Background: Patients with sleep apnea syndrome (SAS) and heart failure (HF) have concomitant different comorbidities and increased risk of morbidity.
Aim: The aim of this study was to analyze differences between patients with SAS and heart failure with preserved ejection fraction (HFpEF; ejection fraction [EF]≥50%) – group 1 and those with SAS and heart failure with reduced ejection fraction (HFrEF; EF<50%) – group 2.
Methods: We evaluated 51 patients with SAS and HF in the sleep laboratory of Timisoara Victor Babes Hospital. We collected general data, sleep questionnaires, anthropometric measurements (neck circumference [NC], abdominal circumference [AC]), somnography for apnea–hypopnea index (AHI), oxygen desaturation index (ODI), echocardiographic data, comorbidities, and laboratory test.
Results: The study included 51 patients who were divided into two groups depending on EF, with the following characteristics: Group 1 (HFpEF): 26 patients, 19 males, seven females, age 61.54±9.1 years, body mass index (BMI) 37±6.4 kg/m2, NC 45.4±3.6 cm, AC 126.6±12.9 cm, AHI 48.3±22.6 events/hour, central apnea 5.6±11.4 events/hour, obstructive apnea 25.7±18.7 events/hour, ODI 41.2±21.2/hour and lowest SpO2 –72.1±14%.
Group 2 (HFrEF): 25 patients, 18 males, seven females, age 63.6±8.8 years, BMI 37.9±7.5 kg/m2, NC 46±4.4 cm, AC 127.2±13.9 cm, AHI 46.4±21.7 events/hour, central apnea 4.6±8.3 events/hour, obstructive apnea 25.9±18.5 events/hour, ODI 44.8±27.1/hour and lowest SpO2 –70.6±12.1%. Differences between groups regarding anthropometric and somnographic measurements and lipidic profile were not statistically significant.
Significant differences were observed regarding stroke (23% vs. 4%, p=0.04) in the group with HFpEF and regarding creatinine measurements (1.1±0.2 vs. 1.4±0.7, p=0.049), aortic insufficiency (11.5% vs. 36%, p=0.04) and tricuspid insufficiency (6.1% vs. 80%, p=0.01) in the group with HFrEF.
Conclusions: Patients with SAS and HFpEF have a higher risk of stroke. Patients with SAS and HFrEF have a significantly increased risk of developing a life-long chronic kidney disease and aortic and tricuspid insufficiency. These results may suggest pathogenic links between SAS and the mentioned comorbidities, and this may explain the higher mortality when this association is present.