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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 acid reflux, and 66% of patients had at least some of their CP episodes attributable to acid reflux [26]. Importantly, following eight weeks of acid suppression, 65% of patients (13/20) had marked improvement or resolution of their symptoms [26].

Further exploring this relationship in a prospective trial of 100 consecutive patients undergoing esophageal manometry with acid infusion provocative testing (Bernstein test) and ambulatory pH monitoring, Hewson et al. found that 48% of patients had abnormal acid exposure times; and among the 83 patients who experienced chest pain, 46% had abnormal reflux parameters, with 60% having a positive symptom index [24]. Interestingly, however, acid provocation testing was positive in only 19% of patients. The authors also prospectively compared the test results of 75 consecutive NCCP patients with both a positive acid perfusion test and CP during a 24‐hour pH monitoring to assess for a positive “symptom index,” whereby pH monitoring identifies reflux events that correlate with patient symptoms [27]. Notably, only 26% of patients (9/34) with abnormal reflux had a positive acid perfusion test, whereas 59% (45/75) had a positive symptom index with pH monitoring.

Another mechanism that may be contributing is the cardio‐esophageal reflex, which occurs when esophageal acid perfusion results in a decreased coronary blood flow velocity [28]. This was explored by Rosztoczy et al. in 51 patients with CP undergoing pH monitoring, esophageal manometry, and acid perfusion testing combined with echocardiography (transesophageal doppler echocardiographic coronary flow measurement in the left anterior descending artery) [25]. Results showed 49% of patients (25/51) had decreased coronary flow velocity during acid perfusion, which was more likely to occur in patients with more severe reflux disease (increased number of reflux episodes, fraction of time below pH 4, and prolonged acid reflux times) (p < 0.05) [25]. These authors therefore suggested that patients with prolonged acid reflux episodes, erosive esophagitis, and coronary spasm may be at higher risk for the development of linked angina.

Finally, another postulated mechanism for GERD in ECP is that of esophageal sensitization of mechanoreceptors. Hu et al. found that in healthy volunteers, acid infusion reduced the first perception (p = 0.05) and pain threshold (p = 0.05) to balloon distension, which was not noted with saline infusion [29]. This relationship between GERD and esophageal hypersensitivity is further discussed in detail in the following section.