Johnson Chris B, Beanlands Rob S, Yoshinaga Keiichiro, Haddad Haissam, Leech Judith, de Kemp Rob, Burwash Ian G
Department of Medicine, University of Ottawa, Ottawa, Canada.
Can J Cardiol. 2008 Sep;24(9):697-704. doi: 10.1016/s0828-282x(08)70668-8.
Obstructive sleep apnea (OSA) may contribute to the pathogenesis of congestive heart failure (CHF). Nocturnal continuous positive airway pressure (CPAP) therapy can alleviate OSA and may have a role in the treatment of CHF patients.
To investigate the acute and chronic effects of CPAP therapy on left ventricular systolic function, diastolic function and filling pressures in CHF patients with OSA.
Twelve patients with stable CHF (New York Heart Association II or III, radionuclide ejection fraction lower than 40%) underwent overnight polysomnography to detect OSA. In patients with OSA (n=7), echocardiography was performed at baseline (awake, before and during acute CPAP administration) and after 6.9+/-3.3 weeks of nocturnal CPAP therapy. Patients without OSA (n=5) did not receive CPAP therapy, but underwent a baseline and follow-up echocardiogram.
In CHF patients with OSA, acute CPAP administration resulted in a decrease in stroke volume (44+/-15 mL versus 50+/-14 mL, P=0.002) and left ventricular ejection fraction ([LVEF] 34.8+/-5.0% versus 38.4+/-3.3%, P=0.006) compared with baseline, but no change in diastolic function or filling pressures (peak early diastolic mitral annular velocity [Ea]: 6.0+/-1.6 cm/s versus 6.3+/-1.6 cm/s, P not significant; peak early filling velocity to peak late filling velocity [E/A] ratio: 1.05+/-0.74 versus 1.00+/-0.67, P not significant; E/Ea ratio: 10.9+/-4.1 versus 11.3+/-4.1, P not significant). In contrast, chronic CPAP therapy resulted in a trend to an increase in stroke volume (59+/-19 mL versus 50+/-14 mL, P=0.07) and a significant increase in LVEF (43.4+/-4.8% versus 38.4+/-3.3%, P=0.01) compared with baseline, but no change in diastolic function or filling pressures (Ea: 6.2+/-1.2 cm/s versus 6.3+/-1.6 cm/s, P not significant; E/A ratio: 1.13+/-0.61 versus 1.00+/-0.67, P not significant; E/Ea ratio: 12.1+/-2.7 versus 11.3+/-4.1, P not significant). There was no change in left ventricular systolic function, diastolic function or filling pressures at follow-up in CHF patients without OSA.
Acute CPAP administration decreased stroke volume and LVEF in stable CHF patients with OSA. In contrast, chronic CPAP therapy for seven weeks improved left ventricular systolic function, but did not affect diastolic function or filling pressures. The potential clinical implications of the discrepant effects of CPAP therapy on left ventricular systolic and diastolic function in CHF patients with OSA warrant further study.
阻塞性睡眠呼吸暂停(OSA)可能参与充血性心力衰竭(CHF)的发病机制。夜间持续气道正压通气(CPAP)治疗可缓解OSA,可能在CHF患者的治疗中发挥作用。
研究CPAP治疗对合并OSA的CHF患者左心室收缩功能、舒张功能及充盈压的急性和慢性影响。
12例稳定期CHF患者(纽约心脏协会II或III级,放射性核素射血分数低于40%)接受整夜多导睡眠监测以检测OSA。在合并OSA的患者(n = 7)中,于基线时(清醒状态、急性CPAP治疗前及治疗期间)及夜间CPAP治疗6.9±3.3周后进行超声心动图检查。未合并OSA的患者(n = 5)未接受CPAP治疗,但进行了基线及随访超声心动图检查。
在合并OSA的CHF患者中,与基线相比,急性CPAP治疗使每搏量降低(44±15 mL对50±14 mL,P = 0.002),左心室射血分数([LVEF] 34.8±5.0%对38.4±3.3%,P = 0.006)降低,但舒张功能或充盈压无变化(舒张早期二尖瓣环峰值速度[Ea]:6.0±1.6 cm/s对6.3±1.6 cm/s,P无统计学意义;舒张早期充盈峰值速度与舒张晚期充盈峰值速度[E/A]比值:1.05±0.74对1.00±0.67,P无统计学意义;E/Ea比值:10.9±4.1对11.3±4.1,P无统计学意义)。相比之下,与基线相比,慢性CPAP治疗使每搏量有增加趋势(59±19 mL对50±14 mL,P = 0.07),LVEF显著增加(43.4±4.8%对38.4±3.3%,P = 0.01),但舒张功能或充盈压无变化(Ea:6.2±1.2 cm/s对6.3±1.6 cm/s,P无统计学意义;E/A比值:1.13±0.61对1.00±0.67,P无统计学意义;E/Ea比值:12.1±2.7对11.3±4.1,P无统计学意义)。未合并OSA的CHF患者随访时左心室收缩功能、舒张功能或充盈压无变化。
急性CPAP治疗使合并OSA的稳定期CHF患者每搏量和LVEF降低。相比之下,7周的慢性CPAP治疗改善了左心室收缩功能,但未影响舒张功能或充盈压。CPAP治疗对合并OSA的CHF患者左心室收缩和舒张功能的不同影响的潜在临床意义值得进一步研究。