Roemheld syndrome: Apprehending arrhythmia in a different perspective

Eka Prasetya Budi Mulia

doi:10.5606/e-cvsi.2022.1261

Introduction

An intriguing article by Bodur et al.[1] investigated the association between premature atrial contractions (PACs) and gastroesophageal reflux disease (GERD).

The authors found that esophagitis and/or gastritis in patients with GERD symptoms were independently associated with the increased prevalence and number of PACs. The exact mechanism of esophagitis and/or gastritis-induced supraventricular arrhythmia is still unclear. However, several hypotheses have been proposed as the underlying pathomechanism discussed by the authors, including alteration in vagal and sympathetic balance and left atrium mechanical stimulation by esophageal distension.

Arrhythmias, particularly supraventricular arrhythmias, can be caused by several predisposing factors, including gastrointestinal problems. Roemheld syndrome, known as gastrocardiac syndrome, an overlap and link between the gastrointestinal symptoms and arrhythmias, was first observed by Ludwig Roemheld[2] later, several subsequent reports described this syndrome.

Finding the link and accurately diagnosing this syndrome is often difficult due to contributions from various possible mechanisms that may cause this syndrome, including vigorous exercise, inflammation within adjacent positioning of esophagus and atria, autoimmune disorders, common nerve innervations, impediments in coronary blood flow, and hiatal hernias.[2] Esophagus stimulation, whether mechanical or chemical by acid reflux, potentiates afferent vagal activity in GERD concomitant arrhythmia patients. Elevated vagal tone shortens effective atrial refractoriness, resulting in development of atrial arrhythmia.[3]

In addition, GERD may release various inflammatory cytokines, i.e., interleukin (IL)-1β and IL-6, which lead to systemic inflammation.

The increase of circulating cytokines may prompt arrhythmia development, particularly atrial fibrillation (AF). In addition, acid reflux may cause lower esophagus inflammation and subsequently penetrate the esophagus wall, affecting the vagal nerves and leading to atrial myocarditis or local pericarditis.[2,3] This may happen due to adjacency of esophageal to atrium and alteration of local receptors. Consequently, cardiac rhythm afferent-efferent reflex mechanisms were induced, secondary to vagal nerve stimulation, thus inducing arrhythmia.[2]

The presence of hiatal hernia can also directly compress atrium, causing a decrease in blood supply to the heart, resulting in relative ischemia that can lead to arrhythmias. This hiatal hernia can also aggravate acid reflux in GERD.[2,3]

Esophageal acid exposure also has potential impact on coronary blood flow. It has been reported that coronary flow was reduced by acid instillation into esophagus. This phenomenon is mediated by autonomic reflex and postulated as one of leading causes of syndrome X, characterized by typical angina despite normal coronary arteries. This phenomenon is absent in denervated heart transplant recipients, supporting that reduced coronary blood flow is achieved through cardioesophageal reflex.[4]

As the first line GERD therapy, proton pump inhibitors (PPIs) may hold potential therapeutic effects in this situation. The PPIs have multimodal effects beyond acid suppression mediated by proton pump (K+-H+ ATPase) inhibition, including antioxidant and anti-inflammatory properties. They have potential antiarrhythmic and cardioprotective agent properties due to functional similarity proteins of the gastric K+-H+ ATPase within cardiac.[2,3]

Quinidine and disopyramide, antiarrhythmics with vagolytic properties,[5] can be used when arrhythmia is suspected due to vasovagal stimulation, while simultaneously treating the underlying gastrointestinal disease.

In conclusion, various pathophysiological mechanisms that may underlie the occurrence of arrhythmias in Roemheld syndrome should be investigated in patients presenting with gastrointestinal complaints and arrhythmias.

Declaration of conflicting interests

The authors declared no conflicts of interest with respect to the authorship and/or publication of this article.

Funding

The authors received no financial support for the research and/or authorship of this article.

References

Bodur O, Yılmaz AS, Akdoğan R, Durakoğlugil ME, Duman H, Kocaman SA, et al. Esophagitis and gastritis are associated with premature atrial contractions in patients with gastroesophageal reflux disease. Cardiovasc Surg Int 2021;8:109-15.

Mohamed A, Ochoa Crespo D, Kaur G, Ashraf I, Peck MM, Maram R, et al. Gastroesophageal reflux and its association with atrial fibrillation: A traditional review. Cureus 2020;12:e10387.

Maruyama T, Fukata M, Akashi K. Association of atrial fibrillation and gastroesophageal reflux disease: Natural and therapeutic linkage of the two common diseases. J Arrhythm 2018;35:43-51.

Lei WY, Wang JH, Wen SH, Yi CH, Hung JS, Liu TT, et al. Risk of acute myocardial infarction in patients with gastroesophageal reflux disease: A nationwide population-based study. PLoS One 2017;12:e0173899.

Price B. Drug therapy of common cardiac disorders. In: Irwin S, Tecklin JS, editors. Cardiopulmonary Physical Therapy: A Guide to Practice. 4th ed. Mosby; 2004. p. 225-39.