Sleep apnea and the heart

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Release date: September 1, 2019
Expiration date: August 31, 2022
Estimated time of completion: 0.75 hour

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The normal sleep-wake cycle is characterized by diurnal variations in blood pressure, heart rate, and cardiac events. Sleep apnea disrupts the normal sleep-heart interaction, and the pathophysiology varies for obstructive sleep apnea (OSA) and central sleep apnea (CSA). Associations exist between sleep-disordered breathing (which encompasses both OSA and CSA) and heart failure, atrial fibrillation, stroke, coronary artery disease, and cardiovascular mortality. Treatment options include positive airway pressure as well as adaptive servo-ventilation and phrenic nerve stimulation for CSA. Treatment improves blood pressure, quality of life, and sleepiness, the last particularly in those at risk for cardiovascular disease. Results from clinical trials are not definitive in terms of hard cardio­vascular outcomes.


  • Diurnal variations in blood pressure, heart rate, and cardiac events occur during normal sleep.
  • While normal sleep may be cardioprotective, sleep apnea disrupts the normal sleep-heart interaction.
  • Untreated severe sleep apnea increases the risk for cardiovascular events.
  • Treatment with continuous positive airway pressure (CPAP) may reduce the risk of cardiac events based on some data, though randomized studies suggest no improvement in cardiovascular mortality.
  • Poor patient adherence to CPAP makes it difficult to evaluate the efficacy of CPAP treatment in clinical trials.




Wakefullness and sleep, the latter comprised of non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep, comprise our primary states of being. Sleep states oscillate between NREM and REM sleep. The first and shortest period of REM sleep typically occurs 90 to 120 minutes into the sleep cycle. Most REM sleep, including the longest period of REM sleep, occurs during the latter part of the sleep cycle.

With these sleep state changes, physiologic changes also occur, such as reduced heart rate and blood pressure because of enhanced parasympathetic tone. During REM sleep, there are also intermittent sympathetic nervous system surges. Other physiologic changes include a regular respiratory rate during NREM sleep and an irregular respiratory rate during REM sleep. Body temperature is normal during NREM sleep and poikilothermic (ie, tends to flucuate) during REM sleep. Blood pressure is reduced 10% to 15% during sleep1 and then rises, so that the highest blood pressure occurs in the morning. Data from 10 million users of activity-monitoring devices show that the heart rate changes during sleep.2 The heart rate is decreased in those who get less than 7 hours of sleep, then increases with longer sleep duration in a U-shaped distribution.

Cardiovascular events are more likely to occur at certain times of day. Myocardial infarction is more likely in the morning, with a threefold increased risk within the first 3 hours of awakening that peaks around 9 AM.3,4 Similar diurnal patterns have been observed with other cardiovascular conditions such as sudden cardiac death and ischemic episodes, with the highest risk during morning hours (6 to 9 AM).4

The reason for this morning predisposition for cardio­vascular events is unclear, but it is thought that perhaps the autonomic fluctuations that occur during REM sleep and the predominance of REM sleep in early morning may be a factor. Diurnal changes in blood pressure and cortisol levels may also contribute, as well as levels of systemic inflammatory and thrombotic markers such as plasminogen activator inhibitor 1.

Arrhythmias are also more likely to occur in a diurnal pattern. Atrial fibrillation (AF), particularly paroxysmal AF, is believed to be vagally mediated in 10% to 25% of patients.5 Therefore, for those who are predisposed, sleep may represent a period of increased risk for AF. In a study of individuals 60 years and older, the maximum duration and peak frequency of AF occurred from midnight to 2 AM.5

Recent studies have found that REM-related obstructive sleep apnea (OSA) is associated with increased cardiovascular risk. Experimental models show that REM sleep may increase the risk for compromised coronary blood flow.6 Increased heart rate corresponds to reduced coronary blood flow and thus, to decreased coronary perfusion time and less time for relaxation of the heart, increasing the risk for coronary artery disease, thrombosis, and ischemia.


The normal physiology of the sleep-heart inter­action is disrupted by sleep apnea. OSA is defined as episodes of complete or partial airway obstruction that occur during sleep with thoraco­abdominal effort. Central sleep apnea (CSA) is the cessation of breathing with no thoracoabdominal effort. The pathophysiology of the sleep-heart interaction varies for OSA and CSA.

Obstructive sleep apnea

OSA is a nocturnal physiologic stressor that is highly prevalent and underrecognized. It affects approximately 17% of the adult population, and the prevalence is increasing with the obesity epidemic. Nearly 1 in 15 individuals is estimated to be affected by at least moderate OSA.7,8 OSA is underdiagnosed particularly in minority populations.9 Data from the 2015 Multi-Ethnic Study of Atherosclerosis (MESA) showed undiagnosed moderate to severe sleep apnea in 84% to 93% of individuals,9 similar to an estimated 85% of undiagnosed cases in 2002.10

OSA is highly prevalent in individuals with underlying coronary disease11–13 and in those with cardiovascular risk factors such as diabetes, hypertension, and heart failure. The prevalence of OSA in patients with cardiovascular disease ranges from 30% (hypertension) to 60% (stroke or transient ischemic attack, arrhythmia, end-stage renal disease).14


Next Article:

Beyond heart health: Consequences of obstructive sleep apnea

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