Otto Maria E, Belohlavek Marek, Romero-Corral Abel, Gami Apoor S, Gilman Gregory, Svatikova Anna, Amin Raouf S, Lopez-Jimenez Francisco, Khandheria Bijoy K, Somers Virend K
Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
Am J Cardiol. 2007 May 1;99(9):1298-302. doi: 10.1016/j.amjcard.2006.12.052. Epub 2007 Mar 20.
Obstructive sleep apnea (OSA) and obesity have been linked to systolic and diastolic dysfunction of the left ventricle. Right ventricular function is poorly understood in the 2 clinical conditions. Data from this study show that otherwise healthy obese patients with OSA had increased an left atrial volume index compared with similarly obese patients without OSA (16.3 +/- 1.2 ml/m in obese patients without OSA vs 20.2 +/- 1.0 ml/m in those with OSA, p = 0.02) and altered diastolic function reflected by changes in mitral annular late diastolic velocity (-5.7 +/- 0.7 cm/s in obese patients without OSA vs -7.3 +/- 0.7 cm/s in those with OSA, p = 0.007), mitral annular early diastolic velocity (-7.9 +/- 0.6 cm/s in obese patients without OSA vs -6.4 +/- 0.3 cm/s in those with OSA, p = 0.05), and early to late diastolic annular ratio >1 (82% of obese patients without OSA vs 26% of those with OSA, p = 0.001), which may be signs of early subclinical impairment of cardiac function. Importantly, healthy obese subjects had similarly increased left ventricular mass compared with obese patients with OSA but normal diastolic function and left atrial size. There was a trend toward abnormal right ventricular filling in patients with OSA, measured by altered superior vena cava diastolic velocity during expiration (-15 +/- 2 cm/s in obese patients without OSA vs -10 +/- 3 cm/s in those with OSA, p = 0.2) and a tendency toward diastolic dysfunction reflected by decreased lateral tricuspid annular early diastolic velocity (-7.2 +/- 0.5 cm/s in obese patients without OSA vs -6.1 +/- 0.5 cm/s in those with OSA, p = 0.1) beyond that seen in obesity alone. In conclusion, OSA independent of obesity may induce cardiac changes that could predispose to atrial fibrillation and heart failure.
阻塞性睡眠呼吸暂停（OSA）与肥胖均与左心室收缩和舒张功能障碍有关。在这两种临床情况下，右心室功能鲜为人知。本研究数据表明，与无OSA的肥胖患者相比，无其他健康问题的OSA肥胖患者左心房容积指数增加（无OSA的肥胖患者为16.3±1.2ml/m，有OSA的患者为20.2±1.0ml/m，p = 0.02），二尖瓣环舒张末期速度变化反映舒张功能改变（无OSA的肥胖患者为-5.7±0.7cm/s，有OSA的患者为-7.3±0.7cm/s，p = 0.007），二尖瓣环舒张早期速度（无OSA的肥胖患者为-7.9±0.6cm/s，有OSA的患者为-6.4±0.3cm/s，p = 0.05），以及舒张早期与晚期环比率>1（无OSA的肥胖患者中82%，有OSA的患者中26%，p = 0.001），这些可能是心功能早期亚临床损害的迹象。重要的是，与有OSA的肥胖患者相比，健康肥胖受试者左心室质量同样增加，但舒张功能和左心房大小正常。通过呼气期间上腔静脉舒张速度改变测量，OSA患者存在右心室充盈异常趋势（无OSA的肥胖患者为-15±2cm/s，有OSA的患者为-10±3cm/s，p = 0.2），并且存在舒张功能障碍倾向，表现为三尖瓣环外侧舒张早期速度降低（无OSA的肥胖患者为-7.2±0.5cm/s,有OSA的患者为-6.1±0.5cm/s，p = 0.1），超过单纯肥胖所见。总之，独立于肥胖的OSA可能诱发心脏变化，进而易患心房颤动和心力衰竭。
