Sleep apnea is highly prevalent in patients with cardiovascular disease. These disordered breathing events are associated with a profile of perturbations that include intermittent hypoxia, oxidative stress, sympathetic activation, and endothelial dysfunction, all of which are critical mediators of cardiovascular disease.
Evidence supports a causal association of sleep apnea with the incidence and morbidity of hypertension, coronary heart disease, arrhythmia, heart failure, and stroke. Several discoveries in the pathogenesis, along with developments in the treatment of sleep apnea, have accumulated in recent years. In this review, we discuss the mechanisms of sleep apnea, the evidence that addresses the links between sleep apnea and cardiovascular disease, and research that has addressed the effect of sleep apnea treatment on cardiovascular disease and clinical endpoints.
Finally, we review the recent development in sleep apnea treatment options, with special consideration of treating patients with heart disease. Future directions for selective areas are suggested.
This review provides an update on sleep apnea and CVD. We hope to provide a catalyst for cardiologists to join with sleep physicians to conduct research, particularly clinical trials, that addresses the role of sleep apnea treatment in patients who are at high risk of or have existing CVD. An apnea is the absence of inspiratory airflow for at least 10 s.
- Pace to breathe — New treatments for sleep apnea - Harvard Health Blog - Harvard Health Publishing;
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A hypopnea is a lesser decrease in airflow, lasting 10 s or longer, and associated with a drop in arterial oxyhemoglobin saturation and or an electroencephalographic arousal. Apneas and hypopneas are classified as obstructive or central, but regardless, they result from an absence or reduction of brainstem neural output to upper airway muscles e. The 2 most common causes in adults are HF and opioid use 4. First tracing is chin electromyogram, second and third are electroencephalogram, fourth is electrocardiogram, fifth and sixth are airflow measured by thermocouple fifth and CO 2 sixth , seventh and eighth are rib cage RC, seventh and abdominal ABD, eighth , ninth is oxyhemoglobin saturation measured by pulse oximetry, and tenth is esophageal pressure.
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Please note that during obstructive apnea, airflow is absent while breathing effort continues. Breathing resumes with the onset of arousal. Reprinted with permission from Javaheri 8. The first 2 tracings are electro-occulogram; otherwise tracings as in Figure 1. Note the smooth and gradual changes in the thoracoabdominal excursions and esophageal pressure in the crescendo and decrescendo arms of the cycle.
There is an intervening central apnea, absence of naso-oral airflow, and excursions in pleural pressure, thorax, and abdomen. The arousal occurs at the peak of hyperventilation.
Desaturation is delayed because of long circulation time in heart failure. Sleep has multiple pronounced effects on the respiratory system and control of breathing. Experimental studies in instrumented cats have shown decreased electrical activity in medullary inspiratory neurons with efferent output to the upper and lower respiratory muscles, reflected in decreased activity of diaphragm and dilator muscles of the upper airway also observed in human studies 9. With reduction in the activity of the genioglossus muscle at the onset of sleep, the tongue falls backward, and individuals with altered mechanical properties of the upper airway are prone to upper airway obstruction.
Several anatomic processes may compromise the patency of the upper airway, including alterations in craniofacial structures, enlarged tonsils, upper airway edema, decreased lung volume, and most importantly, obesity 9, The mechanisms linking obesity to OSA 2,9 are complex, although mostly due to direct mechanical effects on the respiratory system. These include fat deposits within the upper airway and reduction in lung volume, resulting in a loss of caudal traction on the upper airway In these individuals, nonanatomic factors 9,10 , such as upper airway dilator muscle dysfunction, heightened chemosensitivity, and low arousal threshold i.
Specifically, dilator muscle dysfunction should best respond to hypoglossal nerve stimulation, whereas heightened chemosensitivity and low arousal threshold may be amenable to pharmacotherapy to down-regulate ventilatory responses nocturnal oxygen-attenuating hypoxic response , and hypnotics to increase the arousal threshold.
With the push toward personalized medicine, individualizing therapy may be a viable approach for OSA, as the mechanism s underlying disease are better defined and consequently corrected. Much work is needed in this area.follow link
Obstructive Sleep Apnea News and Research
Another risk factor that has received recent attention is that of fluid around the upper airway 5, In individuals with lower-extremity edema, excess fluid may accumulate in the pharyngeal area with cephalad transposition of fluid from lower extremities to the neck area when supine 5,11 , rendering the upper airway susceptible to collapse during sleep.
Redistribution of fluid to the lungs also may potentiate CSA, as discussed later in the text. Apneic threshold is the arterial PCO 2 below which the ponto-medullary respiratory rhythm generator ceases, thereby silencing motor nerves innervating inspiratory thoracic pump muscles.
Consequently, ventilation ceases and CSA occurs. Sleep unmasks a highly sensitive hypocapneic-induced apneic threshold, which in health at sea level, approximates the waking eupneic partial arterial pressure of carbon dioxide PaCO 2 4. When ventilation increases in response to a transient spontaneous arousal or sigh, the subsequent ventilatory overshoot often elicits sufficient hypocapnia i.
Once the central respiratory drive is withdrawn, apnea persists until PaCO 2 rises above the apneic threshold. Loop gain defines the magnitude of a response increased ventilation to a disturbance reduced breathing . The higher the gain, the greater the ventilatory overshoot and undershoot, and the more likely the occurrence of continued ventilatory cycling and repeated apneas.
The role of loop gain in mediating periodic breathing in HF has been reviewed elsewhere 4. Normal sleep provides a time of low physiological stress, which is advantageous to the CV system. However, sleep-disordered breathing SDB disrupts normal sleep. The adverse consequences of SDB have been reviewed elsewhere 4,5,9, We emphasize, however, that the large negative pressure swings due to inspiratory effort against a closed upper airway are reflected in juxtacardiac pressure increasing the transmural pressure of all intrathoracic structures, including atria, ventricles, intrathoracic aorta, and pulmonary vascular beds, with adverse effects on these structures.
Thin-walled atria are vulnerable to surrounding negative pressure, stretching easily, stimulating mechanoreceptors with activation of ion channels that facilitate development of atrial arrhythmias, specifically AF. These effects are most prominent in association with other apnea-related consequences, such as tissue hypoxia and increased sympathetic activity.
Atrial stretch also results in secretion of atrial natriuretic peptide, causing nocturia, a symptom of OSA. The reverse occurs in phasic REM sleep. Pleural pressure Ppl is a surrogate of the pressure surrounding the heart and other vascular structures. OSA is a disorder associated with oxidative stress, up-regulation of redox-sensitive genes, and inflammatory cascade 13, Much of this work has focused on nuclear factor NF -kappaB—mediated pathways. Another molecular signature of OSA is increased catecholamines, consistent with perturbations in the autonomic nervous system.
Many CVD-related biomarkers are also elevated in obesity, and disentangling obesity from OSA-related effects is a challenge, especially given the high correlation between the apnea-hypopnea index AHI and body mass index. Obesity may magnify the effects of OSA because macrophages in fat are likely the target cells for the effects of chronic intermittent hypoxia, leading to increases in inflammatory biomarkers; thus, OSA and obesity may have synergistic effects. The results of a randomized controlled study in obese patients 19 showed that combined treatment with weight loss and CPAP reduced BP more than either therapy alone; however, C-reactive protein levels were only reduced in association with weight loss.
The Icelandic Sleep Apnea Cohort 16 reported that intercellular adhesion molecule levels increase over 2 years in the most obese individuals with untreated OSA, whereas levels decrease in regular CPAP users. Thus, OSA may result in a progressive inflammatory state, which may be 1 mechanism of the vascular damage that occurs from OSA. Inflammatory consequences of OSA may vary with degree of obesity. OSA is independently associated with metabolic syndrome and insulin resistance, with an associated risk for incident CV events In 1 RCT, supervised CPAP treatment for 8 h over 2 weeks nightly significantly improved insulin sensitivity and glucose response in intravenous and oral glucose tolerance tests In another RCT of pre-diabetic patients, the insulin sensitivity index improved significantly in those with severe OSA treated with CPAP 22 , and there was a significant correlation between hours of CPAP use and improvement in insulin sensitivity, emphasizing the critical importance of adherence Thus, current evidence suggests that OSA is associated with insulin resistance, and CPAP treatment may improve insulin sensitivity in pre-diabetic patients.
The epidemiology of these associations has been extensively reviewed 3,5,13,14, We also discuss adjunct therapy of OSA. Studies using h BP monitoring 25—32 consistently report drops of 2 to 2. Summary of different meta-analyses of RCTs. The figure shows 5 randomized controlled trials and 2 meta-analyses. The differences between the 2 meta-analyses depend on the most updated references included in the meta-analysis.
Pace to breathe — New treatments for sleep apnea
There are multiple reasons why the antihypertensive effect of CPAP is limited. However, other pathophysiological mechanisms underlying HTN, such as those associated with obesity, salt intake, and volume overload, may be unaffected by CPAP. Therefore, it is unknown whether BP may fall further in long-term follow-up. Depending on these characteristics, some study patients might have greater antihypertensive benefits from CPAP, whereas others—for example, those with less severe OSA—might not.
This dose-dependent relationship is similar to that for insulin sensitivity 22,23 and other CV outcomes, as discussed later in the text.
There is evidence that the combination of antihypertensive drugs 41 or weight loss 19 with CPAP therapy could have a synergistic effect in reducing BP in OSA patients, supporting the multidimensional pathophysiology of HTN in this population. When hypertensive patients with and without OSA were treated with losartan for 6 weeks, the BP drop measured by h ambulatory BP monitoring was significantly less in those with OSA than without.
Diagnosis and Treatment of Obstructive Sleep Apnea in Adults - American Family Physician
In the only small randomized crossover study therapeutic vs. The reduction was greatest 8. The recommendation comes from the idea that targeted therapy of OSA could either improve or prevent further deterioration in central hemodynamics. Sleep apnea is highly prevalent in patients with stroke or TIA, and OSA also is associated with increased risk for incident stroke 46— There is some evidence that early CPAP therapy has positive effects on long-term survival in ischemic stroke patients with moderate-to-severe OSA 46— Additionally, consistent with observational studies 46—48 , in a recent large RCT 49 , those OSA patients who were adherent to CPAP therapy exhibited reduced risk of incident cerebral events.
Data from observational studies show that CPAP treatment is associated with a significantly decreased recurrence rate of AF, even after electrical cardioversion or ablative therapies, and that patients are less likely to progress to more permanent forms of AF and have significantly reduced occurrence of paroxysmal AF compared with untreated patients 53— On the basis of this evidence, a recent expert consensus document on AF identified OSA as a risk factor for AF recurrence after surgical and catheter ablation, and recommended its treatment Although the reproducibility of these findings from observational studies is compelling, data from clinical trials are needed.
CPAP did not result in a significant reduction in the incidence of the primary composite outcome. The incidence of the primary composite CV endpoint did not differ between the 2 groups. Patients were allocated to CPAP or usual-care treatment for a mean of 3. One-to-one propensity-score matching was performed to compare patients who were adherent to CPAP therapy with patients in the usual-care group. This study has several limitations.
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