The fixed-dose therapy was shown to reduce exacerbations, regardless of patient history, among those with increased cardiovascular risk.
Robert Wise, MD
Aclidinium bromide (Tudorza Pressair) significantly reduced exacerbation rate among patients with chronic obstructive pulmonary disease (COPD) and cardiovascular (CV) risk in new findings from the phase 4 ASCENT-COPD trial.
In new data presented by author Robert Wise, MD, at the CHEST 2019 Annual Meeting in New Orleans, the long-acting meta antagonist (LAMA) therapy was found to significantly benefit moderate-to-very severe COPD patients with comorbid CV risk when compared to placebo.
Wise, of the Johns Hopkins University School of Medicine, noted the findings quell ongoing concern clinicians have had over the cardiovascular safety of aclidinium.
“Although aclidinium has been shown to be a good bronchodilator, the overall study indicates that it is also effective in reducing exacerbations, which is a pivotal finding,” Wise said in a statement.
The fixed-dose combination therapy from Circassia Pharmaceuticals and AstraZeneca was originally approved this year for the maintenance treatment of COPD.
Wise and colleagues conducted the double-blind, parallel-group assessment among 3589 patients with COPD and high CV risk. Patients were randomized 1:1 to either twice-daily therapy or placebo, with treatment lasting up to 3 years.
Investigators assessed for moderate-to-severe exacerbation rate during the first year of treatment, while major adverse cardiovascular events (MACE) and all-cause mortality were assessed over 3 years. Subgroup analyses included the assessment of aclidinium on MACE in patients regardless of previous-year exacerbations.
Mean patient age, gender, and predicted mean post-bronchodilator forced expiratory volume at 1 second (FEV1) were similar across treatment and exacerbation groups. They reported 1068 (59.6%) treated patients had ≥1 exacerbation in the previous year, versus 1088 (60.5%) placebo patients. Exacerbation, MACE, and all-cause mortality rates were markedly higher among patients with a prior COPD exacerbation.
Aclidinium bromide reduced exacerbation rate in both exacerbation and non-exacerbation groups with similar relative benefit compared to placebo (≥1 exacerbation: AB 0.65 vs 0.82; RR .80; 95% CI, 0.68 — 0.94; no exacerbation: AB 0.27 vs 0.38; RR 0.69; 95% CI, 0.54 – 0.89; P = .34).
Investigators found no statistically significant increase in MACE risk between the therapies in either patient group, and aclidinium bromide did not increase all-cause mortality risk irrespective of exacerbation history.
Wise and colleagues concluded aclidinium bromide reduced moderate to severe exacerbation rate versus placebo, without increase all-cause mortality risk in COPD patients with or without a history of exacerbations. Ultimately, that is the objective of any optimal COPD therapy, Wise said—and the addition of the finding being irrespective of patient exacerbation history is potentially a novel one.
“Prevention of exacerbations of COPD should be a treatment goal in COPD patients regardless of whether they have a history of recent exacerbations,” he said. “Aclidinium is a safe and effective maintenance therapy.”
The study, “Aclidinium Bromide Treatment Stratified by Exacerbation History: Effects on Exacerbations and Major Cardiovascular Events in Patients with COPD and High Cardiovascular Risk (ASCENT-COPD),” was presented at CHEST 2019.