Europace Advance Access originally published online on August 4, 2008
Europace 2008 10(9):1029-1033; doi:10.1093/europace/eun190
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REVIEWS
Sleep-disordered breathing in heart failure and the effect of cardiac resynchronization therapy
1 Cardiology Department, Heraklion University Hospital, PO Box 1352, Heraklion, Crete, Greece; 2 Sleep Disorders Unit, Department of Thoracic Medicine, Faculty of Medicine, University of Crete, Crete, Greece
Manuscript submitted 22 April 2008. Accepted after revision 1 July 2008.
* Corresponding author. Tel: +30 2810 392422; fax: +30 2810 542055. E-mail address: cardio{at}med.uoc.gr or mximeris{at}excite.com
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Abstract |
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 Top Abstract IntroductionPathophysiology of sleep...Obstructive sleep apnoea and...Central sleep apnoea and...Cardiac resynchronization...References |
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Respiratory disturbances during sleep are common in patients with heart failure (HF) and can trigger the occurrence of sleep apnoea or deteriorate pre-existing breathing disorder. This in turn may lead to worsening of the HF itself. Optimal treatment for HF has been found to reduce respiratory disturbances during sleep significantly, whereas cardiac resynchronization therapy (CRT), achieved by biventricular pacing, appears to cause a further reduction in episodes of central type apnoea, although it may also have an effect on episodes of obstructive type. The beneficial effect of CRT is due to the patients’ haemodynamic improvement and in the HF amelioration, and not due to some other effect resulting from the electrical stimulation of the heart. However, this therapeutic intervention by itself is insufficient for the effective treatment of respiratory disturbances during sleep and should be considered as an adjunctive treatment in addition to other established therapies.
Key Words: Cardiac resynchronization, Sleep apnoea, Heart failure
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Introduction |
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TopAbstractIntroductionPathophysiology of sleep...Obstructive sleep apnoea and...Central sleep apnoea and...Cardiac resynchronization...References |
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Heart failure (HF) is a syndrome with an epidemic character and important social and economical repercussions.1
Its prevalence ranges from 0.3 to 2% and exceeds 10% in those aged over 70 years. We also know that respiratory disturbances during sleep, often encountered in the general population, are even more common in patients with HF. The central type of sleep apnoea, although seen in other categories of patients, such as those with cerebrovascular stroke, or in healthy individuals at high altitudes, occurs mainly in patients with congestive heart failure (CHF). Its incidence reaches 45% and increases with the severity of CHF.2–4 However, a high percentage of patients with CHF also exhibits the obstructive type of sleep apnoea. In a recent study, 71% of the patients with CHF had sleep apnoea, 28% central, and 43% obstructive type.5 It appears that the latter type can provoke or exacerbate pre-existing CHF, whereas CHF can also influence the pathophysiology of obstructive sleep apnoea. The optimum therapy for CHF appears to have a mitigating effect on sleep apnoea, whereas other measures such as O2 administration or continuous positive airway pressure (CPAP) have been used in order to control the respiratory disturbance further. Although these measures seem to be beneficial, they are not currently recommended in clinical practice because they have no proven effect on mortality and morbidity.6
Recently, the role of cardiac resynchronization therapy (CRT) in the treatment of sleep apnoea has been investigated in CHF patients. In certain subgroups of patients with HF, CRT seems to not only improve their functional capacity, morbidity, and mortality, but also causes reverse remodelling.7–9 As an adjunctive therapy to optimum medication, one would also expect CRT to improve sleep apnoea. Its role, however, has come under close scrutiny because it was recently found that traditional pacing at a rate higher than mean nocturnal heart rate can also improve sleep apnoea in certain patient subgroups.10 This article, after considering the pathophysiology of sleep apnoea in patients with HF, will present the current state of knowledge concerning the role of CRT in the reduction of breathing disorders during sleep in these patients.
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Pathophysiology of sleep breathing disorders in heart failure patients |
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TopAbstractIntroductionPathophysiology of sleep...Obstructive sleep apnoea and...Central sleep apnoea and...Cardiac resynchronization...References |
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Three factors are likely to contribute to the pathogenesis of obstructive sleep apnoea–hypopnoea syndrome (OSAHS): anatomical abnormalities, the ability of the upper airway dilator muscles to respond to respiratory challenge during sleep, and the instability of the respiratory control system (high-loop gain).
Most patients with OSAHS have an anatomically small pharyngeal airway as a result of either increased soft tissue surrounding the airway or a small bony compartment in which the airway is enclosed.11 During sleep, reflex activation of the upper airway dilator muscles is reduced, and if the airway anatomy is quite deficient, these events alone will likely lead to substantial or complete airflow obstruction, yielding a hypopnoea or apnoea–hypopnoea or apnoea. As a result, hypoxia and hypercapnia may develop, ventilation is stimulated, and often arousal from sleep in response to respiratory activation is required to re-establish airway patency and to allow a recovery of ventilation.12
There is also a diminished ability of the upper airway dilator muscles to maintain a patent airway during sleep.13,14 With the onset of sleep, pharyngeal dilator muscle activation falls markedly, leaving the susceptible airway in patients with OSAHS vulnerable to collapse.15 The collapse generally persists until arousal occurs, which leads to reactivation of these muscles.
In addition to anatomical factors and upper airway dilator muscles, loop gain is also important in the pathogenesis of OSAHS. Loop gain is an engineering term used to describe the intrinsic stability or instability of a negative-feedback control system. In the context of ventilation, loop gain can be considered as the propensity of an individual to develop periodic breathing or cycling respiration. A system with a high-loop gain is intrinsically prone to instability, whereas a low-loop gain system tends to be stable. There are two principal components to loop gain: controller gain and plant gain.16,17 With regard to respiratory control, the controller gain refers to the chemoresponsiveness of the system (i.e. hypoxic and hypercapnic ventilatory responses). Thus, a high controller gain is generally due to brisk hypercapnic responsiveness. Plant gain primarily reflects the efficiency of CO2 excretion (i.e. the ability of a given level of ventilation to excrete CO2). Thus, high plant gain would occur if a small change in ventilation produced a large change in PCO2. A third factor, known as circulation time, represents the interval between changes in blood gases in the lung and the arrival of the new blood gases at the CO2 sensor in the brainstem (influenced primarily by cardiac output). In other words, loop gain can be defined mathematically as the response to a disturbance divided by the disturbance itself13 (Figure 1).
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Obstructive sleep apnoea and heart failure |
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TopAbstractIntroductionPathophysiology of sleep...Obstructive sleep apnoea and...Central sleep apnoea and...Cardiac resynchronization...References |
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Obstructive sleep apnoea–hypopnoea syndrome elicits a series of mechanical, haemodynamic, chemical, neural, and inflammatory responses, with adverse consequences for the cardiovascular system.17
Obstructive sleep apnoea–hypopnoea syndrome and HF converge in two areas crucial for the progression of myocardial failure and premature mortality: the negative effect of sympathetic nervous system activation and vagal withdrawal from the cardiovascular system and the deleterious effects of altered loading conditions and hypoxia on the failing ventricle.18,19
Recurrent hypoxaemia and hypercapnia, resulting from obstructive events, stimulate peripheral and central chemoreceptors, which trigger elevated sympathetic nerve activity, known to be cardiotoxic in HF.19
During an obstructive apnoea episode, effort continues against an occluded pharynx, with a consequent abrupt reduction in intra-thoracic pressure. This, in turn, causes an increase in the left ventricular transmural pressure, which reflects the difference between intra-cardiac and intra-thoracic pressure and hence afterload. Venous return is also enhanced, resulting in right ventricular distension and leftward shift of the inter-ventricular septum. This impedes left ventricular filling.18 Therefore, cardiac function is compromised by a combination of diminished left ventricular pre-load and augmented left ventricular afterload, which together reduce the stroke volume.20 Patients with HF experience more profound and prolonged reductions in the stroke volume than control subjects with normal left ventricular function.21 The aforementioned obstructive events are replicated hundred of times during the course of the night, with concomitant reductions in intra-thoracic pressure, which could play a significant role in the development of myocyte slippage, contractile dysfunction, and adverse ventricular remodelling in HF patients.22 In addition, OSAHS prevents the normal drop in heart rate that accompanies the onset of sleep.17 When coupled with reflex increases in central sympathetic outflow (which are greater in HF patients than in normal subjects), these marked elevations in afterload and heart rate increase the metabolic demands of the myocardium, which in turn occurs during reduced oxygen supply, cardiac output, and coronary perfusion and could lead to the development of recurrent nocturnal ischaemia and arrhythmias.18,23 In addition to these adrenergic and mechanical conditions, increased levels of inflammatory mediators, oxidative stress, and vascular endothelial dysfunction in OSAHS have the potential to accelerate atherosclerosis, which could lead to ischaemic heart disease, one of the common causes of HF.24,25
According to large epidemiological studies, OSAHS seems to contribute to the development of systemic hypertension: a precursor of HF that is independent of other known risk factors.26 Left ventricular hypertrophy is more closely linked to hypertension during sleep than during wakefulness. Hypertensive patients with OSAHS experience a higher nocturnal blood pressure than do those without and are at greater risk of left ventricular hypertrophy. As the output from the failing left ventricle is sensitive to increases in afterload, the most direct mechanism by which OSAHS may compromise left ventricular systolic function is through its effect on blood pressure. When HF patients evidence recurrent trends of obstructive events during sleep, blood pressure rises above, rather than descending below, waking values.18,26
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Central sleep apnoea and heart failure |
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TopAbstractIntroductionPathophysiology of sleep...Obstructive sleep apnoea and...Central sleep apnoea and...Cardiac resynchronization...References |
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In contrast to OSAHS, in which ongoing respiratory efforts are observed, central sleep apnoea (CSA) is defined by a lack of respiratory effort during cessations of airflow. However, considerable overlap exists in the pathogenesis and pathophysiology of obstructive and central apnoea, making this distinction somewhat difficult at times. Cheyne–Stokes respiration can be seen in patients with CHF and is a product of high controller gain (increased ventilatory responsiveness to rising CO2), hypocapnia resulting from lung oedema (high filling pressures), and a long circulation time. This combination of traits is particularly destabilizing to ventilation and yields a characteristic crescendo–decrescendo pattern of breathing, with a cycle time of
1 min.13,27,28 Cheyne–Stokes respiration occurs primarily during non-rapid eye movement sleep, although it can be detected during wakefulness if carefully sought. Due to the above combination of traits, it is not seen in all patients with CHF, even in those with severe CHF. Recent data suggest that Cheyne–Stokes respiration is more severe in the supine position than in the lateral.29
It is unclear whether CSA is simply a reflection of severely compromised cardiac function, or whether CSA exerts independent pathological effects on the failing myocardium. The mechanisms responsible involve chemical, neural, and haemodynamic oscillations similar to those observed in OSAHS.27,30,31 There is a marked sympathetic activation, as shown by significantly higher levels of catecholamines in the urine of patients with HF and CSA compared with those without. Patients with CSA and HF also have a surge in blood pressure and heart rate, hypoxaemia, and systemic inflammation and are therefore at increased risk for the development of ventricular and supraventricular arrhythmias.23,30 Importantly, arousals are accompanied by sudden increases in heart rate and blood pressure. Arousal also results in hyperventilation with a subsequent fall in PaCO2, close to the apnoeic threshold. Frequent arousals from sleep lead to destabilization of the respiratory control system, resulting in CSA and periodic breathing with cycles of apnoea. Other major adverse consequences of CSA are intermittent arterial blood gas abnormalities characterized by hypoxaemia–reoxygenation hypercapnia–hypocapnia and large negative swings in intra-thoracic pressure, which increases the wall tension (afterload) and oxygen consumption of the left ventricle.30 With regard to the pulmonary vascular bed, when the patient lies flat, increased venous return from the extremities causes central fluid accumulation and pulmonary and upper airway congestion. In addition, experimental data suggest that pulmonary congestion stimulates vagal irritant receptors in the lung (J-receptors), with concomitant reflex hyperventilation, a fall in PaCO2, and thus hypocapnia and ventilatory destabilization.28,29 These adversely affect various cardiovascular functions and are potentially most detrimental in the presence of established left ventricular systolic and diastolic dysfunction.
There are reports of the coexistence of OSAHS and CSA in HF. According to these, obstructive apnoea shifts to central, depending on the progress of HF, or the presence of OSAHS predisposes the patient with HF to develop CSA.20,31 In a study of patients with HF, the apnoea type shifted overnight from mainly obstructive to mainly central, in association with a reduction in PaCO2 and an increase in periodic breathing cycle duration, suggestive of a fall in the cardiac output.32 Current and ongoing investigation in this area will further elucidate the role of both central and obstructive sleep apnoea in HF.
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Cardiac resynchronization therapy and sleep apnoea |
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TopAbstractIntroductionPathophysiology of sleep...Obstructive sleep apnoea and...Central sleep apnoea and...Cardiac resynchronization...References |
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As HF can cause or exacerbate sleep apnoea, the optimal treatment of HF could reasonably be expected to lead to an improvement in respiratory disturbances during sleep. Indeed, there are data from small studies showing that medical therapy and heart transplantation all significantly reduce the episodes of CSA in HF patients.32
–34
Cardiac resynchronization therapy became part of the HF treatment during the last decade and has had spectacular results. In certain subgroups of patients who have ventricular conduction disturbances, CRT in conjunction with optimal medical therapy appears to improve the patients’ haemodynamic condition and functional capacity; it also leads to the reversal of remodelling and increases survival.7–9,35 It was therefore logical to examine the role of this therapy in the reduction of respiratory disturbances during sleep (Table 1). In addition, as there have been indications that atrial overdrive pacing can limit the obstructive episodes and CSA in patients with bradycardia, by maintaining sympathetic activity and possible by improving patient haemodynamic profile,10 the role of CRT at high cardiac rates has also been investigated.
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An early study by Sinha et al.35
assessed the effect of CRT on the apnoea–hypopnoea index (AHI) and the quality of sleep. The investigators found that after 17 ± 7 weeks of CRT, the AHI decreased significantly from 19.2 ± 10.3 to 4.6 ± 4.4 (P < 0.001), whereas there was a significant correlation between the reduction in AHI and the Pittsburgh sleep quality index. In addition, the desaturation index and ventilation–apnoea length also decreased significantly. In another study,36 the same authors found that CRT reduced Cheyne–Stokes respiration, with an improvement of sleep quality and a decrease in symptomatic depression, whose negative effect on HF is well known.
In a subsequent study, Oldenburg et al.37 investigated the influence of CRT on different types of sleep-disordered breathing. Seventy-seven patients with HF were screened for the presence of sleep-disordered breathing. Central sleep apnoea was recorded in 47% of the patients and obstructive sleep apnoea in 34%. During a follow-up of 5.3 ± 3 months, the investigators found that CRT was associated with a significant improvement in sleep-disordered breathing parameters of central type, whereas the parameters of obstructive sleep apnoea did not change significantly. There was a substantial decrease in total apnoeic–hypopnoeic episodes and maximum apnoea and hypopnoea duration and an increase in minimum oxygen saturation. An important finding was that the improvement in CSA was seen only in the responders to CRT, indicating that the respiratory benefit was the result of the positive change in HF status, rather than a specific effect of pacing.
Similar results were found by Gabor et al.,38 who followed 10 patients with CSA over a period of 27 ± 7 weeks of CRT. In this study, the AHI decreased from 42.7 ± 9.1 to 30.8 ± 18.7 (P < 0.05). A later study by Stanchina et al.39 examined the impact of CRT on obstructive sleep apnoea in 13 patients with HF and attempted to correlate the changes in the severity of the apnoea with changes in the cardiac function assessed by circulation time. In contrast to Oldenburg et al.,37 they found a significant decrease in AHI from 40.9 ± 6.4 to 29.5 ± 5.9 after 6.6 ± 1.4 months of CRT. In addition, this improvement was strongly correlated with circulation time, which is an indirect measure of cardiac output. The same study also investigated whether CRT at a rate of 15 b.p.m. above the mean unpaced rate during sleep, would have a more beneficial effect on sleep parameters. However, the increased pacing rate had no impact on either sleep apnoea or circulation time.
The findings of the above studies demonstrate that CRT, by improving the haemodynamic profile of patients with HF, has a beneficial effect on the central type of sleep apnoea and possibly the obstructive type too. Nevertheless, it should be noted that the findings are indicative rather than conclusive, because the studies were small, may have lacked the necessary statistical power for the detection of differences, and were not controlled. Moreover, the reduction in AHI as a result of CRT was such that CRT cannot be considered alone as an adequate therapy for sleep apnoea but possibly can enhance the effect of CPAP as supplementary therapy, thus leading to a better therapeutic result with regard to the total reduction in the AHI in patients with HF. The magnitude of the reduction in AHI seems to be of great importance. This was shown by a well-organized mortality study, the CANPAP trial, which examined the results of CPAP therapy, a tried and tested treatment for sleep apnoea. Although CPAP was associated with a significant improvement in the sleep apnoea, ejection fraction, and serum catecholamine levels, it had no positive effect on morbidity or mortality in patients with HF and CSA.6 However, a meta-analysis of the same study found that in those patients in whom CPAP reduced the AHI below 15, there was a positive effect on mortality.40 This demonstrates the importance of the degree of reduction of AHI for the therapeutic result.
Although the studies mentioned above are not conclusive, they can contribute to a better understanding of the pathophysiology of sleep apnoea in HF and the important role of the optimum treatment of the latter condition in the improvement of respiratory disturbances. A reduction in apnoea as a result of biventricular pacing in certain patients seems to indicate that those patients are responders to CRT, as in all studies to date only such responders showed an improvement in sleep apnoea. Finally, it should be mentioned that if CRT is combined with pacemakers that have minute ventilation sensors and special algorithms able to record apnoeic episodes, this enables not only an improvement in the benefit but also monitoring of the therapeutic result.
In conclusion, respiratory disturbances during sleep are common in patients with HF. It appears that pathophysiological disturbances occurring in HF are closely related to the mechanisms that cause or exacerbate sleep apnoea. The improvement in HF caused by CRT appears to exert a significant effect in reducing apnoeic episodes of central and possibly obstructive type, although a further reduction using other therapeutic methods is likely to be necessary.
Conflict of interest: none declared.
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TopAbstractIntroductionPathophysiology of sleep...Obstructive sleep apnoea and...Central sleep apnoea and...Cardiac resynchronization...References |
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