OBJECTIVE: To investigate whether obstructive sleep apnea syndrome (OSAS) has any effect on pulmonary artery stiffness (PAS) derived from echocardiographic calculation. METHODS: Fifty-two patients with newly diagnosed OSAS and forty-two subjects without OSAS matched by age and sex were enrolled in the study. OSAS was categorized according to apnea hypopnea index (AHI, event/h) as follows: normal (AHI<5), mild OSAS (AHI 5-15), moderate and severe OSAS (AHI>15). All participants were evaluated by echocardiography to determine PAS and right ventricle functions. PAS was calculated throughout pulmonary artery flow by the formula; PAS (kHz/sec) = maximal frequency shift/acceleration time. RESULTS: Demographic and clinical parameters were similar in both groups. PAS significantly increased in OSAS compared with the control group (26.9 ± 6.1 vs. 18.0 ± 3.5, P < 0.001). Additionally, PAS in severe and moderate OSAS was considerably high compared with that in mild OSAS and control group (P < 0.001). Right ventricular myocardial performance index (MPI) and mean pulmonary artery pressures (mPAP) were considerably higher in OSAS group than control group (P < 0.001). Tricuspid E/A, right ventricle tissue Doppler E'/A', and right ventricular ejection time (RVET) decreased in OSAS group compared with control group (P < 0.001). There was a significantly positive correlation between PAS and AHI, mPAP, and MPI (P < 0.001), and a significantly negative correlation between PAS and tricuspid E/A, E'/A', and RVET (P < 0.001). Linear regression analyses showed that PAS was an independent factor for mPAP (ß = 0.595, P = 0.034). CONCLUSION: Elastic properties of pulmonary artery deteriorate with severity of OSAS and may be responsible for right ventricular dysfunctions in OSAS.
OBJECTIVE: To investigate whether obstructive sleep apnea syndrome (OSAS) has any effect on pulmonary artery stiffness (PAS) derived from echocardiographic calculation. METHODS: Fifty-two patients with newly diagnosed OSAS and forty-two subjects without OSAS matched by age and sex were enrolled in the study. OSAS was categorized according to apnea hypopnea index (AHI, event/h) as follows: normal (AHI<5), mild OSAS (AHI 5-15), moderate and severe OSAS (AHI>15). All participants were evaluated by echocardiography to determine PAS and right ventricle functions. PAS was calculated throughout pulmonary artery flow by the formula; PAS (kHz/sec) = maximal frequency shift/acceleration time. RESULTS: Demographic and clinical parameters were similar in both groups. PAS significantly increased in OSAS compared with the control group (26.9 ± 6.1 vs. 18.0 ± 3.5, P < 0.001). Additionally, PAS in severe and moderate OSAS was considerably high compared with that in mild OSAS and control group (P < 0.001). Right ventricular myocardial performance index (MPI) and mean pulmonary artery pressures (mPAP) were considerably higher in OSAS group than control group (P < 0.001). Tricuspid E/A, right ventricle tissue Doppler E'/A', and right ventricular ejection time (RVET) decreased in OSAS group compared with control group (P < 0.001). There was a significantly positive correlation between PAS and AHI, mPAP, and MPI (P < 0.001), and a significantly negative correlation between PAS and tricuspid E/A, E'/A', and RVET (P < 0.001). Linear regression analyses showed that PAS was an independent factor for mPAP (ß = 0.595, P = 0.034). CONCLUSION: Elastic properties of pulmonary artery deteriorate with severity of OSAS and may be responsible for right ventricular dysfunctions in OSAS.