WHY IS SLEEP RELEVANT TO CARDIOVASCULAR DISEASE?
It is well known that cardiovascular disease is the leading cause of death and disability in the United States and throughout the world. Concurrent with this immense public health problem, we are witnessing an exponential increase in new knowledge about sleep and sleep disorders and growing evidence of the links between sleep and cardiovascular disease and disability. These promising research findings suggest the role of sleep disorders, particularly sleep-disordered breathing, as a pathway to the development of cardiovascular disease (CVD) and a contributor to its exacerbation in patients with CVD. Sleep disorders are also a likely contributor to functional performance and quality of life among cardiovascular patients, although this area has undergone less study. This issue of The Journal of Cardiovascular Nursing (17:1) is devoted to exploring the links between sleep and CVD from a multidimensional biobehavioral perspective. The authors in this issue review the literature on the epidemiologic and physiologic links between sleep-disordered breathing and hypertension, heart failure, and stroke; explore the role of sleep and sleep disorders in cardiac patients in the intensive care unit and across the trajectory of recovery after cardiac surgery; and discuss the implications of heart rate variability for sleep and cardiovascular health. The articles published in this issue provide intriguing insights into the state of the science and directions for future research in these areas. Where appropriate, the authors discuss implications for cardiovascular practice. Although this issue does not pretend to provide comprehensive coverage of all of the avenues through which sleep disorders may contribute to CVD and the lives of people who suffer from it, the articles in this issue provide a substantial overview of several promising research areas that have the potential to reduce morbidity and mortality and improve quality of life and function. It is my goal to raise awareness among cardiovascular nurses, physicians, and other health care providers about the potentially important role of sleep, a biobehavioral phenomenon, for the development of CVD, its implications for people who already have CVD, and its physiologic, functional, and quality-of-life consequences.
Krieger and Redeker review the epidemiologic and physiologic evidence that obstructive sleep apnea-hypopnea syndrome contributes to the development of hypertension and discuss the strengths and limitations of this body of work and its implications for cardiovascular practice. Sleep-disordered breathing, particularly obstructive sleep apnea-hypopnea (OSAHS), is increasingly identified as a pathway to cardiovascular morbidity and mortality. OSAHS is a syndrome characterized by respiratory disturbance resulting from repetitive partial or complete obstruction of the upper airway during sleep in the presence of excessive daytime somnolence.1 Recent work suggests that this syndrome occurs on a continuum ranging from heavy snoring to apneic events during sleep.2 This syndrome results in loud snoring, frequent nocturnal desaturations, and repetitive brief arousals from sleep. A recent estimate of the prevalence of OSAHS at 9% of women and 24% in men,3 as well as more conservative estimates at 2%-4% of the population,4 underscores the public health significance of this problem. Recent studies, such as the Sleep Heart Health Study, funded by the National Heart, Lung, and Blood Institute, have begun to address these issues. In the future, randomized clinical trials to examine the effects of continuous positive airway pressure (CPAP) on hypertension and other cardiovascular outcomes are expected to produce useful findings. Reduction in obesity, a primary risk factor for both OSAHS and CVD, is also a significant goal.
Richards, Hall, Shook, and Brown discuss the links between sleep-related breathing disorders and stroke, the third leading cause of death in the United States. Two possible mechanisms for this relationship include decreased cerebral perfusion, altered cerebral autoregulation, increased platelet aggregation, and plasma fibrinogen. These effects appear to be independent of pre-existing hypertension.5 Increased levels of OSAHS have also been found in patients who had recently had ischemic strokes or transient ischemic attacks compared with control subjects, and age, body mass index, diabetes, and the severity of the stroke were predictive of the apnea-hypopnea index (number of apneas and hypopneas per hour of sleep, a measure of severity of sleep apnea).6 As reviewed by Richards and colleagues, these compelling findings emphasize the need to incorporate screening and treatment for OSAHS into stroke prevention programs, but also highlight the need to evaluate and treat sleep disorders in patients undergoing rehabilitation after transient ischemic attacks or ischemic strokes.
Obstructive sleep apnea has been shown to lead to hypoxemia, sympathetic activation, acute pulmonary and systemic hypertension, and decreased stroke volume. McMillan's article explains the relationships between sleep and heart rate variability, an important marker of autonomic function, and provides useful information on the methods used to evaluate it.
Numerous clinical studies have suggested that OSAHS also contributes to unstable angina, myocardial infarction, and sudden death. For example, myocardial ischemia has been associated with nocturnal respiratory events in several studies (eg, the studies by Hanly and colleagues7 and Guilleminault and colleagues8). Recent epidemiologic data from the Sleep Heart Health Study demonstrated that mild to moderate sleep-disordered breathing was associated with self-reported heart failure, stroke, and coronary heart disease when obesity and other risk factors were controlled.9 Although the odds-ratios for coronary heart disease events were lower than those for heart failure or stroke, the fact that even mild to moderate levels of obstructive sleep apnea were associated with coronary disease suggests the potential benefits of more widespread screening and treatment for this problem.
Although we have not included an article written specifically on insomnia in this issue, there is also interesting evidence that insomnia itself may contribute to the development of CVD. Insomnia is typically defined as difficulty in initiating or maintaining sleep and may include delays in falling asleep, frequent awakenings, premature morning awakening, subjective reports of sleep difficulty or unrefreshing sleep, as well as daytime discomfort. Insomnia has been described as a primary disorder, a complaint, or a condition secondary to another disorder.10 Despite the heterogeneity of definitions and measurement methods, insomnia is the most prevalent sleep disorder across the lifespan. In a recent review of 10 epidemiologic studies,11 trouble falling asleep or difficulty staying asleep predicted coronary events with risk ratios of 1.47-3.9, after adjusting for age and coronary risk factors. The authors suggested that insomnia may be a marker for a syndrome of depression and malaise. Insomnia may also be a marker of autonomic dysfunction, a phenomenon that is undergoing increasing scrutiny as a pathway to coronary disease. Despite the absence of polysomnographic data that might assist in ruling out the presence of sleep-disordered breathing in the study subjects, the authors' premise that insomnia may have significant physiologic consequences warrants further study. However, such studies may need to disentangle depression from disturbed sleep, because insomnia and depression often go hand-in-hand. Insomnia is a frequent sign of depression, but recent findings have also demonstrated that insomnia may be a precursor to depression.12 Given recent increased recognition of the potential influence of depression on CVD, disentangling the effects of depression or insomnia itself is a worthy, if complicated, goal for research. From a clinical perspective, sleep disturbance may reflect underlying mood disturbances that should alert clinicians to the potential need to treat depression in patients with CVD.
Sleep disorders are also relevant to patients who already have CVD and may have an effect on acute care treatment and recovery. However, despite numerous studies of sleep in the acute care environment, until recently there have been few studies that have examined the extent of sleep-disordered breathing in this setting.13 Richards, Anderson, Chesson, and Nagel address this gap in their report of the prevalence of sleep-disordered breathing in male patients who are critically ill with cardiac diagnoses. The presence of sleep-disordered breathing in almost 50% of these patients suggests the potential effect of the desaturations and autonomic changes associated with these events on cardiopulmonary physiology during the acute care period. Increased awareness among acute and critical care personnel of these problems may help to avoid their deleterious effects. Careful monitoring for these events and interventions to maximize oxygenation (eg, use of nasal CPAP, avoidance of sedation) may prevent untoward complications and hasten recovery during acute care hospitalization.
Sleep disturbance in patients who are acutely ill or recovering from CVD appears to change over the course of the illness, and the influences appear to be multifactorial. The literature suggests that in addition to primary sleep disorders, influences on sleep may include cardiovascular illness or its symptoms, comorbid health conditions, medications and other treatments, as well as characteristics of the acute or critical care environment (noise, lighting, nocturnal patient-care interactions). Redeker and Hedges review the literature on the correlates and consequences of sleep disturbance in cardiac surgical patients and propose directions for future research and clinical practice with this large group of patients. Although research has been conducted on the sleep of cardiac patients who are acutely ill (especially patients who have undergone cardiac surgery) for more than 30 years, few researchers have examined the physiologic or functional outcomes of sleep disturbance in these patients, and there have been few clinical trials of sleep-promoting interventions.
From the perspective of chronic illness, disturbed sleep is also a significant problem for the almost 5 million Americans who suffer from heart failure (HF). Cheyne-Stokes breathing or central sleep apnea is "a form of periodic breathing in which central apneas alternate with ventilatory periods that have a gradually waxing-waning pattern of tidal volumes"14(p.1676) is common in as many as 50% of patients with HF and is associated with more severe HF and increased mortality. As many as 33% of patients with HF have obstructive sleep apnea that may occur separately or co-occur with Cheyne-Stokes breathing or central apnea. Parker and Dunbar review the evidence for the physiologic linkages between these sleep-related breathing disorders and discuss some promising findings relative to the use of CPAP as a treatment for sleep-disordered breathing and improvement in cardiac function among these patients. Given the growth in the size of the population with HF and the dire consequences of this syndrome, CPAP may prove to be a valuable adjunct in management of HF.
Although most of the biomedical research on sleep and CVD has focused on the cardiorespiratory consequences of sleep-disordered breathing, sleep disorders are well known to have an effect on quality of life and functional performance. For example, the Wisconsin Sleep Cohort Study demonstrated that sleep-disordered breathing was associated with decrements in general health status15 and increased frequency of motor vehicle accidents.16 Data from the Sleep Heart Health Study demonstrated that sleep-disordered breathing was linearly related to vitality, and persons with high levels of sleep-disordered breathing had poorer quality of life on multiple dimensions of the Medical Outcomes Study SF-36.17 Although neither of these studies consisted entirely of patients with pre-existing cardiac disease, it stands to reason that sleep disorders may contribute or worsen the quality of life or functional performance of patients with CVD. For example, a recent study found that self-reported preoperative sleep quality and sleep efficiency measured with actigraphy contributed to functional performance among patients who had undergone coronary artery bypass surgery 4 weeks after surgery.18 Future studies are needed to evaluate the extent to which sleep-promotion strategies may also improve functional performance and quality of life outcomes in patients with CVD.
The articles in this issue of The Journal of Cardiovascular Nursing and the additional findings discussed in this narrative address multiple ways in which sleep disorders interface with CVD. It is increasingly clear that sleep disorders may influence the evolution of CVD and aggravate existing disease and quality of life for patients with CVD. Although there have been few randomized clinical trials specific to CVD to guide practice, the available epidemiologic evidence suggests that it is prudent to identify individuals with sleep disorders, refer them for treatment when appropriate, and support them in the behaviors necessary to maintain compliance. A detailed discussion of the various sleep disorders and screening methods is beyond the scope of this article, but many references are available on this topic. For example, Sanders and Redline1 published an excellent primer on obstructive sleep apnea. Numerous current scientific resources, including case study materials and patient handouts, are available for no charge on the World Wide Web (see Table 1). Available evidence suggests the relevance of sleep disorders in CVD. The links between sleep and CVD appear to occur on physiologic and behavioral levels and across the trajectory of illness and recovery. Sleep research, including basic, epidemiologic, clinical, and behavioral studies, has grown exponentially over the past few years, and this growth is likely to continue. It is hoped that future studies will lead to the development of strategies to improve sleep as well as reduce the burden of CVD. Cardiovascular nurses and other cardiovascular professionals are likely to contribute substantially to this effort.
—Nancy S. Redeker, PhD, RN, CS
College of Nursing
Rutgers, The State University of New Jersey
Newark, New Jersey
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