Long-Acting Beta2-Agonists Do Not Increase Cardiovascular Risks

Statins may help decrease mortality in patients with COPD.
Statins may help decrease mortality in patients with COPD.
Combination therapy with an inhaled LABA and inhaled corticosteroid did not affect all-cause mortality in patients with COPD compared with inhaled placebo, LABA alone, or corticosterioid alone.

Inhaled long-acting beta2-agonist (LABA) use for moderate chronic obstructive pulmonary disease (COPD) did not increase the risk for cardiovascular disease (CVD) events in patients with heightened risk for CVD.

These findings from the SUMMIT (Study to Understand Mortality and Morbidity; ClinicalTrials.gov identifier: NCT0131676 ) study were published in Heart.1

CVD and COPD are among the 3 leading causes of death in the world, and they commonly co-occur in individual patients. The risk for CVD, which accounts for one-third of deaths in patients with COPD, is higher in these patients than in the general population.2,3

However, the optimal management of COPD in patients with concurrent CVD is unclear and remains controversial.1 “There has been concern for decades that LABA [long-acting beta2-agonist] therapy for patients with COPD might increase cardiovascular events, particularly among high-risk patients,” Robert D. Brook, MD, from the University of Michigan, said in an interview with Cardiology Advisor. However, data on the effects of LABA use on CVD risk are limited and conflicting.1

The SUMMIT trial found that combination therapy with an inhaled LABA (vilanterol) and an inhaled corticosteroid (fluticasone furoate) did not affect all-cause mortality compared with inhaled placebo, vilanterol alone, or fluticasone furoate alone in patients with moderate COPD and high CVD risk.4 Dr Brook and the SUMMIT investigators examined the risk of having a CVD event with LABA treatment in the SUMMIT trial population.1

In SUMMIT, 16,485 patients were randomly assigned to receive inhaled vilanterol, inhaled fluticasone furoate, combination vilanterol and fluticasone furoate, or inhaled placebo.4 The prespecified secondary end point was the first composite CVD event, defined as myocardial infarction, unstable angina, stroke, transient ischemic attack (TIA), or CVD death.1

Of 688 patients who experienced a first composite CVD event, 37% had acute coronary syndrome, 23% had stroke or TIA, and 35% had sudden death.1

No differences in rates of composite CVD events were observed between any of the groups. Time to first composite CVD event was also similar in each treatment group compared with placebo.1

Rates of CVD adverse events (eg, arrhythmia, hypertension) did not differ in the 4 treatment groups.1

“Our findings show in a very large randomized controlled trial that even among patients with established heart disease, a [LABA] does not pose any excess risks for cardiovascular events. Used alone or in conjunction with an inhaled corticosteroid, this treatment can effectively treat COPD in a safe manner,” Dr Brook concluded.

While LABA therapy was safe for treating COPD in patients with high CVD risk, it did not reduce CVD risk in this population.1

“Further studies are required to determine how to optimally reduce heart disease risk among individuals with COPD, if standard treatments (eg, statins) are [as] effective as they are in other populations, and, finally, if certain specialized management (or treatments) of COPD might lead to improvements in cardiovascular health,” Dr Brook said.

The SUMMIT trial was funded by GlaxoSmithKline. Dr Brook is an external member of the SUMMIT Steering Committee.


  1. Brook RD, Anderson JA, Calverley PM, et al; SUMMIT Investigators. Cardiovascular outcomes with an inhaled beta2-agonist/corticosteroid in patients with COPD at high cardiovascular risk [published online April 17, 2017]. Heart. doi:10.1136/heartjnl-2016-310897 
  2. Lozano R, Naghavi M, Foreman K, et al. Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet. 2012;380:2095-2128.

This article originally appeared on The Cardiology Advisor