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  • Updated 09.21.2023
  • Released 11.04.1993
  • Expires For CME 09.21.2026

Sleep and cardiac disorders



In normal subjects, sleep is characterized by physiological changes in cardiovascular parameters (blood pressure, heart rate), but sleep and sleep disorders are also associated with cardiovascular diseases. Patients with cardiovascular diseases may complain of several sleep disturbances, such as sleep fragmentation, insomnia, and breathing disorders, during sleep. On the other hand, patients with sleep disorders seem to be more frequently affected by cardiovascular diseases, so it is often difficult to determine which is the cause and the effect. Quality and duration of nocturnal sleep have been reported as factors affecting the health status of a population, particularly the cardiovascular risk profile, and there is evidence that suggests that they increased risk of adverse cardiac events. Specifically, sleep features and sleep disorders seem to play an important role in determining blood pressure levels, both in the office and over 24 hours, and in modulating the day-night blood pressure profile, which can have an impact on the prognosis of hypertensive patients. However, the most important sleep-related clinical condition affecting cardiovascular control seems to be represented by sleep-related breathing disorders. In this article, the authors summarize the evidence concerning the link between sleep disorders and cardiovascular diseases and the effects of specific treatment.

Key points

• Obstructive sleep apnea is common in the general population, but is increased in frequency in cardiovascular disorders, particularly in heart failure.

• OSA treatment is primarily focused on improving symptoms, which are often very mild in heart failure patients, but also aims at reducing blood pressure and improving cardiac function.

• CPAP can abolish obstructive apneas but may not be sufficient to eliminate central events for which adaptive servo ventilation (ASV) may be considered. However, ASV may be deleterious in heart failure patients.

• Other OSA treatments are available, such as mandibular advancement devices, but studies focusing on cardiovascular outcomes are lacking.

• Current evidence does not show a clear benefit of treating OSA in secondary prevention with the aim of improving cardiovascular outcomes.

Historical note and terminology

The link between sleep and cardiovascular system is a well-known phenomenon. Sleep, in fact, is normally characterized by major changes in the physiologic mechanisms responsible for cardiovascular (CV) regulation. Moreover, increasing evidence shows that there is also an important relationship between sleep, sleep disorders, and cardiovascular diseases (66). Periodic breathing was the first breathing pattern during sleep described in patients with cardiovascular diseases. Periodic breathing is an abnormal ventilatory pattern in which apneas and hypopneas alternate with periods of hyperventilation. Periodic breathing was first observed by Hippocrates (approximately 460 to 377 BCE). Cheyne (20) and Stokes (114) published descriptions of repeated respiratory cycles beginning with central apnea followed by several breaths before the next apnea. Central apneas occur when arterial pCO2 (paCO2) falls below the threshold required to stimulate breathing, whereas hyperpnea occurs with reduced arterial pO2 (paO2), pulmonary congestion, or increased chemosensitivity. Changes in paO2 represent the most important modulator of peripheral chemoreceptor activity, whereas paCO2 is the major stimulus for central chemoreceptors (61). However, it has been proposed that the central and peripheral components of the chemoreflex are not functionally separate, but rather dependent on one another, and that this interaction may affect the appearance and frequency of periodic breathing (112).

Pryor first demonstrated that most patients with Cheyne-Stokes respiration had cardiac enlargement and prolonged circulation time (100). Prolonged transit time had been demonstrated as producing periodic breathing in normal volunteers in breathing experiments (31); this was also shown in experimental animals by delaying flow from the lungs to the brain (46). They also recognized that hypoxia from a decreased vital capacity from pulmonary edema or severe congestion could cause periodic breathing. However, their suggestion that periodic breathing could be caused by an increase in “gain” of the central controller of respiration has never been demonstrated except in mathematic models.

At sea level, periodic breathing has been reported to occur in patients with stroke, metabolic disorders, and heart failure (127). In particular, periodic breathing during sleep in heart failure patients is associated with poor prognosis (22). Periodic breathing has also been described during exposure to hypobaric hypoxia at high altitude in the original work by Angelo Mosso at the end of the XIX century (87), and this breathing pattern during sleep affects males more than females (73) probably because of their increased hypoxic chemosensitivity (17).

Under conditions of hypobaric hypoxia, paO2 and paCO2 values are reduced close to the thresholds that induce hyperpnea and apnea, respectively, so the onset of a cyclic alternation between ventilatory stimulation and inhibition is facilitated at high altitude, thus, leading to periodic breathing (121).

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