## 2 Materials and Methods  
### Study Cohort  
The cohort used in this study included 179 patients recruited from the Cardiology (mainly those on the waiting list for an implantable loop recorder), Neurology, or Emergency Departments between January 2019 and May 2024 at Alvaro Cunqueiro Hospital (Vigo, Spain). The study was approved by the Galicia Ethics and Research Committee under protocol number 2019/048. This work is part of the SINCOSAS study [24], an initiative aimed at exploring the relationship between SUC and sleep apnea (SA), a connection that has been little studied to date. All participants were informed about the nature and objectives of the study, and written informed consent was obtained from all subjects involved. Patients over 18 years of age with a diagnosis of syncope of unknown cause after neurological and cardiological evaluation in accordance with clinical guidelines [1] were included. Patients with a diagnosis of SA, epilepsy, or illicit drug use were excluded. The first column of Tables 1 and 2 presents a summary of the collected variables. Anthropometric variables were recorded [age, sex, body mass index (BMI)], known cardiovascular diseases [ischemic or valvular heart disease, arterial hypertension, stroke, arrhythmias], respiratory diseases (COPD, asthma), dyslipidemia, and diabetes. Smoking habits (status and pack-years), symptoms of SA (daytime sleepiness assessed using the Epworth Sleepiness Scale, awakenings, non-restorative sleep, daytime fatigue), total number of syncopal episodes, and number of episodes in the previous year were also recorded. In addition, the use of negative intotropic (cardioppressive) drugs capable of reducing heart rate was documented. All patients underwent overnight home respiratory polygraphy using the Embletta(r) MPR model (Natus Medical Inc., Middleton, WI, USA), a type III portable system that allows synchronized recording of electrocardiographic signals and automated analysis of heart rate variability (HRV). The device is equipped with sensors to measure nasal airflow (via pressure transducer and thermistor), thoracic and abdominal respiratory effort (inductive bands), and oxygen saturation and heart rate via a finger pulse oximeter, as well as continuous electrocardiographic monitoring. All electrocardiographic signals were obtained with a sampling rate of 200 Hz. Recordings were conducted between 00:00 and 07:00. Respiratory events were initially detected through automated analysis and subsequently reviewed and manually corrected by trained personnel. HRV analysis was performed automatically. The definition and classification of apneas and hypopneas followed the clinical guidelines of the Spanish Society of Pulmonology and Thoracic Surgery (SEPAR) [25]. The apnea-hypopnea index (AHI) was calculated as the total number of apneas and hypopneas divided by the total recording time. The respiratory events included in the AHI are apneas and hypopneas, defined as follows: obstructive apnea: \(\geq\)90% reduction in airflow lasting at least 10 s, with continued respiratory effort; central apnea: \(\geq\)90% reduction in airflow for at least 10 s, without respiratory effort; mixed apnea: initially presents without respiratory effort (as a central apnea), followed by resumption of effort; and hypopneas: \(\geq\)30% reduction in airflow for at least 10 s, associated with a \(\geq\)3% oxygen desaturation. AHI was used to classify SA severity as follows: normal: AHI \(<\) 5 events/h; mid: 5 \(\leq\) AHI \(<\) 15 events/h; moderate: 15 \(\leq\) AHI \(<\) 30 events/h; and severe: AHI \(\geq\) 30 events/h.