Susanna Mak

Influence of obstructive sleep apnea on mortality in patients with heart failure.

OBJECTIVESnThis study sought to determine, in patients with heart failure (HF), whether untreated moderate to severe obstructive sleep apnea (OSA) is associated with a higher mortality rate than in patients with mild to no sleep apnea (M-NSA).nnnBACKGROUNDnObstructive sleep apnea is common in patients with HF and exposes the heart and circulation to adverse mechanical and autonomic effects. However, its effect on mortality rates of patients with HF has not been reported.nnnMETHODSnIn a prospective study involving 164 HF patients with left ventricular ejection fractions (LVEFs) < or =45%, we performed polysomnography and compared death rates between those with M-NSA (apnea-hypopnea index [AHI] <15/h of sleep) and those with untreated OSA (AHI > or =15/h of sleep).nnnRESULTSnDuring a mean (+/- SD) of 2.9 +/- 2.2 and a maximum of 7.3 years of follow-up, the death rate was significantly greater in the 37 untreated OSA patients than in the 113 M-NSA patients after controlling for confounding factors (8.7 vs. 4.2 deaths per 100 patient-years, p = 0.029). Although there were no deaths among the 14 patients whose OSA was treated by continuous positive airway pressure (CPAP), the mortality rate was not significantly different from the untreated OSA patients (p = 0.070).nnnCONCLUSIONSnIn patients with HF, untreated OSA is associated with an increased risk of death independently of confounding factors.

Prevalence and Physiological Predictors of Sleep Apnea in Patients With Heart Failure and Systolic Dysfunction

BACKGROUNDnPrevious studies reported high prevalences of obstructive and central sleep apnea (OSA and CSA, respectively) in patients with heart failure (HF). However, these preceded widespread use of beta-blockers and spironolactone that might have reduced their prevalences. We therefore determined, in patients with HF, prevalences and predictors of OSA and CSA and the influence of changes in HF therapy on prevalences.nnnMETHODS AND RESULTSnA total of 218 HF patients with left ventricular ejection fraction (LVEF) <or=45% underwent sleep studies between 1997 and 2004 and were classified as having moderate to severe sleep apnea (apnea-hypopnea index >or=15 hours of sleep, either OSA or CSA), or mild to no sleep apnea. The prevalence of moderate to severe OSA was 26% and of CSA was 21%. Predictors of OSA were older age, male sex, and greater body mass index, and of CSA were older age, male sex, atrial fibrillation, hypocapnia, and diuretic use. Between 1997 and 2004, the prevalences of OSA and CSA did not change significantly (P(trend) =.460, P(trend) =.211, respectively) despite increased use of beta-blockers and spironolactone (P(trend) < .001, P(trend) < .001, respectively), and an increase in LVEF (P(trend)=.005).nnnCONCLUSIONSnOSA and CSA remain common in patients with HF, despite increases in beta-blocker and spironolactone use.

Relationship Between Sodium Intake and Sleep Apnea in Patients With Heart Failure

OBJECTIVESnThe purpose of this study was to test the hypothesis that severity of sleep apnea (SA), assessed by frequency of apneas and hypopneas per hour of sleep (apnea-hypopnea index [AHI]), is related to sodium intake in patients with heart failure (HF).nnnBACKGROUNDnDependent edema and overnight rostral fluid shift from the legs correlate with the AHI in patients with HF in whom excessive sodium intake can cause fluid retention.nnnMETHODSnSodium intake was estimated by food recordings in 54 HF patients who underwent overnight polysomnography.nnnRESULTSnThirty-one of the 54 patients had SA, and their mean sodium intake was higher than that in those without SA (3.0 ± 1.2 g vs. 1.9 ± 0.8 g, 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 serum creatinine level.nnnCONCLUSIONSnThese findings suggest that in patients with HF, sodium intake plays a role in the pathogenesis of SA.

Cardiac sympathetic activation in patients with pulmonary arterial hypertension.

Patients with congestive heart failure (CHF) due to left ventricular (LV) dysfunction have sympathetic activation specifically directed to the myocardium. Although pulmonary arterial hypertension (PAH) is associated with increased systemic sympathetic activity, its impact on sympathetic drive to ventricular myocardium is unknown. Fifteen patients with PAH (9 women; 54 ± 12 years) were studied: 10 with idiopathic PAH and 5 with a connective tissue disorder. We measured hemodynamics, as well as radiolabeled and endogenous concentrations of arterial and coronary sinus norepinephrine (NE). These measures were repeated after inhaled nitric oxide (NO). Measurement of transcardiac NE concentrations and the cardiac extraction of radiolabeled NE allowed calculation of the corrected transcardiac gradient of NE (CTCG of NE). Comparative data were collected from 15 patients (9 women: 55 ± 12 yr) with normal LV function and 15 patients with CHF (10 women; 53 ± 12 yr). PAH patients had elevated arterial NE concentrations compared with those with normal LV function but were similar to those with CHF. The CTCG of NE was higher in those with PAH than in the normal LV group (3.6 ± 2.2 vs. 1.5 ± 0.9 pmol/ml; P < 0.01) but similar to that seen in those with CHF (3.3 ± 1.4; P = NS). Inhaled NO, which reduced pulmonary artery pressure and increased cardiac output, had no effect on cardiac sympathetic activity. Therefore, cardiac sympathetic activation occurs in PAH. The mechanism of this activation remains uncertain but does not involve elevations in left heart filling pressure.

Effect of a Sodium-Restricted Diet on Intake of Other Nutrients in Heart Failure: Implications for Research and Clinical Practice

BACKGROUNDnSodium restriction is the primary dietary therapy for heart failure (HF) patients. Currently, it is unknown if changing diets to reduce dietary sodium in HF causes secondary changes to the intake of other nutrients in this patient population already at nutritional risk.nnnMETHODS AND RESULTSnHF patients (nxa0= 16; 52 ± 12 years old; 78% male) followed a sodium-restricted diet for 1 week. Nutritional changes were documented at baseline and after a <2,000 mg/d sodium-restricted diet, as measured by food records before baseline and each day during the study. After a 49% reduction in dietary sodium (3,626 ± 956 to 1,785 ± 696 mg/d), we observed a significant reduction in calorie (2,467 ± 748 to 1,931 ± 388 kcal/d; P < .016), carbohydrate (293 ± 108 to 232 ± 56 g/d; Pxa0= .013), calcium (995 ± 496 to 609 ± 208 mg/d; P < .004), thiamine (2.0 ± 0.8 to 1.5 ± 0.8 mg/d; Pxa0= .020), and folate (412 ± 192 to 331 ± 172 μg/d; Pxa0= .019) intakes. There was a decrease in saturated fat (32 ± 18 to 21 ± 6 g/d; Pxa0= .032) and a trend to lower total fat (89 ± 34 to 68 ± 19 g/d; Pxa0= .066) and higher potassium (1,262 ± 328 to 1,405 ± 268 mg/1,000 kcal; Pxa0= .055) intakes.nnnCONCLUSIONSnWe found multiple unintentional nutritional consequences with dietary sodium reduction in HF patients. These findings highlight the need to consider the whole diet when counseling HF patients to lower sodium intake.

Overnight Effects of Obstructive Sleep Apnea and Its Treatment on Stroke Volume in Patients With Heart Failure

BACKGROUNDnWe previously showed in heart failure (HF) patients that obstructive respiratory events during sleep and generation of negative intrathoracic pressure during Mueller manoeuvres, mimicking obstructive apneas, acutely reduced stroke volume (SV). We also showed that treating obstructive sleep apnea (OSA) with continuous positive airway pressure (CPAP) increased left ventricular ejection fraction over a 1-month period. We therefore hypothesized that, in HF patients, those with OSA would have greater overnight declines in SV and cardiac output (CO) than in those without sleep apnea, and that therapy of OSA using CPAP would prevent these declines.nnnMETHODSnWe examined overnight percent change in SV and CO in 32xa0HF patients with and 28 without OSA using digital photoplethysmography. Among patients with OSA, we also examined changes in SV and CO during a CPAP titration study.nnnRESULTSnDuring the baseline polysomnogram SV and CO decreased more overnight in those with OSA than in those without sleep apnea (-12.6 ± 7.7% vsxa0-3.2 ± 6.8%; P < 0.001 andxa0-16.2 ± 9.9% vsxa0-3.7 ± 8.3%; P < 0.001, respectively). Overnight changes in SV and CO correlated inversely with total apnea-hypopnea index (rxa0=xa0-0.551; P < 0.001 and rxa0=xa0-0.522; P < 0.001, respectively). In 21 patients with OSA, CPAP reduced the total apnea-hypopnea index from 37.7 ± 21.4 to 15.0 ± 16.0 (P < 0.001) in association with attenuation of the overnight reduction of SV (fromxa0-14.0 ± 7.9% toxa0-3.4 ± 9.8%; Pxa0=xa00.002) and CO (fromxa0-17.2 ± 9.0% toxa0-9.7 ± 10.7%; Pxa0=xa00.042).nnnCONCLUSIONSnIn patients with HF, coexisting OSA causes overnight declines in SV and CO that are prevented through reversal of OSA by CPAP.