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Albuterol, the short-acting beta-agonist agent, improved pulmonary biomarkers in patients with early and end-stage heart failure with preserved ejection fraction (HFpEF), a 30-person trial found.

Patients randomized to inhaled albuterol 2.5 mg had exercise pulmonary vascular resistance fall soon afterward by -0.6 Wood Units (versus +0.1 for placebo, P=0.003). Change in pulmonary vascular load was observed in all measures (relative changes approximated):

• Pulmonary vascular resistance: -30% versus 0% (P=0.025)
• Pulmonary arterial capacitance: +40% versus 0% (P=0.0005)
• Pulmonary artery elastance: -25% versus -7% (P=0.002)
• Mean pulmonary artery pressure: -20% versus -4% (P=0.0001)
• Incremental pulmonary resistance: -30% versus -4% (P<0.0001)

The decreases in pulmonary vascular resistance and pulmonary vascular load during exercise were associated with an increase in cardiac output, better ventricular-pulmonary arterial coupling, and a decrease in right atrial pressure without elevation in pulmonary capillary wedge pressure, added Yogesh Reddy, MD, MSc, of Mayo Clinic in Rochester, Minn., in his presentation at the Heart Failure Society of America meeting.

An abstract was published in the as well.

These are promising results, given that traditional pulmonary vasodilators (sildenafil for example) don't work in HFpEF and have even shown harm in some cases.

More research on beta-agonists in HFpEF is warranted, according to Reddy.

His team took hemodynamics and echo measurements during rest and exercise among heart failure patients with exercise pulmonary capillary wedge pressure at least 25 mmHg and ejection fraction over 50%. Study participants had to be without pulmonary parenchymal disease and off long-acting beta-agonist inhalers; additionally, they were excluded if they had constrictive pericarditis, valvular heart disease, and high-output heart failure.

Albuterol and placebo groups wound up sharing the same baseline characteristics and pre-randomization hemodynamics.

"This hemodynamics study was very well performed and the design strong," commented Mandeep Mehra, MD, of Brigham and Women's Hospital in Boston. "It sets the rationale for a larger study, but caution should be urged since beta-agonists are not always safe in such patients, and whether arrhythmias and sudden death is provoked with increased frequency will need to carefully watched for in a larger study since chronic use is very different."

Whether the observed hemodynamics benefits persist on chronic use of beta-agonists and what (if any) benefit they translate to clinically remains to studied, he cautioned.

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