
Sleep Apnea as a High-Risk Comorbidity in HFpEF
A FINEARTS-HF subgroup analysis shows patients with HFpEF and comorbid sleep apnea face a 43% higher adjusted cardiovascular risk.
Sleep apnea is common, frequently overlooked, and may carry significant implications for patients with heart failure with preserved or mildly reduced ejection fraction (HFpEF, HFmrEF). At ACC 2026, Pharmacy Times spoke with Sofia Schneider, MD, MS, a resident at Brigham and Women's Hospital, about her poster presentation examining the intersection of sleep apnea and HFpEF within the FINEARTS-HF (NCT04435626) dataset and what the findings mean for how clinicians should be thinking about risk stratification in this population.
Pharmacy Times: What prompted the evaluation of sleep apnea in patients with HFmrEF and HFpEF?
Sofia Schneider, MD, MS: My background is in sleep research. I was interested in clinical questions surrounding sleep even before medical school. When I began working with my mentors, we wanted to investigate sleep apnea specifically within the FINEARTS-HF dataset. Sleep apnea is a common but under-recognized disorder in HFpEF and HFmrEF, and there is significant symptom overlap between the 2 conditions: poor exercise tolerance, dyspnea, poor sleep quality, and fatigue. There is also growing research suggesting a biological connection: both sleep apnea and HFpEF share mechanisms, including increased RAS activation, sympathetic activation, LV remodeling, and elevated blood pressure. We had limited data on whether sleep apnea modifies the response to heart failure therapies, and that's what we set out to explore.
Pharmacy Times: Can you summarize the key findings and their clinical significance?
Schneider: In the FINEARTS-HF trial, we compared patients with heart failure with preserved or mildly reduced ejection fraction who had comorbid sleep apnea to those without. We found that patients with sleep apnea had substantially higher cardiovascular risk and a greater symptom burden. Importantly, finerenone (Kerendia; Bayer) reduced heart failure events consistently regardless of sleep apnea status—but because baseline risk was higher in patients with sleep apnea, the absolute cardiovascular risk reduction was greater in that group. This matters because sleep apnea may represent a high-risk, highly modifiable phenotype within the HFpEF population and targeted risk stratification in this group remains very challenging.
Pharmacy Times: Did identification of sleep apnea translate into measurable improvements in cardiovascular outcomes?
Schneider: To give some more specific numbers, patients with sleep apnea had an approximately 43% higher adjusted risk of the primary end point in FINEARTS-HF, which was a composite of total heart failure events and cardiovascular death. That signal was driven more by recurrent events than by mortality alone. Finerenone worked consistently across both groups, but the absolute benefit was numerically larger in those with sleep apnea. We also saw greater improvement in symptoms and a larger systolic blood pressure reduction at 12-month follow-up in patients with sleep apnea.
Pharmacy Times: Based on these findings, should clinicians be screening more routinely for sleep apnea in patients with HFpEF?
Schneider: Absolutely. I think the most immediate clinical takeaway is heightened recognition. Patients with HFpEF who have unexplained recurrent decompensations, difficult-to-control hypertension, or a disproportionate symptom burden—those are the patients who should raise a red flag. That's where clinicians should be thinking about screening for sleep apnea and considering further risk stratification and treatment.












































































































