{'fraction_non_alphanumeric': 0.03184713375796178, 'fraction_numerical': 0.02847508430123642, 'mean_word_length': 5.068181818181818, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Is obstructive sleep apnea a risk factor for development of venous thromboembolism?

© 2019 The Egyptian Journal of Chest Diseases and Tu Background Obstructive sleep apnea (OSA) is associated with hypercoagulable state that could lead to venous thromboembolism (VTE) occurrence and recurrence. Aim To study the relationship between OSA and the development of VTE. Patients and methods This prospective study was conducted from September 2013 to March 2017 in the sleep laboratory clinic of Zain Hospital in Kuwait. A total of 72 previously diagnosed patients with OSA and 35 controls were included in the study. The patients were presented in the emergency department with acute clinical manifestations of pulmonary embolism or deep vein thrombosis or both. They were subjected to full history, general and local examination, urgent computed tomography pulmonary angiography, or ventilation/perfusion lung scan to confirm the diagnosis of pulmonary embolism. If deep venous thrombosis was also suspected, color Doppler ultrasound was also performed. After clinical stability, full night polysomnography was performed. Laboratory investigations for inherited thrombophilia were also done. Result During the follow-up period, of our 72 patients with OSA, 18 patients developed VTE, which recurred in four patients. Among the 18 patients with OSA who developed VTE, 12 (67%) patients had severe OSA, with apnea–hypopnea index (AHI) more than or equal to 30/h, and six (33%) patients had AHI of 10–29/h. Baseline oxygen saturation (SaO2) was 90±3. Mean nocturnal SaO2 was 79±4. Low nocturnal SaO2 was 73±5. Percentage of total sleep time with SaO2 less than 90% (CT90) was 32±4. Oxygen desaturation index was 29.6±4.2. Among the patients with OSA with VTE, 12 patients were obese (BMI≥30) with a higher incidence of comorbidities. Their Epworth sleepiness score was 17.9±2.5. Overall, 83% of them had severe OSA (AHI ≥30/h), with a significant lower mean nocturnal SaO2, and low nocturnal SaO2 with a higher CT90 and oxygen desaturation index. VTE recurrent patients also showed a higher incidence of comorbidities and worse polysomnographic parameters than patients with one attack of VTE. Conclusion Patients with OSA are likely to be at increased risk for occurrence and recurrence of VTE. This increased risk was attributed to the pathophysiological effects of OSA rather than the effect of obesity alone. OSA and obesity acted additively or synergistically to intensify the risk of VTE. This risk was higher among the patients who were not compliant with continuous positive airway pressure (CPAP) device, suggesting an increased risk with increasing severity of OSA.