Inhibition of Awake Sympathetic Nerve Activity of Heart Failure Patients With Obstructive Sleep Apnea by Nocturnal Continuous Positive Airway Pressure

Usui, Kengo; Bradley, T. Douglas; Spaak, Jonas; Ryan, Clodagh M.; Kubo, Toshihiko; Kaneko, Yasuyuki; Floras, John S.

doi:10.1016/j.jacc.2004.12.080

Cited by 212 publications

(144 citation statements)

References 16 publications

(20 reference statements)

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“…In patients with HFrEF, CPAP improves functional class and reduces sympathetic activity, heart rate, and blood pressure 266, 267, 268. Furthermore, OSA therapy is associated with a trend toward improvement in survival 269.…”

Section: Comorbid Conditionsmentioning

confidence: 99%

Clinical Phenotypes in Heart Failure With Preserved Ejection Fraction

Samson

Jaiswal

Ennezat

et al. 2016

JAHA

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Section: Comorbid Conditionsmentioning

confidence: 99%

Clinical Phenotypes in Heart Failure With Preserved Ejection Fraction

Samson

Jaiswal

Ennezat

et al. 2016

JAHA

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“…In addition to restoring normal sleep architecture, CPAP therapy prevents the extremes of negative intrathoracic pressure and, thus, reduces left ventricular transmural pressure, prevents recurrent hypoxia, reduces sympathetic nervous system activity, decreases blood pressure and heart rate, and increases arterial baroreceptor sensitivity and daytime heart rate variability (1,7,(10)(11)(12)(13)(14)(15)(16). In the normal heart, initiation of CPAP therapy acutely increases intrathoracic pressure, decreases venous return and left ventricular filling, and results in decreased cardiac output (17)(18)(19).…”

mentioning

confidence: 99%

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

Johnson

Beanlands

Yoshinaga

et al. 2008

Canadian Journal of Cardiology

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“…Therapeutic CPAP abolishes these negative intrathoracic pressure swings and reduces LV and intrathoracic aortic transmural pressures. 6 In a heart failure cohort, 1 month of therapeutic CPAP reduced daytime sympathetic vasoconstrictor discharge 7 and BP 9 and improved LV systolic function. 9 Thus, abolition of negative intrathoracic swings is a key mechanism by which treatment of OSA could reduce adverse stimuli to the heart and intrathoracic vessels, yet one that cannot be detected by systemic BP recordings.…”

mentioning

confidence: 99%

“…The first randomized trial of CPAP in OSA with sympathetic vasoconstrictor nerve traffic as its primary end point demonstrated a significant reduction during wakefulness in all of the treated subjects and a parallel decrease in concurrently measured systolic BP. 7 Thus, an important after effect of OSA is its chronic facilitation of sympathetically mediated vasoconstriction during wakefulness. 8 It is, therefore, noteworthy that the trial in which CPAP caused the greatest fall in systolic BP involved patients with OSA with advanced heart failure, individuals with the highest daytime sympathetic nerve traffic of all of those represented in this meta-analysis, 8 and measured BP shortly after waking.…”

mentioning

confidence: 99%

Treating Obstructive Sleep Apnea

Floras

Bradley

2007

Hypertension

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O bstructive sleep apnea (OSA), a common disorder, increases the 4-year risk of developing hypertension by Ϸ3-fold. 1 In an uncontrolled trial, treatment of OSA when present in drug-resistant hypertension by nasal continuous positive airway pressure (CPAP) achieved substantial reductions in both nighttime and daytime blood pressure (BP). 2 However, in controlled and uncontrolled studies involving small cohorts of patients with OSA with stage 1 hypertension, prehypertension, or normal BP, the short-term use of CPAP had less or no effect on BP. A meta-analysis in the present issue of Hypertension 3 attempts to estimate the effect of this intervention on BP.The authors identified all of the published trials that reported BP as a primary or a secondary end point in which adults with OSA diagnosed by polysomnography were randomly allocated to therapeutic CPAP or not for Ն2 weeks. These 16 trials involved 818 participants (86.3% men; mean age: 51 years; mean apnea-hypopnea index: 36.2 events per hour) treated for Յ24 weeks. From the 15 trials that reported systolic and diastolic BP, the authors calculated a significant mean net reduction of 2.46/1.83 mm Hg with CPAP and, from the 7 trials that reported mean arterial BP, a significant net reduction of 2.22 mm Hg. By comparison, in a previous meta-analysis restricted to 12 trials in which the primary variable of interest was 24-hour mean ambulatory BP, the calculated net decrease was still significant at 1.69 mm Hg. 4 In the present analysis by Bazzano et al, 3 the mean net change in systolic BP tended to correlate with the average nightly CPAP use ( Figure 5 in Reference 3; Pϭ0.13). These authors concluded that CPAP decreases BP among those with OSA, and treating OSA with CPAP may help prevent hypertension.There is increasing awareness of the adverse interactions between OSA and several cardiovascular conditions. 5 Consequently, these 2 conclusions are certain to attract attention. However, they are based on a meta-analysis involving a small number of subjects treated briefly. Absent are long-term data confirming that any initial reduction persists, and there has been no randomized, controlled test of the hypothesis that abolition of OSA in prehypertensive patients will prevent the subsequent development of hypertension. Only 2 of these trials recruited specifically hypertensive patients, in whom hypertension was usually treated. The average BP of all 818 subjects was 131/80 mm Hg. In a subsequent subgroup analysis, significant BP reductions were identified only in those with BP Ն130/80 mm Hg. Little or no impact on BP would be anticipated from any intervention in normotensive individuals. The analysis also conflates studies of people with (afterload-insensitive) normal and (afterloadsensitive) impaired ventricular systolic function. Does this meta-analysis then truly provide robust and reliable "level A" evidence for an antihypertensive or hypertensionpreventative effect of CPAP? As we address this question, we will develop 2 concepts: the distinction between "effects...

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Inhibition of Awake Sympathetic Nerve Activity of Heart Failure Patients With Obstructive Sleep Apnea by Nocturnal Continuous Positive Airway Pressure

Abstract: Treatment of coexisting OSA by CPAP in HF patients lowers daytime MSNA, systolic BP, and HR. Inhibition of increased central sympathetic vasoconstrictor outflow is one mechanism by which nocturnal CPAP reduces awake BP in HF patients with moderate to severe OSA.

Cited by 212 publications

References 16 publications

Clinical Phenotypes in Heart Failure With Preserved Ejection Fraction

Clinical Phenotypes in Heart Failure With Preserved Ejection Fraction

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

Treating Obstructive Sleep Apnea

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