Heart Failure Treatment Gaps: Q&A With Advisory Board Member Ileana Piña, MD

Advisory board member, Ileana L. Piña, MD, shares her perspectives on the current state of heart failure, particularly treatment gaps between the genders.


Ileana Piña, MD, is the associate chief for academic affairs at the Montefiore Einstein Center for Heart and Vascular Care in the Bronx, New York, where she is also a professor of medicine and epidemiology and population health.

She previously held the position of director of heart failure and transplantation at University Hospitals of Cleveland, and also completed a quality scholar fellowship at the Cleveland Louis Stokes Veterans’ Administration Medical Center.

Dr Piña’s research relates specifically to heart failure. Most recently, she was a member of the team of investigators in the HF-ACTION trial, which examined psychosocial factors, exercise adherence, and outcomes in heart failure patients.

Q: Describe some neglected aspects of cardiovascular treatment, particularly in heart failure.

A: Even when patients “look good,” medications can probably be uptitrated and/or tweaked, instead of waiting until the next decompensation.1-3

For example, researchers have evaluated the use of beta-blockers in patients with chronic heart failure who met the SHIFT (Systolic Heart failure treatment with the If inhibitor Ivabradine Trial) criteria and the extent to which heart rate reduction was achieved in clinical practice.

Those patients with increased heart rates more often achieved only low doses of beta-blockers compared with patients with lower heart rates, but other randomized trials (eg, MERIT-HF) have failed to show superiority of high beta-blocker doses vs low or moderate doses. Therefore, the solution is not just linked to a general dose-effect relationship—it is more likely motivated by individual patient responses to medication, comorbidities, and genetic predispositions.2   Physicians must, however, make every attempt to uptitrate beta-blockers in heart failure patients with reduced ejection fraction (HFrEF) due to their powerful reduction in mortality and morbidity.

Likewise, heart rate reduction or regulation cannot simply be achieved without regard to the specific drug or mechanism doing so. Reducing a patient’s heart rate does not automatically equate to an improved heart failure prognosis.1  Many drugs can reduce heart rate, but they also have effects beyond a chronotropic action that can alter their efficacy in preventing morbidity and mortality.

In HF-ACTION, a clinical trial I helped conduct, we found that exercise training was well tolerated and safe for patients with systolic heart failure (median left ventricular ejection fraction: 25%).4 Interestingly, only 1 patient in the training group had to be hospitalized during the study compared with 22 patients in the usual care group despite those patients not undergoing any kind of exercise training.4