Abstract 1751: Myocardial Microvasculature Dysfunction and Impaired Left Ventricular Relaxation Revealed by Ultrasonic Strain Rate in Patients with Obstructive Sleep Apnea Syndrome
Introduction: Impairment of left ventricular (LV) diastolic function is common in patients with obstructive sleep apnea syndrome (OSAS). The possible effect of OSAS on the myocardial microvasculature and LV diastolic function, however, has been unclear.
Hypothesis: We investigated whether individuals with OSAS exhibit myocardial microvasculature abnormalities together with LV diastolic dysfunction.
Methods: Intravenous myocardial contrast echocardiography and strain imaging were performed in 22 patients with OSAS (54.8 ± 10.7 years) and 23 control individuals without OSAS who were matched for age and blood pressure. Images of apical two- and four-chamber views were obtained at pulsing intervals of one to four cardiac cycles with bolus infusion of Levovist (Schering). The color pixel intensity was acquired at eight regions of interest (inferior, anterior, septal, and lateral base and apex) in the LV myocardium and in the adjacent chamber. Longitudinal strain and early strain rate (SRdia) were determined for the same segments. Standard polysomnography was performed in OSAS patients to determine the number of apnea and hypopnea episodes per hour (apnea-hypopnea index, or AHI) as well as the oxygen desaturation index (ODI).
Results: The mean contrast intensity difference between the myocardium and chamber in all regions was significantly greater in OSAS patients than in controls (26.1 ± 3.4 vs. 23.9 ± 2.9 dB, P < 0.05). It was also correlated with AHI (r = 0.65, P = 0.001) and ODI (r = 0.68, P = 0.001) but not with LV mass. Strain and SRdia were significantly smaller in OSAS patients than in controls, but the LV ejection fraction did not differ between the two groups. The amount of norepinephrine in 24-h urine specimens was significantly greater in patients with severe OSAS (AHI > 30/h) than in those with mild to moderate OSAS (AHI ≤ 30/h). Strain and SRdia were significantly increased in OSAS patients after treatment for 6 months with continuous positive airway pressure.
Conclusions: The repeated episodes of nocturnal oxygen desaturation, sleep fragmentation, and activation of the sympathoadrenal system in individuals with OSAS may result in myocardial microvasculature dysfunction and thereby contribute to impairment of LV relaxation.