated
intrathoracally without any mucosal abnormalities (Fig. 3).
Spirometry proved mixed ventilator dysfunction with a FVC
of 75%, FEV1 of 55%, Tiffeneau index of 62% and a positive
bronchial challenge test.
The barium swallow revealed important reflux, a giant HH
(13.5 cm) with the GEJ located intrathoracally and containing
almost the whole stomach, except a small portion of the pyloric
antrum that was very thin (Fig. 4a).
The documented correlation between symptoms and HH
and the large size of the hernia led to the indication for surgery
[1]. Pre-operatively she was treated with cardioselective betablockers, low molecular weight heparin and high doses of PPI.
We performed a complete reduction of the herniated stomach,
excision of the sac and crural repair through laparoscopic
Fig. 1. Chest radiography: a) preoperative PA view: mixed hydroaeric image located in
the inferior mediastinum; b) postoperative PA view: ascended left hemidiaphragm and
normal mediastinum; c) preoperative lateral view: mixed hidroaeric retrocardiac image;
d) postoperative lateral view: normal mediastinum.
Fig. 2. Transthoracic echocardiogram: a) preoperative apical window: giant hiatal hernia
compressing the left atrium; b) postoperative apical window: left atrium without any
compression. LV – left ventricle; LA – left atrium; HH – hiatal hernia; X – space previously
occupied by the giant hiatal hernia.
J Gastrointestin Liver Dis, March 2015 Vol. 24 No 1: 113-116
Atrial fibrilation suppressed by hiatal hernia repair Fig. 3. Endoscopic view inside the herniated stomach.
External compression of the left atrium on the stomach wall.
approach. Due to the stomach laxity we achieved a complete
(360º) Nissen fundoplication.
Postoperative barium swallow and chest radiography
showed a subdiaphragmatic stomach and GEJ (Figs. 1, 4).
Transthoracic echocardiography showed that the compression
on the left atrium was relieved and the mild mitral regurgitation
ceased (Fig. 2). Postoperatively, the AF was suppressed and
converted to normal sinus rhythm as per the electrocardiogram
and the Holter monitoring. The patient was discharged 5 days
after surgery in sinus rhythm.
The follow-up at 10 days after surgery revealed that the
shortness of breath improved significantly, the pulse rate was
80 bpm and the electrocardiogram showed no AF.
Discussion
The anatomical proximity of the left atrium to the
HH makes the atria liable to mechanical irritation, neural
connections and inflammation that may increase the risk for
AF [5]. The relationship between gastrointestinal symptoms
and arrhythmias was first described by Ludwig Roemheld,
under the name of “Roemheld gastrocardiac syndrome”,
in which an esophago-gastric stimulus was able to induce
arrhythmia-related symptoms [9, 10].
115
Large PEH predominantly occurs in the elderly population.
Besides causing regurgitation and heartburn due to accompanying
GERD, it may present with a wide spectrum of manifestations
mimicking those of cardiovascular pathology such as postprandial
syncope, angina-like chest pain, recurrent dyspnea and acute
heart failure due to HH induced cardiac compression [11-13].
Further, HH may simulate the appearance of an intra-atrial mass
on transthoracic echocardiography [13, 14].
Giant HH and GERD are two separate diseases, which
frequently coexist, although either can occur without the other
one, both being able to act as risk factors for each other and
also for AF [2, 4]. Our patient was diagnosed with both GERD
and giant HH. There have been numerous case reports and
large retrospective studies that have suggested an association
between AF and GERD due to the locally released cytokines
from esophageal injury or due to the vagal overstimulation that
create an environment that can induce and perpetuate AF [4,
8, 15-18]. On the other hand, the hypothesis that the presence
of HH contributes to the development of AF is supported
by previous reports. Roy et al. demonstrated epidemiologic
association between HH and AF in young patients (age < 55)
due to the cardiac compression and subsequent atrial irritation
[5]. Gillinov et al. reported the case of a patient who had a
surgical correction of a HH and had resolution of AF; however,
this patient also had catheter ablation to treat the AF [19].
Schilling et al. reported that the repair of a large PEH resulted
in the termination of AF [15]. Patel et al. also reported a case
of a patient with atrial flutter caused directly by the mechanical
effect of a large HH that occupied more than 50% of her thorax
without reflux or heartburn that was resolved after surgery [20].
Duygu et al. reported a case of paroxysmal atrial flutter that
was refractory to electrical cardioversion and calcium channel
blockers in a patient with severe acid reflux and daily heartburn
symptoms secondary to a large HH [21].
Patients with large HHs have also significant dyspnea and it
has been suggested that left atrial compression has a causal role
in the pathogenesis of HH-associated dyspnea [22]. Moreover,
in our case the dyspnea was also determined by the rapid
ventricular rate accompanying AF. Our patient’s shortness of
breath improved significantly after the HH repair.
Fig. 4. Barium swallow: a) preoperative: giant sliding
hiatal hernia containing almost the whole stomach with
the gastroesophageal junction located intrathoracally;
b) postoperative: subdiaphragmatic stomach and cardia.
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116
It is not stated yet if AF is caused by the direct compression
of the HH on the left atrium or by the association of GERD,
which accompanies most cases of giant HH.
Besides the direct compression of the HH and the
associated GERD, there are also other possible risk factors that
can induce AF such as ischemic heart disease, chronic heart
failure and thyroid dysfunction. For a 77-year old patient, it
is difficult to completely rule out the presence of ischemic
heart disease without performing coronarography. However,
besides the age, the patient had no other cardiovascular
risk factors (diabetes, obesity, dyslipidemia) and was a nonsmoker. The arterial hypertension mentioned in her medical
history seemed to have been more linked to the previous
episodes of anxiety, as at the time of evaluation the blood
pressure values were normal without any antihypertensive
medication. The cardiac echography showed no sign of
hypertensive cardiopathy either. Furthermore, the good
tolerance of the patient, without any chest pain, at the onset
of fast rhythm AF represents a strong argument against
myocardial ischemia.
The “chronic’’ heart failure mentioned in her medical
history was in fact related to the symptomatology induced by
the non-permanent AF which in its turn was caused by the
cardiac compression of the HH. The normal volume of the
left atrium on echocardiography examination contradicts the
”chronic’’ evolution of the heart failure. In addition, the mild
mitral regurgitation ceased after the reversion of the cardiac
compression as a result of the HH surgical treatment.
Conclusion
Cristian et al
To the best of our knowledge there are no case series and
no case reports in the literature of giant HH associated with
paroxysmal AF which was suppressed after laparoscopic
surgical repair. This could indicate that direct cardiac
compression represents the main mechanism for inducing AF.
In order to determine the full relationship between HH and
AF, future prospective investigation of patients with both AF
and HH would be required.
Conflicts of interest: None to declare.
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