Rare and unusual presentation of gastrocardiac syndrome

Abstract

Gastrointestinal pathology can cause cardiac symptoms and disorders. We present a case of a patient who had worsening of her palpitations with food intake. She was found to have a high burden of premature ventricular contractions in the setting of hiatal hernia and gastro-oesophageal reflux disease. After extensive investigations and ruling out cardiac causes, her arrhythmia resolved with the surgical correction of hiatal hernia.

Background

Gastrocardiac, also known as, Roemheld syndrome is a disorder where maladies in the alimentary tract, usually the upper gastrointestinal tract, are found to be related to cardiac symptoms. The causes of the gastrocardiac syndrome include gastro-oesophageal reflux disease (GERD), transverse colon gas, gall bladder dysfunction and hiatal hernia. Atrial fibrillation is the most commonly described arrhythmia in the setting of GERD and hiatal hernia. Multiple case reports and observational studies have reported these findings, but gastrocardiac syndrome remains a neglected and underdiagnosed factor in the workup of arrhythmias.¹ Since there is rarely a cause traceable to a cardiac condition, patients often end up getting extensive workup before it can be recognised. Herein, we report a case of Roemheld syndrome in the setting of hiatal hernia and GERD presenting as palpitations secondary to premature ventricular contractions (PVCs).

Case presentation

A 62-year-old Caucasian woman presented to our cardiovascular clinic with the chief problem of palpitations. She endorsed palpitations for the past few months which have been progressively getting worse. She described the palpitations as moderate in intensity, intermittent in frequency, non-radiating and fluttering sensation that lasted for a variable amount of time. Her associated symptoms included shortness of breath on exertion, diaphoresis and dizziness. She noticed that her symptoms often got worse with food intake. She denied any chest pain, orthopnoea, paroxysmal nocturnal dyspnoea or syncopal episodes. Her cardiovascular examination revealed a pulse with a normal rate and irregular rhythm with occasional extra beats. The remainder of the physical examination was completely unremarkable. Her medical history was significant for long-standing GERD, hiatal hernia, dyslipidaemia and obesity. Our physical examination was consistent with a mildly obese woman (Body mass index of 32 kg/m²) with a presentation of an arrhythmia who was haemodynamically stable at the time of presentation.

Investigations

Preliminary laboratory testing, including a complete blood count and metabolic panel, was unremarkable. She underwent outpatient 48 hours Holter evaluation, which revealed 35 805 beats of ventricular ectopic activity. Most of the ventricular ectopic activity consisted of PVCs with bigeminy and trigeminy. Her PVC burden was accounted for 14.6% at the time of the initial evaluation. She was advised to maintain a symptom log diary and was found to be symptomatic whenever she had a PVC, often during lunch and dinner times. ECG and rhythm strips documented the presence of PVCs with a very narrow QRS complex along with a QRS axis very similar, but slightly different than the underlying QRS (figures 1 and 2). Her echocardiogram revealed normal ejection fraction 55%–60% with no regional wall motion or valvular abnormalities (videos 1 and 2). She also underwent a nuclear stress test which was unremarkable and did not show any signs of ischaemia or infarction. A fluoroscopic examination of the oesophagus, stomach and duodenum was performed which revealed moderate to large sized hiatal hernia with reflux seen to the upper thoracic region (figure 3). The patient subsequently underwent esophagogastroduodenoscopy for her refractory reflux, which revealed a 5-cm hiatal hernia. The patient was subsequently referred for hiatal hernia surgery as it was thought her symptoms were related to the long-standing GERD.

Figure 1.

ECG with frequent premature ventricular contractions in leads II, V1 and V5.

Figure 2.

Twelve lead ECG revealing frequent premature ventricular contractions in precordial leads.

Video 1.

Download video file ^{(2.7MB, mp4)}

DOI: 10.1136/bcr-2020-236910.video01

Video 2.

Download video file ^{(1.8MB, mp4)}

DOI: 10.1136/bcr-2020-236910.video02

Figure 3.

X-ray oesophagram with double contrast study. The image shows a moderate to large sized hiatal hernia (A, B) along with gastroesophageal reflux (C).

Differential diagnosis

Premature ventricular complexes are a common finding and can occur sporadically in nearly all individuals at some point in time. There are multiple conditions including both cardiac and non-cardiac conditions which are associated with frequent PVCs. In our case, the patient did not have any underlying cardiac risk factors, like hypertension, myocarditis or congenital heart disease which would predispose her to such a huge amount of PVC burden. Also, her transthoracic echocardiogram ruled out any structural or functional disease of the heart which could have been an underlying inciting factor. Catecholamine-induced PVCs may increase during exercise and patients usually complain of palpitations on exertion, which could also be a presenting problem about underlying myocardial ischaemia. In such cases, exercise stress testing, with or without imaging, can reveal an underlying catecholaminergic-sensitive PVCs, which in our case did not show any underlying ischaemia.

Electrolyte derangements, in particular potassium and magnesium, were ruled out with a completely normal metabolic panel. Among patients who abuse certain drugs, for example, cocaine, methamphetamines and other stimulant drugs, PVCs have been known to be one of the reasons for hospital admissions for cardiac arrhythmias. It usually resolves with complete cessation and in our case, the patient denied any substance use and her urine drug screen was also unremarkable.²

Endocrinopathies, like thyroid or adrenal hormone derangements, can also be associated with PVCs. Hyperthyroidism is more commonly associated with cardiac arrhythmias, especially atrial arrhythmias. On the other hand, hypothyroidism is associated with ventricular arrhythmias. In such situations, early and effective treatment of thyroid dysfunction may improve their long-term prognosis. Our patient had a normal thyroid-stimulating hormone and free T4 essentially ruling out any thyroid disease.³

Given that the patient had a long-standing history of reflux disease, gastrocardiac syndrome was also thought to be one of the possibilities in this case. Such patients can present with varying cardiac symptoms, including palpitations, angina, heart failure, paroxysmal tachycardia or PVCs.

Treatment

She was started on beta-blockers after which she felt mild improvement in her symptoms. In the meantime, the patient underwent upper gastrointestinal endoscopy for her long-standing history of GERD which was refractory to medical management. The endoscopy revealed a 5 cm hiatal hernia. Subsequently, she underwent a successful surgical correction (Nissen fundoplication) of hiatal hernia, which also led to the resolution of her symptoms of palpitations and shortness of breath.

Outcome and follow-up

On a 6-month and 12-month follow-up visit in the clinic, after the surgery, the patient was symptom free. Holter evaluation on follow-up revealed decreased PVC burden, which was reduced to 0.1%. Since then, the patient has not reported problem of any palpitations.

Discussion

PVCs are ventricular ectopic beats which lead to direct depolarisation of the ventricles bypassing the His-Purkinje system. It leads to asynchronous activation of the two ventricles and is usually perceived as skipped beats or palpitations. Approximately, 1%–4% of the general population is found to have PVCs on standard ECG. Its prevalence increases to 40%–75% on ambulatory Holter monitoring.⁴ The presentation can vary from asymptomatic healthy individuals to sudden death in an individual with structural heart disease. Medical treatment with beta-blockers or calcium channel blockers is the mainstay of management, but refractory cases need intensive workup to delineate the cause. Our case signifies the importance of gastrointestinal morbidities in the aetiopathogenesis of PVCs.

Ludwig von Roemheld first described the association of cardiac symptomatology with gastric pathology in 1952, which is known as Roemheld gastrocardiac syndrome. He was able to stimulate arrhythmias with an oesophagogastric stimulus.⁵

The exact aetiopathogenesis of gastrocardiac syndrome is unknown. However, multiple mechanisms have been postulated. The oesophageal reflux is associated with an autonomic imbalance from increased vagal tone which predisposes to arrhythmogenicity. Multiple cases of atrial fibrillation (AF) have been reported with an association of oesophagitis and GERD.^6–11 Various underlying risk factors have been postulated including long-standing GERD, oesophagitis, obesity, obstructive sleep apnoea and inflammatory bowel disease.

Large hiatal hernias can lead to direct compression of the left atrium and posterior left ventricular wall, thus inciting atrial arrhythmias and PVCs.^{12 13} A number of studies have also reported the extrinsic cardiac and pulmonary vein compression as the underlying cause of dyspnoea in such patients. One such study of patients with large hiatal hernia reported that 66% had moderate or severe left atrium compression and greater than 40% had pulmonary vein compression. Postoperatively, the symptoms resolved which correlated well with the compression.¹⁴ Lastly, cardio-oesophageal reflex encompasses the reduction in the coronary blood flow from oesophageal acid stimulation, which can lead to chronic ischaemic state generating ectopic foci for PVCs.¹⁵ A retrospective analysis revealed an increased risk of cardiac arrhythmias with hiatal hernias. Moreover, the larger size of hernia was associated with increasing odds of arrhythmia.¹⁶ The prevalence of AF in the general population is age dependent and according to the AnTicoagulation and Risk factors In Atrial fibrillation (ATRIA) study, it was reported as 1%.¹⁷ In one large retrospective study with 111 429 patients found that the hiatal hernia was increasingly associated with AF in both genders, and of all age groups, but was more common in young individuals.¹⁸ Another potential mechanism explained by Linz et al, which summarises the various mechanisms of arrhythmias in patients with GERD, discusses the role of the autonomic nervous system. Acid stimulation and local inflammation directly alter the vagal nerve responses, eventually leading to increased susceptibility for AF and other arrhythmias.¹⁹

Our case was noticed to have a PVC burden of 14.6% on the initial Holter evaluation. The evaluation in the earlier stages was unremarkable for any laboratory or structural heart abnormality. If the PVCs are monomorphic, frequent and patients are symptomatic or have a reduced left ventricular function, seen on the echocardiogram, catheter-based ablation can be considered in such cases.²⁰ Electrophysiology (EP) services were appropriately consulted for evaluation and treatment in our case. However, the patient was hesitant to proceed with ablation and opted to try medical therapy. During this process, we noted the hiatal hernia and refractory GERD, which demanded an upper gastrointestinal endoscopy, eventually revealing the hiatal hernia. This hiatal hernia and GERD was thought to precipitate PVCs by multiple mechanisms. In our case, the most likely mechanism was a combination of long-standing GERD causing localised inflammation and subsequently predisposing her to arrhythmogenic activity, along with mechanical displacement and compression from the hiatal hernia. The patient-reported symptoms during lunch and dinner times on most of the occasions but none during breakfast. This could also possibly be due to the heavy meals during those particular times, which exacerbated her GERD, leading to worsening of her arrhythmia. There have been cases reported where a reduction in the frequency of recurrences of AF with the use of proton-pump inhibitors or after Nissen fundoplication surgery was achieved, therefore suggesting a link between the gastrointestinal tract and atrial arrhythmias.^8–11 Similarly, in our case, after the surgery, her symptoms resolved. The repeat Holter evaluation 6 months and a year after surgery revealed less than 0.1% of PVCs without any symptoms or need of medical intervention. Patients with such a presentation usually undergo extensive cardiac testing to rule out common cardiac conditions, such as ischaemic heart disease. The decrease in PVC burden coupled with the resolution of symptoms after the surgery with unremarkable cardiac investigations (routine echocardiography, nuclear stress testing and EP consultation) makes hiatal hernia and GERD as the underlying cause of PVCs in our patient.

Learning points.

• This case stresses on the importance of considering non-cardiac causes in the patients presenting with palpitations.

• Once identified with thorough history taking and pertinent investigations, the gastrocardiac syndrome is a reversible cause of premature ventricular contractions.

• Because of the rarity of the disease and possibly underdiagnosis, patients often end up getting expensive investigations, which could be halted, if recognised early.