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Severe obstructive sleep apnea impairs left ventricular diastolic function in non-obese men
Yasuhiro Usui1, Yoshifumi Takata, Yuichi Inoue
1Department of Cardiology, Tokyo Medical University, Shinjuku-ku, Tokyo, Japan. kaoyasu@tokyo-med.ac.jp
Sleep Medicine
|March 8, 2011
Summary
Severe obstructive sleep apnea (OSA) directly impairs left ventricular (LV) diastolic function. This dysfunction occurs independently of factors like arterial stiffness and obesity, highlighting OSA as a direct cardiac risk.
Area of Science:
- Cardiology
- Sleep Medicine
- Cardiovascular Physiology
Background:
- Obstructive sleep apnea (OSA) is linked to cardiovascular complications.
- Left ventricular (LV) diastolic dysfunction is an early sign of cardiac disease.
Purpose of the Study:
- To investigate the direct impact of obstructive sleep apnea (OSA) on left ventricular (LV) diastolic function.
- To determine if OSA contributes to LV diastolic dysfunction independent of other cardiovascular risk factors.
Main Methods:
- Seventy-four male patients with OSA (apnea-hypopnea index [AHI] ≥5/h) and no prior cardiac conditions were studied.
- Echocardiography, pulse wave velocity (PWV), and laboratory tests were performed.
- LV diastolic function was assessed using transmitral flow velocity (E/A ratio) and mitral annular velocity (Ea) via tissue Doppler imaging (TDI).
Main Results:
- Severe OSA (AHI ≥30/h) showed significantly lower E/A ratios and Ea compared to mild-to-moderate OSA.
- A higher S/D ratio was observed in severe OSA patients.
- Apnea-hypopnea index (AHI) strongly correlated inversely with the E/A ratio (r=-0.47, P=0.0001).
- Multivariate analysis confirmed severe OSA independently associated with reduced E/A ratio (β=-0.23, P=0.001).
Conclusions:
- Severe obstructive sleep apnea (OSA) appears to directly cause left ventricular (LV) diastolic dysfunction.
- This dysfunction occurs irrespective of LV geometry, arterial stiffness, obesity, and associated cardiovascular risks.
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