Relationship Between Sodium Intake and Sleep Apnea in Patients With Heart Failure
Editor's Note: This review is based on Kasai T, Arcand J, Allard JP, Mak S, Azevedo ER, Newton GE, Bradley TD. Relationship between sodium intake and sleep apnea in patients with heart failure. J Am Coll Cardiol 2011;58:1970-4.
Sleep apnea (SA), including obstructive and central sleep apnea (OSA and CSA, respectively), occurs in approximately 50% of patients with heart failure (HF) in whom it is associated with increased mortality. The observation that OSA is more prevalent in patients with edematous states, such as HF, than in the general population, despite lower body weight, raises the possibility that fluid retention may increase the risk for OSA. Recent studies have shown that fluid retained in the legs during the day can shift rostrally into the neck when recumbentduring sleep, causing peripharyngeal fluid accumulation and upper airway narrowing thereby predisposing to OSA. There is also a strong positive correlation between the amount of fluid displaced from the legs at night and the frequency of apneas and hypopneas per hour of sleep (apnea-hypopnea index, AHI).
CSA is also common in HF patients, and is caused by hyperventilation due to pulmonary vagal irritant receptor stimulation by pulmonary congestion and to increased chemoreceptor sensitivity that together drive PCO2 below the apnea threshold. In HF patients, the degree of overnight rostral fluid displacement from the legs is inversely proportional to PCO2 during sleep and directly related to the AHI, suggesting that some of this fluid is redistributed into the lungs.
Sodium retention, a hallmark of HF, causes fluid retention. We recently demonstrated that high sodium intake is associated with increased risk of HF exacerbations. Since fluid retention in the legs in the daytime contributes to rostral redistribution of fluid into the neck and lungs at night, we hypothesized that in HF patients, sodium intake will be related to the severity of SA assessed by the AHI.
To test this hypothesis, sodium intake was assessed by two three-day food recordings: one at study entry and one six-12 weeks later. Mean daily values were used to estimate habitual intake of sodium and other nutrients in 54 HF patients (left ventricular ejection fraction [LVEF] <35%) in whom age, sex, body mass index (BMI), use of medications, estimated glomerular filtration rate (eGFR), LVEF, caloric, fluid, and potassium intake were also recorded. They underwent overnight polysomnography and were divided into a SA group (AHI ≥15), and a non-SA group (AHI <15).
Of the 54 patients, 31 had SA (mean±SD AHI = 38.2 ± 18.6) and 23 did not (AHI = 7.7 ± 3.6). The SA group had greater fluid, potassium, protein and total calorie intake than the non-SA group, but there was no significant difference in BMI between them. Their mean daily sodium intake was also higher than in those without SA (3.0±1.2g versus 1.9±0.8g, p<0.001). There was a significant correlation between the AHI and sodium intake (r=0.522, p<0.001). Multivariate analysis showed that the significant independent correlates of the AHI were sodium intake, male sex, and eGFR, which together accounted for 69% of the variability in the AHI (p<0.001).
Our findings provide novel insights into the pathogenesis of SA in patients with HF. We found that the AHI was independently and directly related to sodium intake, and inversely related to eGFR. Our findings, therefore, suggest that in addition to high BMI, high sodium intake and impaired renal function increase odds for, and severity of SA in patients with HF. It is likely that this association is due to fluid retention secondary to the combined effects of high sodium intake and impaired renal function, and to overnight rostral fluid shift from the legs. However, we did not measure fluid volume shifts in this study. High sodium intake may therefore play a role in the pathogenesis of SA in HF patients. If so, modulation of sodium intake may be a therapeutic strategy to alleviate SA in HF. Consequently, studies assessing fluid volume and overnight fluid shift, along with their relationships to both sodium intake and severity of SA, as well as interventional studies to assess the effect of reduced sodium intake on fluid volume and severity of SA will be required to test the validity of our findings.
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