Abstract 3162: Diastolic Dysfunction Contributes to Pulmonary Hypertension and Mortality in Sleep Apnea
Sleep apnea is associated with pulmonary hypertension, but the mechanisms for this association are unclear. Nocturnal desaturation, hypoxic vasoconstriction and arterial stiffening can cause precapillary increases in pulmonary artery systolic pressure (PASP); while left ventricular diastolic dysfunction can lead to postcapillary increases in PASP.
Aims: To determine the factors associated with increased PASP and their impact on outcomes in subjects with sleep apnea from the general community
Methods: From a random population-based sample of adults ≥45y in Olmsted County MN, subjects with sleep apnea were identified as those with an apnea hypopnea index (AHI) >5/h by in-lab, attended, multichannel polysomnography. All had Doppler echocardiography and spirometry. Pulse oximetry was used to assess nocturnal desaturation. Brachial pulse pressure was used as an index of arterial stiffening. Diastolic function was determined using the mitral E/e′ ratio. PASP was derived from the tricuspid regurgitant jet. Subjects were followed for a median of 9 years.
Results: Among 60 subjects with sleep apnea, median (interquartile range) PASP was 28 (26 –30) mmHg. PASP correlated with mean nocturnal O2 saturation (r=−0.36; p=0.005), pulse pressure (r=0.29; p=0.03) and E/e′ (r=0.34; p=0.01) but not with AHI or spirometry values. Compared to subjects with PASP<30 (Table⇓), those with PASP≥30 had more hypertension, arterial stiffening, diastolic dysfunction and nocturnal desaturation despite similar lung function and severity of sleep apnea. In multivariate analysis only E/e′ was independently associated with PASP (p<0.001) and all-cause mortality (p=0.002).
Conclusions: While both pre- and post-capillary factors contribute to pulmonary hypertension in sleep apnea, the independent effect of diastolic dysfunction and its impact on mortality suggest an important pathophysio-logic role for diastolic dysfunction in sleep apnea.