How useful are proton-pump inhibitors for diagnosis and therapy of patients with noncardiac chest pain?

Non-cardiac chest pain mimics angina pectoris but generally originates from the oesophagus. Visceral hypersensitivity may contribute, but its neurophysiological basis is unclear. We investigated whether central sensitisation, an activity-dependent amplification of sensory transfer in the central nervous system, underlies visceral pain hypersensitivity and non-cardiac chest pain. We studied 19 healthy volunteers and seven patients with non-cardiac chest pain. Acid was infused into the lower oesophagus. Sensory responses to electrical stimulation were monitored within the acid-exposed lower oesophagus, the non-exposed upper oesophagus, and the cutaneous area of pain referral, before and after the infusion. In healthy volunteers, acid infusion into the lower oesophagus lowered the pain threshold in the upper oesophagus (mean decrease 18.2% [95% CI 10.4 to 26.0]; p=0.01) and on the chest wall (24.5% [10.2 to 38.7]; p=0.01). Patients with non-cardiac chest pain had a lower resting oesophageal pain threshold than healthy controls (45 [30 to 58] vs 64 [49 to 81] mA; p=0.04). In response to acid infusion, their pain threshold in the upper oesophagus fell further and for longer (mean fall in area under threshold/time curve 26.7 [11.0 to 42.3] vs 5.8 [2.8 to 8.8] units; p=0.04). The finding of secondary viscerovisceral and viscerosomatic pain hypersensitivity suggests that central sensitisation may contribute to visceral pain disorders. The prolonged visceral pain hypersensitivity in patients with non-cardiac chest pain suggests a central enhancement of sensory transfer. New therapeutic opportunities are therefore possible.

To assess (i) the efficacy of short-term proton pump inhibitors (PPIs) in non-cardiac chest pain (NCCP) and (ii) the performance of an empirical short-term treatment with PPI (PPI test) to establish a diagnosis of abnormal acid reflux in NCCP. Metaanalysis of English language studies identified by searching MEDLINE (1966-May 2004), EMBASE (1980-May 2004), Cochrane Controlled Trials Register, and abstract books from major gastroenterology meetings (1993-2004). For the metaanalysis of PPI efficacy in NCCP, we selected randomized controlled trials (parallel group and crossover designs) comparing PPI therapy with placebo. For the metaanalysis of PPI test performance, we selected uncontrolled studies comparing the test with a standard reference. Eight studies were included in the PPI efficacy analysis. The pooled risk ratio for continued chest pain after PPI therapy was 0.54 (95% CI 0.41-0.71). The overall number needed to treat was 3 (95% CI 2-4). The pooled sensitivity, specificity, and diagnostic odds ratio for the PPI test versus 24-h pH monitoring and endoscopy were 80%, 74%, and 13.83 (95% CI 5.48-34.91), respectively. All studies were small and there was evidence of publication bias or other small study effects. PPI therapy reduces symptoms in NCCP and may be useful as a diagnostic test in identifying abnormal esophageal acid reflux.

This study assessed whether childhood and current adversities: (a) were more prevalent in patients with functional dyspepsia (FD) or non-cardiac chest pain (NCCP) than in patients with gastro-oesophageal reflux disease (GORD) or ischaemic heart disease (IHD); and (b) predicted health related quality of life in these disorders.