title: Cardiovascular safety of salmeterol in COPD.
abstract: BACKGROUND
  Patients with COPD have an increased risk of cardiovascular disease. Despite the clinical benefits of long-acting beta-agonist agents in the treatment of COPD, patients may be at an increased risk of cardiovascular toxicity, including tachyarrhythmia due to beta-adrenergic stimulation.
  
  
  OBJECTIVE
  To evaluate the cardiovascular safety of salmeterol in COPD patients by conducting a pooled analysis of cardiovascular safety data.
  
  
  METHODS
  Randomized, double-blind, parallel group, multiple-dose studies, which included salmeterol, 50 micro g bid, and placebo arms.
  
  
  METHODS
  Seven of a total of 17 studies met the predefined inclusion requirements and were pooled. A total of 1,443 patients received placebo, while 1,410 patients received salmeterol, 50 micro g bid. The median duration of treatment was 24 weeks (range, 12 to 52 weeks).
  
  
  RESULTS
  Treatment with salmeterol, 50 micro g bid, showed no increased risk of cardiovascular adverse events (AEs) compared with placebo (relative risk, 1.03; 95% confidence interval, 0.8 to 1.3; p = 0.838). Both groups had a similar incidence of cardiovascular events (8%), including cardiovascular deaths. The incidence of cardiovascular AEs increased with age, concurrent cardiovascular conditions, and treatment with antiarrhythmic/bradycardic agents, although increases were comparable in both treatment groups. There were no episodes of sustained ventricular tachycardia, and no clinically significant differences were observed in 24-h heart rate, ventricular and supraventricular ectopic events, qualitative ECGs, QT intervals, or vital signs between the salmeterol, 50 micro g bid, group and the placebo group. Similar findings were observed when patients were stratified for age of > 65 years or the known presence of cardiovascular disease.
  
  
  CONCLUSIONS
  Treatment with salmeterol, 50 micro g bid, does not increase the risk of cardiovascular AEs in this population of COPD patients compared with placebo.
authors.affiliation: Pulmonary Research Institute of SouthEast Michigan, Livonia, MI 48152, USA.
authors.forename: Gary T
authors.initials: GT
authors.lastname: Ferguson
authors.forename: Christian
authors.initials: C
authors.lastname: Funck-Brentano
authors.forename: Tracy
authors.initials: T
authors.lastname: Fischer
authors.forename: Patrick
authors.initials: P
authors.lastname: Darken
authors.forename: Colin
authors.initials: C
authors.lastname: Reisner
mesh_terms: D000318:Adrenergic beta-Agonists / Q000008:administration & dosage / Q000009:adverse effects*; D000368:Aged; D000420:Albuterol / Q000008:administration & dosage / Q000009:adverse effects* / Q000031:analogs & derivatives*; D001993:Bronchodilator Agents / Q000008:administration & dosage / Q000009:adverse effects*; D002318:Cardiovascular Diseases / Q000139:chemically induced; D002319:Cardiovascular System / Q000187:drug effects*; D004311:Double-Blind Method; D004562:Electrocardiography; D015716:Electrocardiography, Ambulatory; D005260:Female; D006801:Humans; D008297:Male; D029424:Pulmonary Disease, Chronic Obstructive / Q000188:drug therapy* / Q000503:physiopathology; D000068299:Salmeterol Xinafoate; D013610:Tachycardia / Q000139:chemically induced
chemical_list: D000318:Adrenergic beta-Agonists; D001993:Bronchodilator Agents; D000068299:Salmeterol Xinafoate; D000420:Albuterol