Abstract 2209: Velocity Vector Imaging in Evaluation of Subclinical Right Ventricular Dysfunction in Obstructive Sleep Apnea Patients without Systemic and Pulmonary Arterial Hypertension

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Aylin Tugcu ◽  
Ozlem Yildirimturk ◽  
Yelda Tayyareci ◽  
I C Demiroglu ◽  
Saide Aytekin
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Right Ventricular ◽  
Strain Rate ◽  
Velocity Vector ◽  
Strain Rates ◽  
Obstructive Sleep ◽  
Pulmonary Arterial

To evaluate regional right ventricular (RV) myocardial velocity, strain and strain rate alterations in newly diagnosed obstructive sleep apnea (OSA) patients without systemic and pulmonary arterial hypertension and to correlate OSA severity to RV dysfunction using Velocity Vector Imaging (VVI). The OSA group consisted of 27 obese patients who were found to have moderate-to-severe OSA, and the control group of 26 age and body mass index-matched healthy subjects who were found not to have OSA on their first polysomnographic testing. All subjects underwent 24-hour ambulatory blood pressure monitoring and conventional echocardiography to exclude systemic and pulmonary arterial hypertension. Peak systolic myocardial velocities, strain and strain rates were determined at the basal and mid segments of RV free wall by VVI. Systemic and pulmonary artery pressures were within normal limits in both groups. Peak systolic myocardial velocities, strain and strain rates were significantly impaired in patients with OSA compared to controls (Table 1 ). The apnea hypopnea index (AHI) correlated strongly with all indices obtained by VVI (basal velocity: r=−0.563, p<0.001; basal strain: r=−0.587, p<0.001;basal strain rate: r=−0.372, p<0.006, mid velocity: r=−0.559, p<0.001, mid strain: r=−0.689, p<0.001;mid strain rate: r=−0.658, p<0.001). The structural consequences of OSA in the RV is influenced by the severity of AHI. These effects occur independently from obesity and systemic hypertension. VVI can accurately recognize and quantify abnormalities of RV function in these subgroup of patients. Table 1

846 Pulmonary Arterial Hypertension as a Sequela of Untreated Obstructive Sleep Apnea in a Patient with Prader-Willi Syndrome

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A329-A329
Author(s):  
Hina Emanuel ◽  
Kevin Kaplan
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Systolic Dysfunction ◽  
Morbidity And Mortality ◽  
Prader Willi Syndrome ◽  
Obstructive Sleep ◽  
Pulmonary Arterial

Abstract Introduction Prader-Willi Syndrome (PWS) is a complex neurogenetic disorder characterized by hypotonia, behavioral problems, endocrinopathies, sleep and respiratory abnormalities. Morbidity and mortality in the PWS population is attributable to obesity, cardiovascular problems, and sleep apnea. We report a patient with PWS presenting with pulmonary arterial hypertension (PAH) due to untreated obstructive sleep apnea (OSA). Report of case(s) Our patient is a 17-year-old female with a past medical history of PWS, scoliosis, obesity (BMI 52.46), hypogonadotropic hypogonadism, and type II diabetes. Baseline echocardiogram (ECHO) performed at age 9 revealed an estimated right ventricular systolic pressure (eRVSP) of 32mmHg above right atrial pressure (RAP), tricuspid regurgitation (TR) at 2.8 m/sec with no interventricular septal flattening (IVSF) and right ventricle (RV) systolic dysfunction suggestive of mild PAH. Given significant scoliosis the patient did not qualify for growth hormone therapy. She underwent a polysomnogram (PSG) at age 14 showing severe obstructive sleep apnea; apnea-hypopnea index (AHI) of 22.6 (oAHI 22.6). Patient was subsequently lost to follow up until presenting in acute respiratory failure at age 17. She required endotracheal intubation and was extubated to bilevel PAP (BPAP) with inability to wean off BPAP. At that time an ECHO revealed eRVSP of 55 mmHg above RAP, IVSF, TR at 3.7 m/sec, and RV systolic dysfunction suggestive of moderate to severe PAH and developing right sided heart failure. A PAP titration PSG during this admission revealed hypoxemia with oxygen saturation less than 90% (O2 nadir 70%) 12.6% of total sleep time (TST) and hypoventilation (transcutaneous CO2 max of 57 mmHg with an elevation above 50 mmHg for 100% of TST). Using an inspiratory PAP (IPAP) of 24 cmH2O and expiratory PAP (EPAP) of 14 cmH20 with supplemental O2 of 4LPM the respiratory events and hypoxemia resolved but there was persistence of hypoventilation. Tadalafil was initiated for PAH and BPAP therapy for OSA. Follow up visits 4- and 8-weeks post discharge shows improving PAH (TR 3.6 m/sec, eRSVP 52 mmHg, and mild IVSF) due to BPAP and tadalafil therapies. Conclusion This case highlights the importance of treating OSA in patients with PWS to prevent cardiorespiratory complications and reduce morbidity and mortality. Support (if any) None

scholarly journals Pericardial Effusion in Obstructive Sleep Apnea without Pulmonary Arterial Hypertension and Daily Hypoxemia - is it Unusual?

2018 ◽  
Vol 35 (3) ◽  
pp. 233-237
Author(s):  
Emil Ivanov Manov ◽  
Ventsislava Pencheva Pencheva ◽  
Nikolay Margaritov Runev ◽  
Stefan Naydenov Naydenov ◽  
Daniela Stoychkova
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Pulmonary Arterial Hypertension ◽  
Pericardial Effusion ◽  
Arterial Hypertension ◽  
Obstructive Sleep ◽  
Pulmonary Arterial

Prognostic relevance of sleep apnea syndrome in patients with pulmonary arterial hypertension

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J Precek ◽  
K Vykoupil ◽  
F Kovacik ◽  
M Hutyra
Keyword(s):  
Pulmonary Hypertension ◽  
Sleep Apnea ◽  
Pulmonary Arterial Hypertension ◽  
General Population ◽  
Arterial Hypertension ◽  
Left Ventricular ◽  
Sleep Study ◽  
Prognostic Relevance ◽  
Obstructive Sleep ◽  
Pulmonary Arterial

Abstract Introduction Sleep disordered breathing (SDB) is a group of ventilatory disorders during sleep which includes obstructive sleep apnea (OSA), central sleep apnea (CSA), and sleep related hypoventilation. In patients with SDB, the prevalence of pulmonary hypertension (PH) ranges from 17% to 52%. While SDB is prevalent in the general population with recent estimates of 20% to 30%, in those with cardiovascular disease, particularly left ventricular failure, there is a higher reported prevalence of 47%. Aims The aims of this study were to determine the prevalence and prognostic relevance of sleep apnea in a cohort of patients with newly diagnosed pulmonary arterial hypertension (ESC/WHO Group 1 pulmonary hypertension). Methods We evaluated prospectively 76 patients with the pulmonary arterial hypertension (mean age 54±16 years; 45% male). All patients underwent right heart catheterisation, clinical assessments, sleep study, standard laboratory testing and evaluation of subjective sleepiness by the Epworth Sleepiness Scale. Sleep test was provided with an ApneaLink Plus, consisting of nasal pressure sensor, respiratory effort band, and pulse oximeter worn on the finger. Subjects previously treated for or diagnosed with SDB were excluded from the study. Results Sleep apnea (SA) – defined as apnea-hypopnea index (AHI) ≥5/h – was found in 59 (77.6%) of the pulmonary arterial hypertension (PAH) patients. Mean AHI in the cohort of PAH patients with SA was 26.1±16.6/h. Mean follow-up was 24 months, during which 15 (19.7%) patients died. Characteristics of parameters related to SA in groups of survivors and deceased are in table 1. From the sleep apnea-related parameters, only time with O2Sat &lt;90% – T90 was significantly associated with mortality (AUC 0.856; 95% CI 0.693 – 1.019; p&lt;0.001). Conclusions The presence of sleep apnea in pulmonary arterial hypertension patients is high. The prevalence of sleep apnea is higher in PAH patients than in the general population. The presence of sleep apnea in patients with PAH was not associated with worse prognosis, but noctural hypoxemia (time with O2Sat &lt;90%) was related to poor prognosis. Sleep apnea in patients with PAH should be screened for systematically. Funding Acknowledgement Type of funding source: None

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