OBJECTIVE: To evaluate whether obstructive sleep apnea (OSA) contributes directly to left ventricular (LV) diastolic dysfunction. METHODS: Seventy-four non-obese male OSA (apnea hypopnea index (AHI)⩾5/h) patients without cardiac disease, hypertension or diabetes were enrolled. Echocardiography, pulse wave velocity (PWV) measurements and laboratory testing were performed in all patients. LV diastolic function was assessed by the transmitral flow velocity (E/A ratio), and mitral annular velocity (Ea) was derived from tissue Doppler imaging (TDI). RESULTS: The E/A ratio and Ea in the severe OSA group (AHI⩾30/h) was significantly lower than those in the mild to moderate OSA group (5⩽AHI<30/h) (P<0.0001), whereas the S/D ratio, an indicator of pulmonary vein flow velocity, in the severe OSA group was significantly higher than that in the mild to moderate OSA group (P=0.04). AHI exhibited a statistically significant inverse correlation with the E/A ratio (r=-0.47, P=0.0001), but not with relative wall thickness (RWT), LV mass index (LVMI) or PWV. RWT, LVMI and PWV exhibited an inverse correlation with the E/A ratio. Multivariate linear regression analysis revealed that severe OSA was independently associated with the E/A ratio even after adjusting for age, insulin resistance, blood pressure, LV geometry, and PWV (β=-0.23, P=0.001). CONCLUSIONS: These results indicate that severe OSA itself may contribute directly to LV diastolic dysfunction irrespective of LV geometry, arterial stiffness, obesity and its associated cardiovascular risk factors.
OBJECTIVE: To evaluate whether obstructive sleep apnea (OSA) contributes directly to left ventricular (LV) diastolic dysfunction. METHODS: Seventy-four non-obese male OSA (apnea hypopnea index (AHI)⩾5/h) patients without cardiac disease, hypertension or diabetes were enrolled. Echocardiography, pulse wave velocity (PWV) measurements and laboratory testing were performed in all patients. LV diastolic function was assessed by the transmitral flow velocity (E/A ratio), and mitral annular velocity (Ea) was derived from tissue Doppler imaging (TDI). RESULTS: The E/A ratio and Ea in the severe OSA group (AHI⩾30/h) was significantly lower than those in the mild to moderate OSA group (5⩽AHI<30/h) (P<0.0001), whereas the S/D ratio, an indicator of pulmonary vein flow velocity, in the severe OSA group was significantly higher than that in the mild to moderate OSA group (P=0.04). AHI exhibited a statistically significant inverse correlation with the E/A ratio (r=-0.47, P=0.0001), but not with relative wall thickness (RWT), LV mass index (LVMI) or PWV. RWT, LVMI and PWV exhibited an inverse correlation with the E/A ratio. Multivariate linear regression analysis revealed that severe OSA was independently associated with the E/A ratio even after adjusting for age, insulin resistance, blood pressure, LV geometry, and PWV (β=-0.23, P=0.001). CONCLUSIONS: These results indicate that severe OSA itself may contribute directly to LV diastolic dysfunction irrespective of LV geometry, arterial stiffness, obesity and its associated cardiovascular risk factors.
Authors: Emilia Sforza; Mouhamed Sabri; Antoine DaCosta; Karl Isaaz; Jean Claude Barthélémy; Frédéric Roche Journal: J Clin Sleep Med Date: 2015-09-15 Impact factor: 4.062
Authors: Pedro Pujante; Cristina Abreu; Jose Moreno; Eduardo Alegria Barrero; Pedro Azcarate; Arantxa Campo; Elena Urrestarazu; Camilo Silva; Jesus Gil Maria; Javier Tebar; Gema Frühbeck; Javier Salvador Journal: J Clin Sleep Med Date: 2013-11-15 Impact factor: 4.062