Pathological bolus exposure plays a significant role in eliciting non-cardiac chest pain


Professor Poong-Lyul Rhee, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, #50 Irwon-dong, Gangnam-gu, Seoul 135-710, Korea. Email:


Background and Aim:  Pathological bolus exposure is defined in the present study as cases in which all reflux percentage times are above 1.4% of the total reflux number, as revealed by impedance–pH monitoring. The role of pathological bolus exposure in the pathogenesis of non-cardiac chest pain (NCCP) is poorly known. We aimed to classify and characterize NCCP using combined impedance–pH monitoring.

Methods:  Seventy-five consecutive patients with NCCP were prospectively enrolled from January 2006 to October 2008. All the patients underwent upper endoscopy, esophageal manometry, and 24-h multichannel intraluminal impedance (MII)–pH metering.

Results:  Sixteen patients (21.3%) had esophageal erosion upon endoscopy. Upon esophageal manometry, 37 patients (49.3%) had esophageal dysmotility. When the patients were classified based on MII–pH metering, 16 (21.3%) showed pathological acid exposure, and 40 (53.3%) showed pathological bolus exposure. The DeMeester score of patients with pathological acid exposure was higher than that of patients with pathological bolus exposure (P = 0.002). There was no significant difference in age, sex, typical esophageal symptoms, presence of esophageal erosion, esophageal dysmotility, improvement with proton pump inhibitor medication, symptom index ≥50%, percentage of time clearance pH below 4 ≥4%, and all reflux time ≥1.4% in the fasting period between the two groups. When the patients were divided into gastroesophageal reflux disease (GERD)-related NCCP and non-GERD-related NCCP groups based on MII–pH metering and upper endoscopy, there was no difference between the two groups.

Conclusions:  Combined impedance–pH monitoring improves the detection and characterization of NCCP. This study suggests that pathological bolus exposure plays a major role in eliciting NCCP.