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2 Diagnosis and Treatment of Esophageal Chest Pain
Edward C. Oldfield, IV1, Parth J. Parekh2, and David A. Johnson3
1 Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Virginia, Charlottesville, VA, USA
2 Division of Gastroenterology, Department of Internal Medicine, Eastern Virginia Medical School, Norfolk, VA, USA
3 Division of Gastroenterology, Department of Internal Medicine, Eastern Virginia Medical School, Norfolk, VA, USA
Introduction
Recurrent noncardiac chest pain (NCCP) is a common clinical scenario with a global prevalence of up to 13%, with related expenditures exceeding $10 billion annually in the United States [1, 2]. Beyond the musculoskeletal etiologies, the majority are esophageal in origin [3]. Recognizably, esophageal chest pain (ECP) manifests from a heterogeneous group of causes, albeit only some of which are well understood. Among these, gastroesophageal reflux disease (GERD) is the primary etiology for approximately 50% of cases, whereas other causes include esophageal hypersensitivity, functional gastrointestinal (GI) disorders, and esophageal dysmotility [4–6]. This discussion will highlight the most recent available evidence‐based literature on the epidemiology, pathophysiology, and treatment of GERD, esophageal hypersensitivity, and esophageal dysmotility as they relate to ECP.* Additionally, a practical clinical algorithm is provided with evidence‐based recommendations for treatment and diagnosis.
Epidemiology
The treatment and evaluation of chest pain (CP) is one of the most frequently encountered emergent clinical scenarios comprising 5.7% of all emergency visits [4]. Recent estimates suggest that in the US, the costs are $10 billion annually, with only 10% of these patients ultimately having acute coronary syndrome or other diagnosis requiring admission [2]. Shockingly, these staggering costs already represent a significant improvement in the utilization of resources, as admissions for CP have decreased from 21% in 2006 to 11.8% in 2013, reflecting nearly $8 billion in estimated savings [5].
Importantly, there are some differences between inpatient and outpatient evaluation of CP, related mostly to the proportion of patients presenting with NCCP. Whereas studies in the emergency department found NCCP represents about 50% of the cases, in the outpatient setting, causes represent 70–80% of cases [6, 7]. In the outpatient evaluation of CP, the main causes are musculoskeletal (33%), gastrointestinal (10–20%), cardiac (stable angina or acute myocardial ischemia) (12–14%), and respiratory (5%) [8–12]. Recognizably, these complaints must be taken seriously, as life‐threatening causes of chest pain may be identified in 5.5–8.4% of patients [12, 13].
Gastroenterologists play an essential role in the evaluation of NCCP, as nearly 10–20% of patients will present with GI causes of CP, the majority of which are esophageal in origin [3]. Esophageal CP is common, with population‐based surveys estimating an annual prevalence of 19–33% with only mild geographic variation (China 19%, Argentina 23.5%, United States 23%, Australia 33%) [14–17]. There is a nearly equal gender distribution, but the prevalence decreases with age [14, 15]. Some studies have also found a correlation between ECP and younger age, increased alcohol and/or tobacco use, and in patients reporting anxiety [18]. This last point is especially important, as 80% of ECP patients have an overlap with a functional GI disorder, half of which were either irritable bowel syndrome (27%) or functional bloating (22%) [19]. Furthermore, 84% of patients with abnormal esophageal manometry (vs. 31% with normal) had a psychiatric diagnosis, with 25% of these patients meeting the criteria for panic disorder [20, 21].
The net effect of this disease prevalence and overlap with a number of functional and mental health disorders has significant negative adverse effects. In an analysis of patients presenting to a tertiary hospital emergency department over a one‐year period, a total of 212 patients were found to have noncardiac chest pain, which resulted in high rates of work absenteeism (29%) and interruptions to daily activities (63%) [22].
Gastroesophageal reflux
Pathophysiology
Gastroesophageal reflux disease (GERD) represents the main cause of ECP [23–25]. This section will discuss not only GERD but also other physiologic mechanisms such as the cardio‐esophageal reflex and the overlap between GERD and esophageal hypersensitivity.
Reflux as an etiology of ECP was originally noted by DeMeester et al. back in 1982 when they reviewed symptom questionnaires and 24‐hour esophageal pH monitoring of 50 patients with severe CP but normal cardiac function and imaging [23]. A total of 46% of patients (23/50) had abnormal pH monitoring, with 57% (13/23) reporting CP, which further coincided with a reflux episode in all but one patient [23]. Additionally, even in patients with angiographic evident coronary artery disease and persistent atypical chest pain, Singh et al. found that 23.2% of chest pain episodes correlated with