Sleep Disorders and Heart Disease: A Reciprocal Relationship

Poor sleep quality and cardiovascular disease often go hand in hand.

The Centers for Disease Control and Prevention calls Americans’ propensity to skimp on sleep “a national epidemic.” The agency reports that up to 70 million American adults have a sleep disorder.¹ Cardiovascular disease—another epidemic—kills 1 in 4 Americans.² Disturbed sleep and cardiovascular disease (CVD) have a reciprocal relationship: poor sleep quality may cause or contribute to CVD, and CVD may perturb sleep (Table 1^3-20). This hand-in-hand relationship should encourage health care providers to ask about and monitor both issues when patients present with either. This article examines the sleep-CVD relationship and potential interventions to create a health care win-win.

Sleep-Disordered Breathing and Cardiovascular Disease

Sleep-disordered breathing (SDB) is a spectrum of conditions that can alter sleep. Most SDB leads to sleep deprivation. Results of physiologic studies demonstrate that sleep deprivation can impair insulin sensitivity and create hormonal changes that increase hunger and appetite. ^20,21 As a manifestation of this change, individuals who sleep fewer than 7 hours a night are more likely to carry excess weight—a CVD risk factor—than those who sleep more than 7 hours.²²

Specific sleep disturbances seem to have unique effects on CVD. For example, 1 in 15 Americans, or roughly 7% of the population, has obstructive sleep apnea, the most common form of SDB.²³ This condition is clearly associated with CVD, and results of well-controlled studies show that patients’ blood pressure improves when their sleep apnea is treated adequately.²⁴ Researchers believe that sleep apnea creates nocturnal blood pressure surges that contribute to plaque rupture.²⁵ They also suspect that autonomic factors—inflammation mediators, oxidative stress, negative intrathoracic pressure, hypoxemia, arousal from sleep—and metabolic factors conspire to cause acute hemodynamic alterations.^26,27 Hypoxemia in particular boosts venous return and increases pulmonary arterial pressure, which elevates right ventricular pressure, blood pressure, and heart rate.²⁸ Nitric oxide is critical in cardiovascular pathways, and reactive oxygen species decrease nitric oxide production and may inactivate bioavailable nitric oxide.²⁹

More than half of patients with heart failure have sleep abnormalities, which generally fall into 2 categories.^30,31 About one-third of heart failure patients with left ventricular dysfunction have obstructive sleep apnea, and one-third experience Cheyne-Stokes respirations, a form of central apnea characterized by deeper, faster breathing. The remaining third have miscellaneous CVD conditions that disturb sleep.³⁰

On the other hand, SDB is a risk factor for recurrence and mortality following stroke or transient ischemic attack. Evidence suggests a dose-response relationship between the severity of a patient’s SDB and his or her risk for serious adverse outcomes after stroke and transient ischemic attack.³² Within the first 48 hours after a stroke, most patients experience nocturnal deterioration. Researchers think that dysregulated autonomic function exaggerates hemodynamic changes during sleep, causing arrhythmia and blood pressure fluctuations in stroke patients.³³

Managing the Sleep—Cardiovascular Disease Combination

Clinicians need to screen for comorbid SDB and CVD and establish accurate diagnoses. A full diagnostic workup includes a medical history and physical examination. If obstructive sleep apnea cannot be ruled out, a sleep study (polysomnography in a sleep laboratory or a home sleep test) should be conducted.³⁴

The clinician’s first step in treating patients with heart failure is to optimize medical therapy because adequate dosing of cardiac medications resolves Cheyne- Stokes respirations.³⁵

General steps to improve sleep are listed in Table 2.³⁴ In addition, clinicians should consider prescribing sedatives/ hypnotics if the patient’s comorbidities and demographic factors are not contraindications. Cautious use is advised due the possibility of addiction to some drugs as well as the propensity to cause daytime drowsiness or falls.

Patients who have sleep apnea should be considered for continuous positive airway pressure (CPAP) because it positively influences hemodynamics (Table 3^36,37). It is critical to remember that the effects of CPAP on hypertension are generally modest, and patients will still require concomitant antihypertensive therapy.³⁵ In addition, many patients have difficulty adhering to CPAP, with total adherence defined as using the CPAP machine every night throughout the entire night. Failure to use CPAP, even for 1 night, allows the symptoms of SDB—daytime sleepiness, neurobehavioral decline, increased sympathetic activity, and significant driving impairment—to return.^37,38

Conclusion

The association between sleep and CVD and metabolic health is receiving more attention in the medical literature. Pharmacists can help patients and other members of the health care team appreciate the importance of these conditions. Pharmacists can also suggest appropriate interventions. As our understanding of the mechanisms underlying both becomes clearer, we will have more opportunities to tailor care to specific targets. Until then, we need to help patients sleep as soundly as possible and address CVD conditions as well.

Ms. Wick is a Visiting Professor at the University of Connecticut School of Pharmacy and a former National Cancer Institute employee.

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