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M. Ito, J. Tanaka, K. Kubota, H. Sato, M. Takahashi, H. Tanaka, T. Ohdaira, H. Yoshizawa, Y. Muramatsu, M. Satoh, E. Suzuki, M. Arakawa and F. Gejyo, “Obstructive Sleep Apnea Syndrome in a Patient with Superior Vena Cava Syndrome Caused by Lung Cancer,” The Journal of the Japanese Respiatory Society, Vol. 38, No. 6, 2000, pp. 471-475.

has been cited by the following article:

• TITLE: Association of Superior Vena Cava Syndrome with Sleep Apnea: Investigation Using an Impulse Oscillometry System

  AUTHORS: Masanori Yokoba, Naohito Ishii, Tsuyoshi Ichikawa, Mayuko Wada, Hisashi Mitsufuji, Masaru Kubota, Noriyuki Masuda, Masato Katagiri

  KEYWORDS: Upper Airway Resistance; Central Respiratory Resistance; Peripheral Respiratory Resistance; Impulse Oscillometry System; Ios; Pulmonary Neoplasm

  JOURNAL NAME: International Journal of Clinical Medicine, Vol.3 No.4, July 12, 2012

  ABSTRACT: Superior vena cava syndrome (SVCS) patients sometimes show signs of obstructive sleep apnea (OSA). However, the mechanism causing hypoxia during sleep in SVCS patients is still uncertain. The aim of this study was to elucidate 1) the changes in central and peripheral respiratory resistance with SVCS, and 2) interpret the mechanism underlying the development of hypoxia during sleep in patients with SVCS related to OSA. Ten SVCS patients related to a neoplasm were recruited for this study. The degree of apnea hypopnea index (AHI) for OSA was evaluated by portable diagnosing device before and after SVCS treatment. We also analyzed the airway resistance and reactance quantitatively in the supine position by Master Screen impulse oscillometry system (MS-IOS?). After SVCS treatment, mean values of AHI were significantly decreased from 30.9 to 16.9 (/hour) (p = 0.001). Central respiratory resistance (R20) also decreased significantly from 0.40 to 0.33 kPa/L/s (p = 0.025) in the supine position. In contrast, peripheral respiratory resistance (R5-R20) and distal capacitive reactance (X5) did not change significantly. It is thought that the exacerbation of OSA due to SVCS is caused by increasing upper airway resistance related to reversible edema of the upper airway mucous or tissue. In contrast, SVCS may not cause peripheral respiratory tract and lung parenchyma edema.