Acute and chronic effects of continuous positive airway pressure therapy on left ventricular systolic and diastolic function in patients with obstructive sleep apnea and congestive heart failure.

BACKGROUND: 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. OBJECTIVES: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

The effects of continuous positive airway pressure on myocardial energetics in patients with heart failure and obstructive sleep apnea.

OBJECTIVES: We sought to examine the short-term and longer term (6-week) effects of continuous positive airway pressure (CPAP) on myocardial energetics. BACKGROUND: Obstructive sleep apnea (OSA) and heart failure (HF) are both states of increased afterload and metabolic demand. Treatment with CPAP may initially reduce stroke volume but subsequently improves left ventricular function. However, it is not clear whether CPAP therapy favorably affects myocardial energetics and hence improves cardiac efficiency. METHODS: Twelve patients with HF were divided into two groups: 7 patients with OSA were treated with CPAP (group I), and 5 patients without OSA served as a control group (group II). Oxidative metabolism was measured using the mono-exponential fit of the myocardial [(11)C] acetate positron emission tomography time-activity curve (k-mono). Myocardial efficiency was derived using the work metabolic index (WMI = [heart rate x stroke volume index x systolic blood pressure]/k-mono) measured at baseline, during short-term CPAP, and after 6 +/- 3 weeks of CPAP. RESULTS: In group I, short-term CPAP tended to reduce SVI (p = 0.063) and reduced oxidative metabolism (p = 0.031). Work metabolic index did not change. However, longer term CPAP improved left ventricular ejection fraction (38.4 +/- 3.3% to 43.4 +/- 4.8%, p = 0.031), tended to reduce oxidative metabolism (0.047 +/- 0.012 to 0.040 +/- 0.008 min(-1), p = 0.078), and improved WMI (7.13 +/- 2.82 x 10(6) to 8.17 +/- 3.06 x 10(6) mm Hg.ml/m(2), p = 0.031). In group II (control), these parameters did not change. CONCLUSIONS: In this cohort of patients with HF and OSA, short-term CPAP decreased oxidative metabolism and tended to decrease SVI, but did not alter cardiac efficiency. Longer term CPAP improved cardiac efficiency, indicating an energy-sparing effect. These effects may contribute to the benefits of CPAP therapy.