Sustained effect of continuous positive airway pressure on baroreflex sensitivity in congestive heart failure patients with obstructive sleep apnea
Sleep and Cardiovascular Physiology Research Laboratories of the Mount Sinai Hospital, Toronto, Ontario, Canada. Journal of Hypertension
(Impact Factor: 4.72).
07/2008; 26(6):1163-8. DOI: 10.1097/HJH.0b013e3282fb81ed
Patients with either heart failure or obstructive sleep apnea have a reduced baroreflex sensitivity for heart rate, a sign of poor prognosis. We previously demonstrated that nocturnal application of continuous positive airway pressure to heart failure patients with obstructive sleep apnea increased baroreflex sensitivity acutely, but it is not known whether these effects persist into wakefulness.
To determine whether treating obstructive sleep apnea in heart failure patients with continuous positive airway pressure improves baroreflex sensitivity during wakefulness.
Spontaneous baroreflex sensitivity was assessed during wakefulness in 33 heart failure patients (left ventricular ejection fraction < or = 45%) with obstructive sleep apnea (apnea-hypopnea index > or = 20). Subsequently, baroreflex sensitivity was reassessed 1 month after patients were randomly allocated to nocturnal continuous positive airway pressure treatment or no treatment (control).
Compared with the 14 control patients, the 19 continuous positive airway pressure-treated patients experienced a greater increase in baroreflex sensitivity [median, (25%, 75%)] [from 5.4 (2.2, 8.3) to 7.9 (4.4, 9.4) ms/mmHg; P = 0.01] and left ventricular ejection fraction (P < 0.001). In addition, daytime systolic blood pressure and heart rate decreased more in the continuous positive airway pressure group (from 122 +/- 15 to 113 +/- 12 mmHg; P = 0.02, and from 66 +/- 8 to 62 +/- 8 bpm; P < 0.001, respectively) than in the control group.
Treatment of coexisting obstructive sleep apnea by continuous positive airway pressure in heart failure patients improves baroreflex sensitivity during wakefulness in addition to improving left ventricular ejection fraction and lowering blood pressure and heart rate. These data indicate that the improved autonomic regulation of heart rate in heart failure patients treated for obstructive sleep apnea during sleep persists into wakefulness.
Available from: PubMed Central
- "Impairment of the baroreflex sensitivity is directly associated with this autonomic dysfunction (Creager, 1992). Many studies have demonstrated that the arterial baroreflex sensitivity is attenuated in both clinical and experimental CHF (White, 1981; Floras, 1993; Frenneaux, 2004; Pinna et al., 2005; Ruttanaumpawan et al., 2008), which is a predictive risk factor for sudden cardiac death (Kleiger et al., 1987) and is associated with mortality of CHF (Nolan et al., 1998; Cygankiewicz et al., 2008; Boogers et al., 2011; Hauptman et al., 2012). Although the precise mechanisms responsible for blunted arterial baroreflex in the CHF state are not fully understood, activation of the arterial baroreflex (as a long-term therapeutic approach) has been shown to have numerous beneficial effects on CHF treatments in both clinical and experimental studies (Zucker et al., 2007; Sabbah, 2012; Doumas et al., 2014; Gronda et al., 2014; Halbach et al., 2014; Iliescu et al., 2014; Liao et al., 2014; Madershahian et al., 2014; Schmidli et al., 2014). "
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ABSTRACT: Chronic heart failure (CHF) affects approximately 5.7 million people in the United States. Increasing evidence from both clinical and experimental studies indicates that the sensitivity of arterial baroreflex is blunted in the CHF state, which is a predictive risk factor for sudden cardiac death. Normally, the arterial baroreflex regulates blood pressure and heart rate through sensing mechanical alteration of arterial vascular walls by baroreceptor terminals in the aortic arch and carotid sinus. There are aortic baroreceptor neurons in the nodose ganglion (NG), which serve as the main afferent component of the arterial baroreflex. Functional changes of baroreceptor neurons are involved in the arterial baroreflex dysfunction in CHF. In the CHF state, circulating angiotensin II (Ang II) and local Ang II concentration in the NG are elevated, and AT1R mRNA and protein are overexpressed in the NG. Additionally, Ang II-superoxide-NFκB signaling pathway regulates the neuronal excitability of aortic baroreceptors through influencing the expression and activation of Nav channels in aortic baroreceptors, and subsequently causes the impairment of the arterial baroreflex in CHF. These new findings provide a basis for potential pharmacological interventions for the improvement of the arterial baroreflex sensitivity in the CHF state. This review summarizes the mechanisms responsible for the arterial baroreflex dysfunction in CHF.
Frontiers in Neuroscience 11/2015; 9:382. DOI:10.3389/fnins.2015.00382 · 3.66 Impact Factor
- "Patients with untreated SDB consume twice as many healthcare resources for treatment of cardio-respiratory diseases as subjects without SDB . In contrast, treating SDB alleviates hypersomnolence, lowers blood pressure, and improves cardiovascular function in patients with hypertension or HF     . Therefore, widespread diagnosis and treatment of SDB could have a considerable beneficial medical and public health impact . "
American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado; 05/2011
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- "On the other hand, Valipour , using the sequence method, described a decline in the mean slope of spontaneous baroreceptor sequences at pressure levels > 10 cmH2O, compared to lower pressure levels (0, 3 or 5 cmH2O). Significant increases in the baroreflex gain were also described with PEEP in severe obstructive sleep apnea, with  or without  heart failure, and in snorers . In critical care, mechanically ventilated patients, we observed a decrease in baroreflex sensitivity with increasing PEEP. "
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ABSTRACT: Baroreflex allows to reduce sudden rises or falls of arterial pressure through parallel RR interval fluctuations induced by autonomic nervous system. During spontaneous breathing, the application of positive end-expiratory pressure (PEEP) may affect the autonomic nervous system, as suggested by changes in baroreflex efficiency and RR variability. During mechanical ventilation, some patients have stable cardiorespiratory phase difference and high-frequency amplitude of RR variability (HF-RR amplitude) over time and others do not. Our first hypothesis was that a steady pattern could be associated with reduced baroreflex sensitivity and HF-RR amplitude, reflecting a blunted autonomic nervous function. Our second hypothesis was that PEEP, widely used in critical care patients, could affect their autonomic function, promoting both steady pattern and reduced baroreflex sensitivity.
We tested the effect of increasing PEEP from 5 to 10 cm H2O on the breathing variability of arterial pressure and RR intervals, and on the baroreflex. Invasive arterial pressure, ECG and ventilatory flow were recorded in 23 mechanically ventilated patients during 15 minutes for both PEEP levels. HF amplitude of RR and systolic blood pressure (SBP) time series and HF phase differences between RR, SBP and ventilatory signals were continuously computed by complex demodulation. Cross-spectral analysis was used to assess the coherence and gain functions between RR and SBP, yielding baroreflex-sensitivity indices.
At PEEP 10, the 12 patients with a stable pattern had lower baroreflex gain and HF-RR amplitude of variability than the 11 other patients. Increasing PEEP was generally associated with a decreased baroreflex gain and a greater stability of HF-RR amplitude and cardiorespiratory phase difference. Four patients who exhibited a variable pattern at PEEP 5 became stable at PEEP 10. At PEEP 10, a stable pattern was associated with higher organ failure score and catecholamine dosage.
During mechanical ventilation, stable HF-RR amplitude and cardiorespiratory phase difference over time reflect a blunted autonomic nervous function which might worsen as PEEP increases.
Respiratory research 04/2010; 11(1):38. DOI:10.1186/1465-9921-11-38 · 3.09 Impact Factor
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