Obstruktive Schlafapnoe und kardiovaskuläre Komorbidität

Obstructive sleep apnea (OSA) is the most common entity of sleep-disordered breathing in Germany. OSA is independently associated with an increased risk of cardiovascular disease. It predisposes to arterial hypertension in particular, but also to coronary artery disease, cardiac arrhythmias and atrial fibrillation. OSA has been established as an independent risk factor for arterial hypertension, and treatment of OSA with continuous positive airway pressure (CPAP) causes a significant and persistent drop in blood pressure. Long-term CPAP treatment reduces the rate of important cardiovascular comorbidities.     

Exacerbation of ventricular arrhythmias by continuous positive airway pressure treatment in idiopathic dilated cardiomyopathy

Continuous positive airway pressure (CPAP) therapy can be beneficial in patients with obstructive sleep apnea (OSA) and cardiovascular diseases, reducing arrhythmia frequency and improving cardiac function. We describe a case of moderate OSA with idiopathic dilated cardiomyopathy, in which the frequency of premature ventricular contraction (PVC) and non-sustained ventricular tachycardia (NSVT) increased immediately after initiating CPAP therapy. Although PVC and NSVT are benign cardiac arrhythmias, they are associated with an increased risk of sustained lethal ventricular tachyarrhythmias. Therefore, when initiating CPAP therapy, the possibility of increased arrhythmia should be considered.     

Obstructive Sleep Apnea as a Cardiovascular Risk Factor—Beyond CPAP

Patients with obstructive sleep apnea (OSA) experience repetitive partial or complete airway collapse during sleep resulting in nocturnal hypoxia-normoxia cycling, and are at increased cardiovascular risk. The number of apneas and hypopneas indexed per hour of sleep (apnea-hypopnea index) along with the associated intermittent hypoxia predict the increased cardiovascular risk; thus, their attenuation or prevention are objectives of OSA therapy. Continuous positive airway pressure (CPAP) is the gold standard treatment for OSA and, when effective, mitigates the apnea-hypopnea index and hypoxemia. As such, it is reasonable to expect CPAP would decrease cardiovascular risk. However, 3 recent randomized clinical trials of CPAP vs usual care did not show any significant effects of CPAP in attenuating incident cardiovascular events in patients with OSA. In this review, we discuss these studies in addition to potential complementary therapeutic options to CPAP (eg, neurostimulation) and conclude with suggested therapeutic targets for future interventional studies (eg, the autonomic nervous system). Although these areas of research are exciting, they have yet to be tested to any similar degree of rigour as CPAP.     

慢性间歇低氧对心脏B超和血压影响的观察

目的 探讨慢性间歇低氧对OSAHS患者左心功能的影响,以及持续气道正压通气(CPAP)治疗后左心功能和血压的变化.方法 顺序收集2007年5月至2008年12月于吉林大学第一医院就诊的、符合OSAHS诊断标准的门诊或住院患者75例(OSA组),其中非高血压者35例,合并高血压者40例.另选30名健康人为对照组,其中男20名,女10名,年龄30～65岁,与患者组年龄匹配,均为经系统检查无异常发现的健康人.对两组左心室射血分数(left ventricular ejection fraction,LVEF)、短轴缩短率(shortening fraction,FS)、E峰、A峰,并计算E/A进行比较.CPAP治疗后的血压、LVEF、E/A进行分析.结果 所有患者晨起血压(150.80±20.73/108.0±15.34)mm Hg(1 mm Hg=0.133 kPa)均较睡前血压(134.16±18.33/90.09±11.24)mm Hg明显升高.OSA组E/A明显降低(P<0.01),LVEF、FS明显降低(P<0.05);与对照组及OSA非高血压组比较,OSA合并高血压的患者左室射血分数和短轴缩短率均减少,提示高血压的出现是OSA左室收缩功能减退的重要因素;与对照组比较,OSA非高血压组E/A明显降低;非高血压组和高血压组比较,高血压组E/A下降显著,说明OSA本身可直接影响左心室舒张功能,而高血压的出现加重了左心室的舒张功能的降低.经CPAP治疗6个月后晨起血压(142.59±15.34/96.52±9.81)mmHg较治疗前(150.80±20.73/108.0±15.34) mm Hg显著下降(P<0.001);左室射血分数(59.70±11.1)%较治疗前(56.40±9.74)%增加(P<0.05);E/A值1.16±0.25较治疗前0.87±0.17明显增加(P<0.01).结论 (1)CIH可引起左心结构和功能发生改变,高血压的出现加重了这种变化.(2)CPAP对于纠正OSA患者高血压、改善左心功能,提高生活质量有重要意义.     

Obstructive Sleep Apnea and Hypertension

Obstructive sleep apnea (OSA) and hypertension commonly coexist. Observational studies indicate that untreated OSA is associated with an increased risk of prevalent hypertension, whereas prospective studies of normotensive cohorts suggest that OSA may increase the risk of incident hypertension. Randomized evaluations of continuous positive airway pressure (CPAP) indicate an overall modest effect on blood pressure. However, these studies do indicate a wide variation in the blood pressure effects of CPAP, with some patients, on an individual basis, manifesting a large antihypertensive benefit. OSA is particularly common in patients with resistant hypertension. The reason for this high prevalence of OSA is not fully explained, but data from our laboratory suggest that it may be related to the high occurrence of hyperaldosteronism in patients with resistant hypertension. We hypothesize that aldosterone excess worsens OSA by promoting accumulation of fluid in the neck, which then contributes to increased upper airway resistance.     

快速眼动睡眠期的阻塞型呼吸暂停与高血压

快速眼动(REM)睡眠期阻塞型睡眠呼吸暂停(OSA)是指发生在REM期的阻塞型睡眠呼吸暂停综合征,由于REM期交感神经活性异常增高,因此发生在此期的OSA可以使交感神经活性更高,心血管功能更不稳定。目前认为REM-OSA很可能是OSA相关高血压发生的主要原因,并且也可能是目前OSA相关高血压用持续正压通气(CPAP)治疗效果不明显的重要原因。临床工作中应重视对REM-OSA的诊断和治疗,这对OSA相关高血压的防治具有重要意义。     

Obstructive sleep apnea and hypertension: Mechanisms,evaluation, and management

Obstructive sleep apnea (OSA) is a recognized cause of secondary hypertension. OSA episodes produce surges in systolic and diastolic pressure that keep mean blood pressure levels elevated at night. In many patients, blood pressure remains elevated during the daytime, when breathing is normal. Contributors to this diurnal pattern of hypertension include sympathetic nervous system overactivity and alterations in vascular function and structure caused by oxidant stress and inflammation. Treatment of OSA with nasal continuous positive airway pressure (CPAP) abolishes apneas, thereby preventing intermittent arterial pressure surges and restoring the nocturnal “dipping” pattern. CPAP treatment also has modest beneficial effects on daytime blood pressure. Because even small decreases in arterial pressure can contribute to reducing cardiovascular risk, screening for OSA is an essential element of evaluating patients with hypertension.     

Cardiovascular Implications in the Treatment of Obstructive Sleep Apnea

Epidemiological studies provide strong evidence that obstructive sleep apnea (OSA) is associated with cardiovascular complications such as systemic hypertension, congestive heart failure, and atrial fibrillation. Successful OSA treatment with continuous positive airway pressure (CPAP) has resulted in coincident reductions in systemic hypertension, improvements in left ventricular systolic function, and reductions in sympathetic nervous activity. These data suggest that successful treatment of OSA may reduce cardiovascular morbidity in such patients. Although CPAP is the more successful treatment for OSA when used properly and consistently, its clinical success is often limited by poor patient and partner acceptance, which leads to suboptimal compliance. Oral appliances or upper airway surgeries are considered a second line of treatment for patients with mild to moderate OSA who do not comply with or refuse long-term CPAP treatment. Oral devices such as mandibular repositioning appliances were recently shown to improve arterial hypertension in OSA patients. Electrical stimulation of the hypoglossal nerve is a new investigational therapy for patients with moderate to severe OSA. This new treatment option, if proven effective, may provide cardiovascular benefits secondary to treating OSA.     

Cardiovascular diseases in obstructive sleep apnea

Obstructive sleep apnea (OSA) affects approximately 5% of women and 15% of men in the middle-aged adults, and associated with adverse health outcomes. Cardiovascular disturbances are the most serious complications of OSA. These complications include heart failure, left/right ventricular dysfunction, acute myocardial infarction, arrhythmias, stroke, systemic and pulmonary hypertension. All these cardiovascular complications increase morbidity and mortality of OSA. Several epidemiologic studies have demonstrated that sleep related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic activity, and altered baroreflex control during sleep. Arterial hypertension, obesity, diabetes mellitus and coronary artery disease (CAD) which are independent predictors of left ventricular dysfunction, often have co-existence with OSA. Especially severe OSA patients having diastolic dysfunction might have an increased risk of heart failure, since diastolic dysfunction might be combined with systolic dysfunction. Early recognition and appropriate therapy of ventricular dysfunction is advisable to prevent further progression to heart failure and death. Patients with acute myocardial infarction, especially if they had apneas and hypoxemia without evident heart failure should be evaluated for sleep disorders. So, patients with CAD should be evaluated for OSA and vice versa. Early recognition and treatment of OSA may improve cardiovascular functions. Continuous positive airway pressure (CPAP) applied by nasal mask, is still the gold standard method for treatment of the disease and prevention of complications.     

Deleterious effects of sleep-disordered breathing on the heart and vascular system

Obstructive sleep apnea (OSA) is the most common form of sleep-disordered breathing, affecting 5-15% of the population. It is characterized by intermittent episodes of partial or complete obstruction of the upper airway during sleep that disrupts normal ventilation and sleep architecture, and is typically associated with excessive daytime sleepiness, snoring, and witnessed apneas. Patients with obstructive sleep apnea present risk to the general public safety by causing 8-fold increase in vehicle accidents, and they may themselves also suffer from the physiologic consequences of OSA; these include hypertension, coronary artery disease, stroke, congestive heart failure, pulmonary hypertension, and cardiac arrhythmias. Of these possible cardiovascular consequences, the association between OSA and hypertension has been found to be the most convincing. Although the exact mechanism has not been understood, there is some evidence that OSA is associated with frequent apneas causing mechanical effects on intrathoracic pressure, cardiac function, and intermittent hypoxemia, which may in turn cause endothelial dysfunction and increase in sympathetic drive. Therapy with continuous positive airway pressure has been demonstrated to improve cardiopulmonary hemodynamics in patients with OSA and may reverse the endothelial cell dysfunction. Despite the availability of diagnostic measures and effective treatment, many patients with sleep-disordered breathing remain undiagnosed. Therefore, OSA continues to be a significant health risk both for affected individuals and for the general public. Awareness and timely initiation of an effective treatment may prevent potential deleterious cardiovascular effects of OSA.     

Sleep apnea and heart failure

Sleep apnea is frequently observed in patients with heart failure (HF). In general, sleep apnea consists of two types: obstructive and central sleep apnea (OSA and CSA, respectively). OSA results from upper airway collapse, whereas CSA arises from reductions in central respiratory drive. In patients with OSA, blood pressure is frequently elevated as a result of sympathetic nervous system overactivation. The generation of exaggerated negative intrathoracic pressure during obstructive apneas further increases left ventricular (LV) afterload, reduces cardiac output, and may promote the progression of HF. Intermittent hypoxia and post-apneic reoxygenation cause vascular endothelial damage and possibly atherosclerosis and consequently coronary artery disease and ischemic cardiomyopathy. CSA is also characterized by apnea, hypoxia, and increased sympathetic nervous activity and, when present in HF, is associated with increased risk of death. In patients with HF, abolition of coexisting OSA by continuous positive airway pressure (CPAP) improves LV function and may contribute to the improvement of long-term outcomes. Although treatment options of CSA vary compared with OSA treatment, CPAP and other types of positive airway ventilation improve LV function and may be a promising adjunctive therapy for HF patients with CSA. Since HF remains one of the major causes of mortality in the industrialized countries, the significance of identifying and managing sleep apnea should be more emphasized to prevent the development or progression of HF.     

Cardiovascular consequences of obstructive sleep apnea

Sleep apnea is associated with several cardiovascular disease conditions. A causal relationship between sleep apnea and each of these diseases is likely, but remains to be proven. The clearest evidence implicating OSA in the development of new cardiovascular disease involves data that show an increased prevalence of new hypertension in patients with OSA followed over 4 years [3]. Circumstantial evidence and data from small study samples suggest that OSA, in the setting of existing cardiovascular disease, may exacerbate symptoms and accelerate disease progression. The diagnosis of OSA always should be considered in patients with refractory heart failure, resistant hypertension, nocturnal cardiac ischemia, and nocturnal arrhythmias, especially in individuals with risk factors for sleep apnea (e.g., central obesity, age, and male gender). Treating sleep apnea may help to achieve better clinical control in these diseases and may improve long-term cardiovascular prognosis.     

Effect of continuous positive airway pressure treatment on pulmonary artery pressure in patients with isolated obstructive sleep apnea: a meta-analysis

Pulmonary hypertension (PH) can occur in patients with obstructive sleep apnea (OSA) in the absence of cardiac or lung disease. Data on the development and severity of PH, and the effect of continuous positive airway pressure (CPAP) therapy on pulmonary artery (PA) pressures in these patients have been inconsistent in the literature. We sought to determine whether CPAP therapy affects PA pressures in patients with isolated OSA in this meta-analysis. We searched PubMed, Medline, EMBASE and other databases from January 1980 to August 2015. Studies of patients with OSA, defined as an apnea–hypopnea index >10 events/h, and PH, defined as PA pressure >25 mmHg were included. Two reviewers independently extracted data and assessed risk of bias. A total of 222 patients from seven studies (341.53 person-years) had reported PA pressures before and after treatment with CPAP therapy. 77 % of participants were men, with a mean age of 52.5 years, a mean apnea–hypopnea index of 58 events/h, and mean PA pressure of 39.3 ± 6.3 mmHg. CPAP treatment duration ranged from 3 to 70 months. Using fixed effects meta-analysis, CPAP therapy was associated with a decrease in PA pressure of 13.3 mmHg (95 % CI 12.7–14.0) in our study population. This meta-analysis found that CPAP therapy is associated with a significantly lower PA pressure in patients with isolated OSA and PH.     

Sleep disorders in patients with congestive heart failure

PURPOSE OF REVIEW: This review of recent literature pertains to the growing evidence that obstructive sleep apnea contributes to the development of systemic hypertension and congestive heart failure. RECENT FINDINGS: There is irrefutable evidence that OSA causes systemic hypertension and that continuous positive airway pressure (CPAP) treatment of OSA causes a reduction in blood pressure. Moreover there is evidence that untreated OSA is associated with left ventricular diastolic and systolic failure and that treatment with CPAP improves systolic function. SUMMARY: OSA should be considered in patients with systemic hypertension or heart failure.     

Obstructive sleep apnea therapy for cardiovascular risk reduction—Time for a rethink?

Obstructive sleep apnea (OSA) is a highly prevalent and underdiagnosed medical condition, which is associated with various cardiovascular and metabolic diseases. The current mainstay of therapy is continuous positive airway pressure (CPAP); however, CPAP is known to be poorly accepted and tolerated by patients. In randomized controlled trials evaluating CPAP in cardiovascular outcomes, the average usage was less than 3.5 hours, which is below the 4 hours per night recommended to achieve a clinical benefit. This low adherence may have resulted in poor effectiveness and failure to show cardiovascular risk reduction. The mandibular advancement device (MAD) is an intraoral device designed to advance the mandible during sleep. It functions primarily through alteration of the jaw and/or tongue position, which results in improved upper airway patency and reduced upper airway collapsibility. The MAD is an approved alternative therapy that has been consistently shown to be the preferred option by patients who are affected by OSA. Although the MAD is less efficacious than CPAP in abolishing apnea and hypopnea events in some patients, its greater usage results in comparable improvements in quality‐of‐life and cardiovascular measures, including blood pressure reduction. This review summarizes the impact of OSA on cardiovascular health, the limitations of CPAP, and the potential of OSA treatment using MADs in cardiovascular risk reduction.     

Resistant hypertension, obstructive sleep apnoea and aldosterone

Obstructive sleep apnoea (OSA) and hypertension commonly coexist. Observational studies indicate that untreated OSA is strongly associated with an increased risk of prevalent hypertension, whereas prospective studies of normotensive cohorts suggest that OSA may increase the risk of incident hypertension. Randomized evaluations of continuous positive airway pressure (CPAP) indicate an overall modest effect on blood pressure (BP). Determining why OSA is so strongly linked to having hypertension in cross-sectional studies, but yet CPAP therapy has limited BP benefit needs further exploration. The CPAP studies do, however, indicate a wide variation in the BP effects of CPAP, with some patients manifesting a large antihypertensive benefit such that a meaningful BP effect can be anticipated in some individuals. OSA is particularly common in patients with resistant hypertension (RHTN). The reason for this high prevalence of OSA is not fully explained, but data suggest that it may be related to the high occurrence of hyperaldosteronism in patients with RHTN. In patients with RHTN, it has been shown that aldosterone levels correlate with severity of OSA and that blockade of aldosterone reduces the severity of OSA. Overall, these findings are consistent with aldosterone excess contributing to worsening of underlying OSA. We hypothesize that aldosterone excess worsens OSA by promoting accumulation of fluid within the neck, which then contributes to increased upper airway resistance.     

Obstructive sleep apnea: an update on mechanisms and cardiovascular consequences

Background and aimThere is growing recognition of the widespread incidence and health consequences of obstructive sleep apnea (OSA). This review examines the evidence linking sleep apnea with cardiovascular disease and discusses potential mechanisms underlying this link.Data synthesisThe weight of evidence provides increasing support for a causal relationship between OSA and hypertension. Furthermore, OSA may contribute to the initiation and progression of cardiac ischemia, heart failure and stroke. Chronic sympathetic activation appears to be a key mechanism linking OSA to cardiovascular disease. Other potential mechanisms include inflammation, endothelial dysfunction, increased levels of endothelin, hypercoagulability and stimulation of the renin angiotensin system. OSA, hypertension and obesity often coexist and interact, sharing multiple pathophysiological mechanisms and cardiovascular consequences. Effective treatment of OSA may attenuate neural and humoral abnormalities in circulatory control, improve blood pressure control and conceivably reduce the risk of future cardiovascular events.ConclusionPatients with OSA are at increased risk for cardiovascular disease. OSA should be considered in the differential diagnosis of hypertensive patients who are obese. In particular, OSA should be excluded in patients with hypertension resistant to conventional drug therapy.     

Influence of obstructive sleep apnea and treatment with continuous positive airway pressure on fractional flow reserve measurements for coronary lesion assessment

Obstructive sleep apnea (OSA) and sleep‐disordered breathing have been implicated in the progression of cardiovascular disease and with increased risk of coronary artery disease, congestive heart failure, and stroke. Fractional flow reserve (FFR) is used to evaluate the physiological significance of coronary artery stenosis, and this technique is largely thought to be independent of systemic hemodynamic changes. Herein, we describe a case of OSA and sleep‐disordered breathing cyclically altering FFR measurements from normal to abnormal in a patient with coronary artery disease. More specifically, we show that the abnormal FFR across a coronary lesion in a patient with sleep disordered apnea improves (to a normal threshold) with the initiation of continuous positive airway pressure (CPAP). This finding may have implications for the mechanisms of cardiac dysfunction in patients with OSA. © 2009 Wiley‐Liss, Inc.     

New developments in the use of positive airway pressure for obstructive sleep apnea

Obstructive sleep apnea (OSA) is a disorder which afflicts a large number of individuals around the world. OSA causes sleepiness and is a major cardiovascular risk factor. Since its inception in the early 1980’s, continuous positive airway pressure (CPAP) has emerged as the major treatment of OSA, and it has been shown to improve sleepiness, hypertension, and a number of cardiovascular indices. Despite its successes, adherence with treatment remains a major limitation. Herein we will review the evidence behind the use of positive airway pressure (PAP) therapy, its various modes, and the methods employed to improve adherence. We will also discuss the future of PAP therapy in OSA and personalization of care.     

Diagnostic and therapeutic approach to nonsleepy apnea

Epidemiological and observational studies suggest that sleep-disordered breathing is associated with the subsequent development of hypertension and ultimately with cardiovascular consequences. It may therefore be assumed that continuous positive airway pressure (CPAP) not only avoids sleep-related symptoms but could also mitigate cardiovascular consequences. Short-term studies have revealed a drop in blood pressure, especially in more severe, symptomatic cases of obstructive sleep apnea. Two recent studies have reported that nonsleepy obstructive sleep apnea is associated with an absence of reduced blood pressure after CPAP treatment. This suggests that this group of patients is less susceptible to the consequences of apneas, even those with mild-moderate hypertension or other cardiovascular disorders. However, in patients with severe cardiovascular disease or a higher number of obstructive events, CPAP treatment should be seriously considered.