Influence of nocturnal hypoxemia on follow-up course after type B acute aortic syndrome

Introduction Association between sleep nocturnal breathing disorders and acute aortic syndrome (AAS) has been described but mid-term data are scarce. Objectives We assessed the prognostic value of sleep apnea parameters and their relationship with aortic morphology after the onset of a type B AAS. Methods Between January 2010 and January 2018, sleep apnea screening in post type B AAS was prospectively performed. The association of sleep apnea parameters with aortic morphology and aortic expansion during follow-up was studied. Results Over the 8-year-study period, 103 patients were included, with a mean age of 57.8 ± 12.1 years old. Median follow-up was 25.0 months (11.0–51.0). Thirty-two patients (31%) required aortic stenting during the acute phase. In patients treated by aortic stenting, the descending thoracic aortic diameter was positively associated with a higher percentage of nocturnal time of saturation ≤ 90% after adjustment (p = 0.016). During follow-up, the nocturnal time of saturation ≤ 90% in patients treated by medical therapy was the only parameter associated with significant aortic expansion rate (r = 0.26, p = 0.04). Thirty-eight patients started and sustained nocturnal ventilation during follow-up. The association between aortic expansion rate and nocturnal time of saturation ≤ 90% did not persist during follow-up after adjustment on nocturnal ventilation initiation (r = 0.25, p = 0.056). Conclusions Nocturnal hypoxemia parameters are positively associated with the max onset aortic diameter and significant aortic growth after type B AAS. Nocturnal ventilation seems to mitigate aortic expansion during follow-up.

Correlation arterial stiffness and central blood pressure with obstructive sleep apnea in patients with resistant arterial hypertension

The aim assess correlation the arterial stiffness in patients with resistant arterial hypertension (AH) and obstructive sleep apnea (OSA) Design 185 patients with AH were enrolled into the study. They were divided on 2 groups: OSA group – 148 patients were found to have OSA, indicated by at mean AHI of 38.1±2.5 h–1, and control group – 37 patients without OSA, mean AHI 3.02±0.25 h–1 (P<0.001). Patients of both groups were comparable on age, growth, total cholesterol level and office systolic blood pressure (SBP) and diastolic blood pressure (DBP). Results Patients with RAH and OSA (mean apnea-hypopnea index (AHI) 36.5±2.7 event/h) in comparison with patients with RAH without OSA (mean AHI 3.4±0.2 event/h) had significantly higher body mass index (34.2±0.7 vs 31.6±0.7 kg/m2, P<0.05), uric acid level (6.7±0.1 vs 5.6±0.4 mg/dl, P<0,05), higher carotid-femoral pulse wave velocity (PWVcf) (12.1±0.5 vs 10.2 m/s, P<0,05) and central systolic blood pressure (CSBP) (143.8±2.7 vs 136.2±3.4 mm Hg, P<0,05). Patients of both groups had comparable office blood pressure (SBP 145.6±1.67 vs 138.4±3.66 mm Hg, P=0.057 and DBP 93.6+±1.18 vs 89.1±2.11 mm Hg, P=0.073), but significantly higher 24-h systolic and diastolic blood pressure. We suggest that in the study some patients with OSA had masked arterial hypertension. Daytime sleepiness in OSA patients was associated with structural remodeling of the left ventricle myocardium and more expressed arterial stiffness: ESS score was independently correlated with snoring duration (β=−0.008; P=0.021), interventricular septum thickness (β=0.023; P=0.026), LVMI (β=−0.037; P=0.039) and indexes of central pulse wave: ejection duration (ED) (β=−0.020; P<0.001) and subendocardial viability ratio (SEVR) (β=−0.224; P=0.012). Nocturnal hypoxemia in OSA patients was associated with increased aortic stiffness and higher central blood pressure: desaturation index was independently correlated with Aix (β=4.167; P=0.009), Aix75 (β=−3.929; P=0.006) and central DBP (β=0.151; P=0.004). Conclusion In patients with RH and OSA nocturnal hypoxemia correlation with increased aortic stiffness and higher central blood pressure. FUNDunding Acknowledgement Type of funding sources: None.

Nocturnal Hypoxemia Rather Than Obstructive Sleep Apnea Is Associated With Decreased Red Blood Cell Deformability and Enhanced Hemolysis in Patients With Sickle Cell Disease

Background: Although obstructive sleep apnea (OSA) could act as a modulator of clinical severity in sickle cell disease (SCD), few studies focused on the associations between the two diseases.Research Question: The aims of this study were: (1) to explore the associations between OSA, nocturnal oxyhemoglobin saturation (SpO2) and the history of several acute/chronic complications, (2) to investigate the impact of OSA and nocturnal SpO2 on several biomarkers (hematological, blood rheological, and coagulation) in patients with SCD.Study Design and Methods: Forty-three homozygous SCD patients underwent a complete polysomnography recording followed by blood sampling.Results: The proportion of patients suffering from nocturnal hypoxemia did not differ between those with and those without OSA. No association between OSA and clinical severity was found. Nocturnal hypoxemia was associated with a higher proportion of patients with hemolytic complications (glomerulopathy, leg ulcer, priapism, or pulmonary hypertension). In addition, nocturnal hypoxemia was accompanied by a decrease in RBC deformability, enhanced hemolysis and more severe anemia.Interpretation: Nocturnal hypoxemia in SCD patients could be responsible for changes in RBC deformability resulting in enhanced hemolysis leading to the development of complications such as leg ulcers, priapism, pulmonary hypertension or glomerulopathy.Clinical Trial Registration:www.ClinicalTrials.gov, identifier: NCT03753854.

843 Paradoxical Waking Hypoxemia that Improves with Sleep

Introduction We present a case of paradoxically worsened hypoxia during wake phase of polysomnography while undergoing a CPAP titration study. Nighttime hypoxemia is a common feature in obstructive sleep apnea, due to obstructive events that manifest while sleeping. Excluding OSA, there remains an extensive differential for disease processes that cause hypoxemia while asleep; however, none of these processes can explain waking hypoxemia that improves upon sleeping. Report of case(s) A 70 year old male with severe OSA diagnosed by home sleep test (REI 46.5, nadir O2=76%) underwent polysomnography with PAP titration and demonstrated several hours of interrupted sleep without hypoxia and minimal obstructive events on CPAP 9–13 cmH2O. During the study, while awake at CPAP of 14 cmH2O, he developed hypoxia to mid-high 80s and supplemental oxygen bleed in was added starting at 3L and increased to 5L during a prolonged period of wakefulness. On CPAP 15 cmmH2O with 5L bleed-in, the patient fell asleep and oxygen saturation again increased to low 90s. He underwent an extensive workup for other cardiopulmonary causes of hypoxemia, with pulmonary function testing showing moderate obstructive ventilatory defect and mild DLCO impairment. An echocardiogram with saline contrast bubble study was relatively unremarkable, without evidence of right to left shunting. He underwent a chest CTA which was negative for pulmonary embolism, though it did reveal an enlarged pulmonary artery consistent with pulmonary hypertension. His chronic hypoxemia was treated with 2L supplemental oxygen during the day and bleed-in with CPAP at night. Conclusion Though nocturnal hypoxemia is common with OSA, polysomnography with paradoxical hypoxemia during wake phase has not been reported. Notably, the patient was without prolonged hypoxia during his sleep phase while on CPAP treatment with minimal apneic/hypopneic events. Pulmonary hypertension can also present as nocturnal hypoxemia, but it should worsen with sleep, rather than improve. There are case reports of right to left shunting worsened by PAP, though his hypoxemia persisted despite PAP. His paradoxical worsening hypoxemia with wakefulness is still unexplained. Support (if any):

Sleep-Disordered Breathing and Nocturnal Hypoxemia in Precapillary Pulmonary Hypertension: Prevalence, Pathophysiological Determinants, and Clinical Consequences

<b><i>Background and objective:</i></b> The clinical relevance and interrelation of sleep-disordered breathing and nocturnal hypoxemia in patients with precapillary pulmonary hypertension (PH) is not fully understood. <b><i>Methods:</i></b> Seventy-one patients with PH (age 63 ± 15 years, 41% male) and 35 matched controls were enrolled. Patients with PH underwent clinical examination with assessment of sleep quality, daytime sleepiness, 6-minute walk distance (6MWD), overnight cardiorespiratory polygraphy, lung function, hypercapnic ventilatory response (HCVR; by rebreathing technique), amino-terminal pro-brain natriuretic peptide (NT-proBNP) levels, and cardiac MRI (<i>n</i> = 34). <b><i>Results:</i></b> Prevalence of obstructive sleep apnea (OSA) was 68% in patients with PH (34% mild, apnea-hypopnea index [AHI] ≥5 to &#x3c;15/h; 34% moderate to severe, AHI ≥15/h) versus 5% in controls (<i>p</i> &#x3c; 0.01). Only 1 patient with PH showed predominant central sleep apnea (CSA). Nocturnal hypoxemia (mean oxygen saturation [SpO₂] &#x3c;90%) was present in 48% of patients with PH, independent of the presence of OSA. There were no significant differences in mean nocturnal SpO₂, self-reported sleep quality, 6MWD, HCVR, and lung and cardiac function between patients with moderate to severe OSA and those with mild or no OSA (all <i>p</i> &#x3e; 0.05). Right ventricular (RV) end-diastolic (<i>r</i> = −0.39; <i>p</i> = 0.03) and end-systolic (<i>r</i> = −0.36; <i>p</i> = 0.04) volumes were inversely correlated with mean nocturnal SpO₂ but not with measures of OSA severity or daytime clinical variables. <b><i>Conclusion:</i></b> OSA, but not CSA, is highly prevalent in patients with PH, and OSA severity is not associated with nighttime SpO₂, clinical and functional status. Nocturnal hypoxemia is a frequent finding and (in contrast to OSA) relates to structural RV remodeling in PH.