Reversible atrial fibrillation secondary to a mega-oesophagus
© Upile et al; licensee BioMed Central Ltd. 2006
Received: 10 October 2006
Accepted: 13 December 2006
Published: 13 December 2006
Atrial fibrillation (AF) is the most common cardiac arrhythmia, and it increases in prevalence with advancing age to about 5% in people older than 65 years.
We present a rare case of atrial fibrillation secondary to a mega-oesophagus occurring in an 84-years-old Caucasian woman. The patient had a history of progressive dysphagia and the accumulation of food debris lead to mega-oesophagus.
The diagnosis was made by barium swallow and electrocardiogram; evacuations of 300 ml of the food debris lead to complete resolution of the arrhythmia. The possible aetiology leading to this AF is discussed.
Causes of Atrial Fibrillation
Mitral valve disease
Sick sinus syndrome
When the atria are in fibrillation, contraction occurs at rates of 350–900 per minute. The AV node may conduct these impulses to the ventricles at 90–170 beats per minute, and often higher. There are several complementary and competing theories regarding the pathophysiology of AF initiation and propagation. The occasional impulses conducted by the atrio-ventricular node results in a totally irregular ventricular rhythm which is a characteristic of the condition which can be either continuous (acute or chronic) or paroxysmal .
Achalasia is primarily associated with a degeneration of ganglion cells of Auerbach's plexus resulting in an absence of oesophageal peristalsis and failure of lower oesophageal sphincter relaxation. This results in oesophageal dilatation or mega-oesophagus .
We present a rare case of a patient with achalasia in which accumulation of undigested food lead to mega-oesophagus and atrial fibrillation.
An 84-year-old Caucasian women referred by her General Practitioner complaining of dysphagia and dyspnoea exacerbated by swallowing. She reported a 3 week history of progressive dysphagia, initially for solids and subsequently for fluids leading to total dysphagia. Other reported symptoms included regurgitation, cough and hoarseness of voice. There was no significant medical, family or social history.
Clinical examination revealed a rapid, irregularly irregular pulse; no other cardiovascular-respiratory abnormalities were identified. Abdominal examination also revealed no abnormality; indirect laryngoscopy which was carried out by the same examining clinician showed pooling of saliva in the hypopharyngx.
There is a correlation between achalasia and cardiac arrhythmia . Many patients with achalasia are known to perform a temporary valsalva manoeuvre to aid the transit of food over the functionally stenotic segment of their oesophagus. The anatomical proximity of the oesophagus with the left atria is further evidenced by the rare but severe complication of left atrial radiofrequency ablation of oesophageal perforation and mediastinitis .
Using 3 non-invasive tests, abnormalities of cardiovascular reflex function were found in 7 of 15 patients with achalasia. Abnormalities of heart rate responses to the valsalva manoeuvre, deep breathing, and standing were noted in patients with autonomic neuropathy defect. The findings are consistent with the hypothesis that an abnormality of vagal function may contribute to the pathogenesis of achalasia .
Achalasia itself may be a result of an abnormality of vagal function due to an autonomic neuropathic defect and therefore abnormalities of cardiovascular response are not uncommon .
In this patient, the removal of the food debris from the cervical oesophagus caused reversion of this arrhythmia back into sinus rhythm. This can be justified as either due to vagal repression or the relief of the pressure effect of the volume of the food debris transmitted directly to the atria. The evacuation may have resulted in either a sinus massage or a forced valsalva leading to reversion of the rhythm.
There are several confounding factors as to the exact cause of the transient atrial arrhythmia in this patient. Previous electrocardiograms exhibit a degree of ischaemia which may predispose to transient arrhythmias in situations of vagal repression especially in the circumstances of extra-cardiac intra-thoracic pathology as in this case.
Written consent was obtained from the patient or their relative for publication of study.
- Roberts R: Mechanisms of disease: Genetic mechanisms of atrial fibrillation. Nat Clin Pract Cardiovasc Med. 2006, 3 (5): 276-82. 10.1038/ncpcardio0509.View ArticlePubMedGoogle Scholar
- Andrews M, Nelson BP: Atrial fibrillation. Mt Sinai J Med. 2006, 73 (1): 482-92.PubMedGoogle Scholar
- Richards WO, Torquati A, Lutfi R: The current treatment of achalasia. Adv Surg. 2005, 39: 285-314. 10.1016/j.yasu.2005.04.002.View ArticlePubMedGoogle Scholar
- Sperry K: Achalasia, the Valsalva maneuver, and sudden death: a case report. J Forensic Sci. 1994, 39 (2): 547-51.View ArticlePubMedGoogle Scholar
- Ren JF, Lin D, Marchlinski FE, Callans DJ, Patel V: Esophageal imaging and strategies for avoiding injury during left atrial ablation for atrial fibrillation. Heart Rhythm. 2006, 3 (10): 1156-61. 10.1016/j.hrthm.2006.06.006.View ArticlePubMedGoogle Scholar
- Ge F, Li Z, Ke M: Abnormal cardiovascular reflexes in patients with achalasia. Chin Med Sci J. 1994, 9 (3): 194-6.PubMedGoogle Scholar
- Eckardt VF, Stenner F, Liewen H, Roder R, Koop H, Bernhard G: Autonomic dysfunction in patients with achalasia. Neurogastroenterol Motil. 1995, 7 (1): 55-61.View ArticlePubMedGoogle Scholar
- The pre-publication history for this paper can be accessed here:http://www.biomedcentral.com/1472-6815/6/15/prepub
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