Do calcium antagonists contribute to gastro‐oesophageal reflux disease and concomitant noncardiac chest pain?

What is already known about this subject • Calcium antagonists (CA) are listed in textbooks as potential causes of gastro‐oesophageal reflux disease (GORD). • There have been two studies which have documented increased use of acid suppressant therapy amongst patients taking CAs. What this study adds • This study provides the first data on the frequency of exacerbation and precipitation of gastro‐oesophageal reflux symptoms amongst users of CAs. • It also provides evidence of the likely potential of the different CAs to cause such symptoms and highlights the need for a prospective study into CA therapy. • The data from the study should heighten prescribers' awareness of the potential of these agents to exacerbate/precipitate GORD, and to consider avoiding CAs in patients with GORD or withdrawing them in patients in whom GORD symptoms develop or worsen. Aims A cohort retrospective observational study was undertaken to determine the relationship between calcium antagonist (CA) use and gastro‐oesophageal reflux disease (GORD), as well the ability of CAs to precipitate or exacerbate noncardiac chest pain, an atypical symptom of GORD. Methods Eligible patients were those prescribed CAs for hypertension without a history of ischaemic heart disease or nitrate use. Patients were recruited through 15 pharmacies (hospital 1, community 14). Patients giving informed consent were administered a standard questionnaire to obtain information including history of reflux symptoms before and during treatment with CAs, and the management of these symptoms. Results Three hundred and seventy‐one participants were enrolled. Their mean age was 64 years (SD ± 12.7 years), 51.2% were females and 48.8% males. Of the 130 patients with pre‐existing gastrointestinal (GI) symptoms, 59 (45.4%) reported a worsening of reflux symptoms during CA therapy. Increases in both frequency and severity of symptoms were most common amongst patients on amlodipine (61.3%; P  ≤ 0.0001) and least common amongst those taking diltiazem (12.5%). Reflux‐related symptoms developed in 85 (35.3%) of the 241 previously asymptomatic patients during CA therapy, with verapamil having the greatest number of reports (39.1%; P  = 0.001) and diltiazem the least (30.7%). Conclusions Diltiazem appears the least likely of the CAs to precipitate or exacerbate reflux symptoms. Further research using a prospective design could test whether it may be more appropriate to use diltiazem in patients with ischaemic heart disease and could assess the appropriateness of CA therapy in patients with moderate to severe GORD. Increasing prescriber and pharmacist awareness of these adverse effects may result in better patient outcomes and potentially reduce treatment costs.