Abstract Introduction Obstructive sleep apnea (OSA) is associated with increased cardiovascular morbidity and mortality. Standard management typically involves in-person diagnosis, PAP initiation, and follow-up, but many older adults experience fragmented care due to mobility limitations, comorbidities, or transportation barriers. Telemedicine offers an alternative model that may improve continuity, access, and patient engagement. This case describes five years of virtual OSA management in an older adult with changing medical needs. Report of case(s) An 82-year-old man with atrial fibrillation/flutter (status post multiple ablations and cardioversions), gastroesophageal reflux disease, hyperlipidemia, OSA, and insomnia was followed entirely through telemedicine. Home sleep apnea testing (HSAT) in 2020 revealed mild OSA (REI 12/hour, nadir SpO₂ 79%, 74 minutes < 88%). The patient declined CPAP and chose a mandibular advancement device (MAD). Telemedicine visits from 2020–2022 documented high adherence, symptom improvement, and reduced REI with the MAD. Repeat HSAT showed persistent hypoxemia not explained by residual apneas, prompting in-lab polysomnography (PSG). PSG with the MAD demonstrated REI ~9/hour without significant hypoxemia, supporting continued MAD therapy. Following influenza A pneumonia requiring ICU admission in 2023–2024, the patient experienced functional decline, recurrent atrial fibrillation, 26-lb weight loss, and new oxygen dependence. Because untreated OSA can exacerbate arrhythmia recurrence, repeat evaluation was pursued. In 2025, PSG with the MAD showed progression to severe OSA (REI 32.9/hour, nadir SpO₂ 83%, 24 minutes < 88%). A titration PSG was scheduled to assess supplemental alternative therapies. Conclusion This case illustrates how telehealth can support long-term OSA management in medically complex patients. Virtual care enabled timely reassessment, coordination with dental sleep medicine, and rapid adjustments during periods of clinical instability. Telemedicine was particularly useful for this elderly patient, who faced mobility challenges, hospitalizations, and comorbidities that made in-person visits difficult. Regular virtual follow-up promoted adherence, facilitated recognition of disease progression, and allowed treatment to be individualized over time. Telemedicine represents an effective model for continuous, patient-centered OSA care, especially for older adults and individuals with limited access to traditional sleep medicine services. This case highlights the value of virtual care in maintaining continuity, supporting multidisciplinary collaboration, and adapting therapy to evolving clinical needs. Support (if any)

Sleep apnea is a sleep-related breathing disorder characterized by repeated interruptions in breathing, encompassing two main types: obstructive sleep apnea (OSA), caused by airway obstruction, and central sleep apnea (CSA), resulting from diminished respiratory effort. Sleep apnea is associated with significant health risks, including cardiovascular disease, metabolic dysfunction, and reduced quality of life. Polysomnography (PSG) is the diagnostic gold standard, with positive airway pressure (PAP) therapy as the primary treatment. This study evaluates the demographic, clinical, and treatment characteristics of patients assessed for sleep apnea in a large cohort. A retrospective chart review was conducted for patients referred for sleep studies for evaluation of sleep apnea from November 2020 to March 2024 at an academic medical center. Diagnoses were determined using PSG or home sleep apnea testing (HSAT) and categorized as OSA, CSA, a combination of OSA and CSA, or no sleep apnea. Heart failure comorbidities were identified through transthoracic echocardiograms (TTE) and medical records. Of 1,103 patients evaluated (mean age: 54 ± 16 years; mean BMI: 34.2; 49% male; 61% Caucasian), 76% were diagnosed with OSA, 4% with combined OSA and CSA, and 0.7% with CSA alone. Nineteen percent had no sleep apnea. The mean apnea-hypopnea index (AHI) for patients with available PSG results was 43.9 ± 33.9, indicating severe disease. PAP therapy was prescribed to 69% of patients, including 49% on CPAP, 18% on BiPAP, 1.5% on adaptive servo-ventilation (ASV), and 0.5% on oral appliances. Heart failure was observed in 13.3% of patients, with 9.7% presenting with heart failure with preserved ejection fraction (HFpEF) and 3.6% with heart failure with reduced ejection fraction (HFrEF). This study demonstrates the high prevalence of OSA and its significant association with comorbidities, such as heart failure. These findings highlight the need for early diagnosis and individualized treatment strategies to improve patient outcomes and mitigate the broader health impacts of sleep apnea. AASM Foundation (203-JF-18)

Positional obstructive sleep apnea (POSA) is characterized by a significant increase in airway obstruction and breathing disturbances when a patient sleeps in the supine position compared to sleeping on their side. While mandibular advancement devices (MADs) are effective in managing obstructive sleep apnea (OSA), their efficacy in treating POSA remains uncertain. This study evaluates the effectiveness of MADs in improving clinical and polysomnographic outcomes for patients with POSA. Clinical notes and sleep studies (in-lab polysomnography or home sleep apnea test) were reviewed from patients who received a MAD for OSA treatment between 2019 and 2023. Patients who met the diagnostic criteria for POSA (supine AHI at least double the lateral AHI) were analyzed. Sleep parameters, including the Epworth Sleepiness Scale (ESS), Apnea-Hypopnea Index (AHI), and minimum oxygen saturation (SpO2), were compared between baseline and follow-up visits after MAD titration and optimization. Of 167 patients, 49.7% (n=83) had POSA. The POSA cohort had a median baseline ESS of 8 (range 0-20, n=69), AHI of 13.3 events/hour (range 5.7-62.2, n=67), supine AHI of 19.2 events/hour (range: 8-109.8, n=67), lateral AHI of 5.3 events/hour (range 0-44; n=67), minimum SpO2 of 82% (range 0.7-90, n=67), sleep efficiency of 73.4% (range 37.2-78.9, n=6), and arousal index of 13.2 events/hour (range 6.8-36, n=6). After MAD intervention, the cohort demonstrated a median ESS of 6 (range 0-20), AHI of 8.7 events/hour (range 0.5-88.9), supine AHI of 11.4 events/hour (range 0-85.9), lateral AHI of 4.1 events/hour (range 0-100.8), minimum SpO2 of 82% (range 64-91), sleep efficiency of 81.5% (range 65.4-95.8), and arousal index of 22.7 events/hour (range 2.8-41.9). Patients experienced significant reductions in median overall AHI (p< 0.001) and supine AHI (p< 0.001) and improvement in sleep efficiency (p< 0.001). Similar outcomes were observed in the non-POSA cohort (n=84, 50.3%), including significant reductions in median overall AHI (p< 0.05) and lateral AHI (p< 0.001). Mandibular advancement devices (MADs) effectively improved clinical and polysomnographic outcomes in patients with POSA. Similar benefits in AHI reduction were observed in non-POSA patients, supporting MADs as a viable treatment for both groups. American Academy of Dental Sleep Medicine

The goal of this study was to evaluate the association between a polygenic risk score (PRS) for QT prolongation (QTc-PRS), corrected QT intervals (QTc) and sudden cardiac death (SCD) in participants enrolled in the UK Biobank with and without sleep-disordered breathing (SDB). The QTc-PRS was calculated using allele copy number and previously reported effect estimates for each single nuclear polymorphism. Competing-risk regression models adjusting for age, sex, body mass index, QT prolonging medication, race, and comorbid cardiovascular conditions were used for SCD analyses. A total of 500,584 participants were evaluated (56.5 ± 8 years, 54

Abstract Introduction Obstructive sleep apnea (OSA) is characterized by episodes of partial or complete collapse of the upper airway. OSA has been associated with increases in QTc interval and QT variability—risk factors for ventricular arrhythmias and death. This study explores how QTc and QT Variability change with positive airway pressure therapy (PAP) in patients without heart failure (HF), HF with preserved ejection fraction (HFpEF), and HF with reduced ejection fraction (HFrEF) based on sleep stage. Methods Consecutive patients with OSA undergoing diagnostic and PAP titration polysomnography (PSG) were included for analysis. Electrocardiogram (ECG) analysis during PSG was performed using Comprehensive Analysis of Repolarization Signal (COMPAS) software for the longest apnea/hypopnea events in NREM and REM for the diagnostic period as well as on the highest CPAP or BPAP pressure delivered for the titration PSG. Both Bazett’s (QTbc=QT/RR1/2) and Fridericia’s (QTfc=QT/RR1/3) corrections were used to calculate corrected QT. QT variability measures included the standard deviation of QT intervals (SDQT), normalized QT interval variance (QTVN), short-term interval beat-to-beat QT variability (STVQT) and QT Variability Index (QTVi). Sleep stages were characterized as Non-Rapid eye movement (NREM) vs. REM. Results Ninety two patient diagnostic and 92 titration PSG were reviewed (54% male, age 54 ± 15 years, BMI 38.5 ± 8.9, AHI 51.8/hr ± 39.0, minimum spO2 74.9% ± 14.4). Only eight percent of the patients had HF. There were no significant differences in QTfc and QTbc in NREM and REM. In the no HF cohort, QTVi decreased significantly in REM (n=31) during titration (0.78 ±1.79) when compared to baseline (1.64 ± 1.65), p=0.0026. In the no HF cohort, no significant changes were noted in QT variability during NREM (n=66) in the titration PSG when compared to the diagnostic PSG. No other findings in QT variability were statistically significant including the HFrEF and HfpEF cohorts however those sample sizes were very small. Conclusion PAP in patients with no HF may result in decreased QT variability and the effects may be varied based on sleep stage. Our findings need to be verified in larger cohorts. Support (if any) American Academy of Sleep Medicine Foundation, National Institutes of Health , The University of Arizona

This perspective on alternatives to positive airway pressure (PAP) therapy for the treatment of obstructive sleep apnea (OSA) summarizes the proceedings of a focus group that was conducted by the Sleep Research Society Foundation. This perspective is from a multidisciplinary panel of experts from sleep medicine, dental sleep medicine, and otolaryngology that aims to identify the current role of oral appliance therapy and hypoglossal nerve stimulation for the treatment of OSA with emphasis on the US practice arena. A secondary aim is to identify-from an implementation science standpoint-the various barriers and facilitators for adoption of non-PAP treatment that includes access to care, multidisciplinary expertise, reimbursement, regulatory aspects, current treatment guidelines, health policies, and other factors related to the delivery of care. The panel has contextualized the review with recent events-such as a large-scale PAP device recall compounded by supply chain woes of the pandemic-and emerging science in the field of OSA and offers solutions for multidisciplinary approaches while identifying knowledge gaps and future research opportunities.

Abstract Introduction Effective obstructive sleep apnea (OSA) treatment can potentially reduce the risk and the public health burden of OSA. While continuous positive airway pressure (CPAP) therapy remains the gold standard for treating OSA, long-term adherence is suboptimal. Although adherence to mandibular advancement devices (MADs) is higher, long-term data is lacking. This study explores the potential of MAD to i) improve patient symptoms and clinically relevant parameters and ii) evaluate telehealth as a platform to increase MAD accessibility and address the public health burden of OSA. Methods The electronic medical records of patients administered a MAD for OSA at an academic medical facility from 2019 to 2023 were evaluated. Patient demographics and mode of healthcare delivery were extracted. For patients who received a MAD, variables from their diagnostic polysomnography, like the Epworth Sleepiness Scale (ESS) and the apnea-hypopnea index (AHI), were compared with those from follow-up polysomnography with the MAD. These variables were also compared between the in-person and telehealth cohorts. Results 176 patients received a MAD for OSA treatment (56 ± 16 years of age, BMI 31 ± 7 kg/m2, 59% female, 82 White, 20% Hispanic/Latino). 37% and 59% of initial visits used telemedicine or teledentistry, respectively. Insurance coverage included AHCCS (26%), Medicare (20%), and commercial insurance (79%) as primary or secondary. The baseline ESS was 8 ± 4 (range 1-24). Initial diagnostic sleep study noted an AHI of 18 ± 15/hour (range 5-109.9/hour; supine 22±18/hour, lateral 14±25/hour), minimum oxygen saturation of 81 ± 7, sleep efficiency of 74 ± 16/hour, and an arousal index of 24 ± 19/hour. In the follow-up polysomnography with the MAD, significant differences were noted in AHI (p=0.0062) regardless of the frequency of in-person or telehealth encounters. While significant differences were not noted in ESS for the overall cohort (p=0.11), ESS improvement was significant in the telemedicine (p=0.03) and teledentistry (p=0.018) cohorts. Conclusion MAD use can improve clinically relevant parameters in OSA. Telehealth can deliver clinically effective treatment of OSA. Support (if any) American Academy of Dental Sleep Medicine, American Academy of Sleep Medicine Foundation, National Institutes of Health, The University of Arizona.

Introduction:The goal of this study was to evaluate the association between a polygenic risk score (PRS) for QT prolongation (QTc-PRS), QTc intervals and mortality in patients enrolled in the UK Biobank with and without sleep apnea. Methods:The QTc-PRS was calculated using allele copy number and previously reported effect estimates for each single nuclear polymorphism SNP. Competing-risk regression models adjusting for age, sex, BMI, QT prolonging medication, race, and comorbid cardiovascular conditions were used for sudden cardiac death (SCD) analyses. Results:500,584 participants were evaluated (56.5 ±8 years, 54% women, 1.4% diagnosed with sleep apnea). A higher QTc-PRS was independently associated with the increased QTc interval duration (p<0.0001). The mean QTc for the top QTc-PRS quintile was 15 msec longer than the bottom quintile (p<0.001). Sleep apnea was found to be an effect modifier in the relationship between QTc-PRS and SCD. The adjusted HR per 5-unit change in QTc-PRS for SCD was 1.64 (95% CI 1.16 - 2.31, p=0.005) among those with sleep apnea and 1.04 (95% CI 0.95 - 1.14, p=0.44) among those without sleep apnea (p for interaction =0.01). Black participants with sleep apnea had significantly elevated adjusted risk of SCD compared to White participants (HR=9.6, 95% CI 1.24 - 74, p=0.03). Conclusion:In the UK Biobank population, the QTc-PRS was associated with SCD among participants with sleep apnea but not among those without sleep apnea, indicating that sleep apnea is a significant modifier of the genetic risk. Black participants with sleep apnea had a particularly high risk of SCD.

INTRODUCTION:Patients with obstructive sleep apnea (OSA) are at risk for QTc prolongation, a known risk factor for increased mortality. The pro-QTc score can help identify individuals at increased risk for mortality associated with increased QTc however, it has not been evaluated in patients with OSA. The goal of this study was to evaluate the pro-QTc score in patients with OSA. METHODS:Medical records of patients undergoing a sleep study at our sleep center from February 2012 to August 2020 were analyzed. Presence or absence of OSA was determined by polysomnography. The pro-QTc score was calculated with 1 point assigned for each of the following: female sex, QT-prolonging diagnoses and conditions, QT-prolonging electrolyte abnormalities, and medications with known risk for QT-prolongation. Mortality was determined from the electronic medical record of an integrated healthcare system. RESULTS:There were 2246 patients (age 58 ± 15 years, 54% male, 82 dead) with OSA and 421 patients (age 54 ± 18 years, 43% male, 18 dead) without OSA. Of those with OSA, 1628 (72.5%) had at least one risk factor for QTc prolongation. A higher pro-QTc score was associated with greater mortality in patients with OSA (HR 1.48 per pro-QTc score, p < 0.001, 95% CI 1.3-1.7) but not in patients without OSA (HR 1.25 per pro-QTc score, p = 0.30, 95% CI 0.82-1.9), after adjusting for age, body mass index (BMI), and smoking status. CONCLUSION:In patients with OSA, a higher pro-QTc score was associated with greater mortality.

Abstract Introduction Heart failure and sleep disordered breathing are prevalent in the United States and often co-exist; diagnostic strategy and management for sleep disordered breathing may change based on the presence, absence and type of heart failure. The goal of this study was to evaluate how many additional patients would be identified with either heart failure with reduced (HFrEF) or preserved (HFpEF) ejection fraction through existing echocardiogram results when this diagnosis is not explicitly stated in the medical records for patients evaluated at a single academic sleep center. Methods A retrospective chart review was performed for all patients undergoing for a sleep study and/or a PAP device from February 2012 through September 2019 at the University of Arizona. Sleep disordered breathing was identified through either polysomnography (PSG) or home sleep apnea testing (HSAT). Patients were identified with heart failure with reduced ejection fraction if an echocardiogram (TTE) listed ejection fraction Results 2,817 patients were evaluated (age 57 (±16 years), 53% male and 77% Caucasian). Ninety-nine patients (3.51%) were noted to have HFrEF based on past medical history and an additional 38 patients were identified through TTE. One hundred and fifteen patients (4.08%) were noted to have HFpEF based on past medical history and an additional 265 patients were identified through TTE. Among these, a majority had OSA (77% HFrEF and 83% HFpEF), followed by combined OSA and CSA (7% HFrEF and 5% HFpEF), and primary CSA (5% HFrEF and 3% HFpEF). Of the patients identified after having reviewed TTE results, 6 (16%) with HFrEF and 42 (16%) with HFpEF developed treatment emergent central sleep apnea. Conclusion Existing echocardiography data in the electronic medical record can identify additional patients with HFrEF and HFpEF which may impact clinical diagnosis and management of sleep disordered breathing. Support (if any) AASM Foundation (203-JF-18), NIH (HL126140, 2L30HL154400-023), University of Arizona (5299903; 5833261; 4258021)

Abstract Introduction Obstructive sleep apnea (OSA) is associated with prolonged ventricular repolarization at baseline that further increases during sleep when an apnea/hypopnea event occurs. Aggressive treatment of OSA with positive airway pressure therapy (PAP) may further prolong ventricular repolarization during apnea/hypopnea events particularly in patients with heart failure (HF). The goal of this study was to evaluate how ventricular repolarization changes during apnea/hypopnea events in patients with heart failure with reduced (HFrEF) and preserved (HFpEF) ejection fraction and in those patients without HF. Methods Thirty patients with OSA in each of the following groups were randomly selected from a dataset of 2,817 patients: HFrEF, HFpEF and no HF failure. Overnight polysomographies (PSG) for these patients were reviewed and beat-to beat measurements during apnea/hypopnea events were obtained at baseline (without PAP) and on the highest PAP setting attempted. Fridericia’s heart rate corrections were used to calculate QTc. QT variability was measured as the standard deviation of QT intervals (SDQT). Results The electrocardiogram was analyzable for n=11 with HFrEF (age 71± 17 years , 91% male) , n=28 with HFpEF (age 71± 12 years , 43% male) and n=30 without HF (age 57± 12 years , 50% male). In those with HFrEF, the mean (SD) QTc increased from 442(12)ms to 452(13)ms and SDQT increased from 9(2) to 13 (2) from baseline to the highest level of PAP attempted. In those with HFpEF, the mean (SD) QTc decreased from 448 (8) to 436 (8) ms and SDQT increased from 10 (1) to 11 (1) from baseline to the highest level of PAP attempted. In those without HF, the mean (SD) QTc increased from 429(37) to 439(56) and SDQT was stable from 8(6) to 8(8) from baseline (no PAP) to the highest level of PAP attempted. There were significant differences noted between the groups in changes in QTc (p=0.002) and SDQT (p=0.048) on PAP when compared to baseline. Conclusion Patients with HFrEF had increases in both QTc and SDQT with PAP at high pressures placing them at greater risk for ventricular arrhythmias. Support (if any) AASM Foundation (203-JF-18), NIH (HL126140, 2L30HL154400-023), University of Arizona (5299903; 5833261; 4258021)

Abstract Introduction Positive airway pressure (PAP) therapy is the mainstay treatment for obstructive sleep apnea (OSA). Continuous PAP (CPAP) therapy has been shown to decrease QTc length in electrocardiograms in patients with OSA in small studies. The impact of higher pressures of CPAP and Bilevel PAP (BPAP) on ventricular repolarization—QTc length and QT variability in OSA is unknown. The goal of this pilot study is to explore this relationship. Methods 10 consecutive patients who underwent polysomnography during which they had a diagnostic, CPAP titration, and BPAP titration portion were included for analysis. Bazett’s heart rate correction was used to calculate QTc. QT variability was measured as short-term interval QT variability (STVQT) and normalized QT interval variance (QTVN). All variables were analyzed for the entire duration of the diagnostic period, on the highest CPAP pressure and highest BPAP pressure delivered. Results The patients were 49 ± 15 years of age and 60% women. Median CPAP pressure was 14.5 cm H2O (mean 13.5 ± 5 cm H2O). For BPAP, the median inspiratory PAP was 21.5 cm H2O (mean 20.5 ± 5 cm H2O) and EPAP median was 16 cm H2O (mean 15.9 ± 4 cm H2O). Mean QTc for the diagnostic portion, highest CPAP pressure and highest BPAP pressure were 430 ± 17 ms, 445 ± 15 ms and 441 ± 21 ms, respectively (p=0.141). Mean QTVN for the diagnostic portion, highest CPAP pressure and highest BPAP pressure settings were 0.0011 ± 0.0008 dimensionless units (du), 0.0012± 0.0008 du and 0.002 ± 0.0012 du, respectively (p=0.127). STVQT for the diagnostic portion, highest CPAP pressure and highest BPAP pressure settings were 6.62 ± 4.13 ms, 9.12 ± 4.7271 ms and 12.62 ± 4.99 ms, respectively (P=0.041). Post-hoc pairwise comparisons between BPAP and diagnostic portions of the study were significant for STVQT (P=0.034). Conclusion Short-term QT variability, STVQT, was significantly increased on BPAP when compared to the diagnostic portion of the study. Support (If Any) American Academy of Sleep Medicine Foundation (203-JF-18), National Institutes of Health (HL126140, 2L30HL154400-023) University of Arizona Health Sciences Career Development Award (5299903), and University of Arizona Faculty Seed Grant (5833261)

Abstract Introduction Evidence suggests that patients with obstructive sleep apnea (OSA) are at risk for QTc prolongation which, is a known risk factor for arrhythmias, sudden cardiac death and all cause mortality. QTc risk scores have been implemented widely to help physicians identify patients at risk for mortality however, these risk scores have not been routinely implemented in patients undergoing sleep studies or those diagnosed with OSA. The goal of this study was to evaluate the distribution of pro-QTc risk scores for patients with and without OSA diagnosed at our facility and its relationship to mortality. Methods Medical records of all patients undergoing a sleep study at our sleep center from 2/2012 through 8/2020 were analyzed. Patients were identified with or without OSA based on polysomnography or Type III home sleep study. The pro-QTc risk score was calculated with 1 point assigned for: female sex, QT-prolonging diagnoses and conditions, QT-prolonging electrolyte abnormalities, and QT-prolonging medications defined as medications with known and possible risk of torsades de Pointes based on the CredibleMeds website. Mortality was determined if a death date was noted in the electronic medical record. Results A total of 2,834 patient records (54% male, age 58 ± 16 years, n=106 dead) were evaluated. A total of 2,265 patients (age 58 ±15, 54% male, 89 dead) were identified as having OSA and 428 patients (age 54 ± 18, 41% male, 17 dead) did not have OSA. The remaining patients (n=141) had either central sleep apnea or a combination of both obstructive and central sleep apnea. A higher pro-QTc score was associated with greater mortality regardless of presence of OSA (HR 1.3, p<0.0001, 95% CI 1.12 -1.46) after adjusting for age. The association of pro-QTc with mortality was not increased in the moderate or severe OSA groups compared to those without OSA or mild OSA (p=0.36). Conclusion Increased pro-QTc scores were associated with greater mortality in all patients undergoing sleep studies. OSA status did not affect this association. Support (If Any) American Academy of Sleep Medicine Foundation (203-JF-18), National Institutes of Health (HL126140, 2L30HL154400-023), University of Arizona Health Sciences Career Development Award (5299903), and University of Arizona Faculty Seed Grant (5833261)

Introduction: Variability and prolongation of ventricular repolarization -measured by changes in QT interval and QT variability are independently associated with ventricular arrhythmias, sudden death, and mortality but such studies did not examine the role of sleep-disordered breathing. We aimed to determine whether sleep-disordered breathing moderated the association between measures of ventricular repolarization and overall mortality. Methods: Eight hundred participants were randomly selected from each of the following four groups in the Sleep Heart Health Study: mild, moderate, severe or no sleep disordered breathing (n = 200 each). Overnight electrocardiograms were analyzed for QTc duration and QT variability (standard deviation of QT intervals, normalized QT interval variance and the short-term interval beat-to-beat QT variability). Cox proportional hazards penalized regression modeling was used to identify predictors of mortality. Results: Eight hundred of 5600 participants were randomly selected. The participants (68 +/- 10 years; 56.8% male) were followed for an average of 8.2 years during which time 222 (28.4%) died. QTc, SDQT, and QTVN were associated with the presence of SDB (p = 0.002, p = 0.014, and p = 0.024, respectively). After adjusting for covariates, the presence of sleep-disordered breathing did not moderate the association between QTc length, QT variability and mortality (p > 0.05). Conclusion: Sleep-disordered breathing was associated with some measures of ventricular repolarization. However, sleep-disordered breathing was not an effect modifier for the relationship between QTc and QT variability and mortality. (C) 2022 Elsevier B.V. All rights reserved.

Abstract Introduction The apneas and hypopneas that characterize sleep-disordered breathing (SDB) are associated with QTc prolongation and increased QT variability. There have been mixed results as to whether QTc and QT variability increase with increasing SDB severity. This study assesses whether QTc prolongation and QT variability are likely to increase with increasing severity of SDB in a large multi-center cohort. Methods 200 subjects with no SDB and approximately 600 with three levels of SDB (mild, moderate, severe) were randomly selected from the Sleep Heart Health study and matched by age, gender and BMI. SDB was defined as an apnea/hypopnea index ≥5. Respiratory and electrocardiograms (ECG) signals from polysomnography studies were analyzed. Bazett’s heart rate correction was used to calculate QTc. QT variability was measured as standard deviation of QT intervals (SDQT) and short-term interval QT variability (STVQT), at 5-minute intervals. Subjects were excluded if there were missing data or low-quality ECG. Results Seven hundred and seventy-one subjects (age 68±10 years, 51% female, 92% Caucasian) were included. One hundred and sixty-five subjects had no SDB, 235 mild, 195 moderate and 176 had severe SDB. The mean (SD) QTc was 422(29), 411(26), 419 (34) and 418 (36) ms for the no SDB, mild, moderate, and severe SDB groups, respectively (p=0.017). The mean (SD) STVQT was 7 (9), 11 (16), 8 (9) and 9 (11) for the no SDB, mild, moderate severe SDB groups, respectively (p=<0.001). The mean (SD) STVQT was 3 (2), 4 (4), 4 (3) and 4(4) for the no SDB, mild, moderate severe SDB groups, respectively (p=<0.001). There was no statistically linear relationship between QT prolongation or QT variability and SBD severity. Conclusion QTc duration and QT variability were not increased with SDB severity. Support (if any) American Academy of Sleep Medicine Foundation (203-JF-18), National Institutes of Health (HL126140), University of Arizona Health Sciences Career Development Award (5299903), and University of Arizona Faculty Seed Grant (5833261)

Sleep disordered breathing (SDB) is associated with increased mortality. Obstructive apneas/hypopneas have been associated with an increase in both QTc duration and QT variability. These markers of ventricular repolarization are associated with arrhythmias and death. It is unknown whether SDB-related QTc changes are responsible for the relationship between QTc/QT variability and cardiovascular death (CVD). From the Sleep Heart Health Study, we randomly selected 200 subjects in each of four groups based on overall apnea/hypopnea index: those with no SDB and those in either, mild, moderate or severe SDB at baseline, matched for gender, age and BMI. Respiratory-related channels and electrocardiograms (ECG) from each polysomnography were analyzed. QTc was calculated using Bazett’s heart rate correction. The following measures of QT variability were obtained: i) standard deviation of QT intervals (SDQT) at 1- and 5-minute intervals and ii) short-term interval QT variability (STVQT) at 5-minute intervals. Cox proportional hazards regression models were used to evaluate potential predictors of CVD. Twenty-nine subjects were excluded either due to missing data or low quality ECG. The 771 subjects included were 68±10 years of age, half were female. During follow-up, 220 subjects (28.5%) died of CVD among whom, 67 (30.5%) had comorbid severe SDB, 45 (20.5%) had no SDB, and the remaining CVD deaths had mild (47, 21.4%) and moderate 61 (27.7%) SDB. The CVD patients were more likely to be older(p<0.001), hypertensive (p<0.001), diabetic(p<0.001), and had increased SDQT(p<0.001), STVQT(p<0.001) and QTc (0.017). After adjusting for covariates, the presence of mild (p=0.562), moderate(p=0.439) and severe SDB (p=0.912) did not moderate the association between QTc prolongation and CVD. Additionally, mild (p=0.486), moderate(p=0.478) and severe SDB (p=0.849) did not moderate the association between SDQT and CVD. Similarly, mild (p=0.144), moderate(p=0.594) and severe SDB (p=0.508) did not moderate the association between STVQT and CVD. However, QTc, SDQT, STVQT, mild and severe SDB were individually associated with CVD (p=0.004, 0.000, 0.000, 0.014, 0.022, respectively). SDB was not a factor in the relationship between QTc prolongation/QT variability and CVD. American Academy of Sleep Medicine Foundation (203-JF-18), National Institutes of Health (HL126140), University of Arizona Health Sciences Career and Development Award (5299903)