Snoring: Its Connection to Daytime Sleepiness and Cardiovascular Disease

At Sleep Consultants, our typical patient is referred for evaluation because of loud and obnoxious snoring and excessive daytime sleepiness. Most are on an antihypertensive medication and a history of heart disease is common. The majority are males who are also overweight. A typical patient is a male who is over 35, weighs about 235 pounds, snores loudly and is sleepy whenever quiet. Several epidemiological studies have demonstrated that people who habitually snore loudly have an increased incidence of cardiovascular disease. This is true even if obesity is not a factor. These individuals experience more hypertension, cardiac arrhythmias, strokes and heart attacks than similar people who do not snore. They may also exhibit more hostility. At our clinic, the link to cardiovascular disease and daytime sleepiness is usually because of coexisting sleep apnea. Briefly, this is a syndrome involving episodes of hypoxemia in sleep induced by airway collapse that is reversed but repeated many times across the night. We will discuss this in more detail later. However, why most loud snoring individuals have an increased risk for these problems is unclear. The purpose of this paper is to discuss what we know about snoring and probable mechanisms for this link.

Anatomy of the airway

Snoring is a noise made by vibration of soft tissues in the throat when a person is asleep. The pharynx (throat) begins behind the nose (nasopharynx) and extends inferiorly past the back of the mouth (oropharynx) to end at and around the epiglottis (hypopharynx). Its walls are made of muscles which contract and collapse the lumen during swallowing but otherwise maintain an open airway for breathing.

The pharynx also contains a flap of muscular tissue called the soft palate. It is innervated by five different cranial nerves. It contracts and elevates to act as a check valve during swallowing to prevent regurgitation of fluids into the nose. It relaxes during breathing to allow airflow from the nasopharynx through the oropharynx on its way to the epiglottis and larynx. Normal muscle tone while awake keeps the airway open for breathing and the soft palate directs traffic of air and fluids as appropriate to our need at the moment.

Normal breathing
Normal breathing
Throat muscles relax, airway collapses. The soft palate or other throat tissue flutters.
Breathing resumes with a gasp

Since muscle tone is reduced in sleep, the potential for snoring is introduced. As the throat muscles relax, the airway reduces in size. During inspiration a negative pressure or vacuum develops in the pharynx that is created by the descent of the diaphragm. This results in a further reduction in airway size. In the patient who snores, tissue vibration results from two things that happen to airflow in a smaller airway. Firstly, to compensate for the reduced diameter, air velocity increases significantly. This creates a higher negative pressure resulting from the Bernoulli effect. This effect is defined as a pressure reduction resulting from an increased stream velocity in a fluid. Secondly, turbulence increases with increased air velocity. Therefore, we have higher negative pressures and they oscillate with turbulence resulting in vibration of either the soft palate or other throat tissue. This is the same reason why a flag flutters or ripples in the wind. The soft palate is particularly prone to flutter in a similar manner in the snoring patient. Microscopic examination of the soft palate of snorers shows that it suffers deterioration from the trauma of snoring.

Snoring in men and women. These data were obtained from 5,713 people living in San Marino. Data from Lugarest E, Cirignotta F, Coccagna G, Plana C. 1980. Some epidemiological data on snoring and cardiocirculatory disturbances. Sleep 3:222.

Snoring has been the subject of much humor. But as anyone who has slept with a chronic snorer can tell you, it is not funny. At our sleep center, many of our patients come because their spouses cannot tolerate the snoring. Snoring has been measured to be at about 70 decibels. This is roughly equivalent to heavy traffic noise or a diesel freight train. Despite this loud noise, most snorers never are aware of their own snoring. In a typical couple, the wife is talking and the husband falls asleep. She will then remark, “You are not paying attention!” His usual “honest” reply is, “Oh, I could not have been asleep. I heard every word you said.” She then remarks, “You could not have been awake. You were beginning to snore.” The truth is that each of their observations are correct. It is their conclusions that are fallacious. We know from experiments that the mind continues to function in sleep. Patients who sleep for up to ten minutes will usually deny having been asleep. We know it usually takes about 15 minutes of sleep to gain amnesia for wakefulness. Therefore, the husband heard everything just as he said. However, he was asleep and snoring just as accused. Why snoring remains unheard by the snorer is an unanswered mystery.

The purpose of sleep is to provide restitution of energy and vigor for a succeeding 16-hour interval of activity. In normal sleep, there is a decrease in heart rate, respiratory rate, blood pressure and body temperature across the night. With loud snoring, this process is modified. There are brief arousals (Micro Arousals) which may be associated with K-complexes in the EEG and increases in chin muscle tone. We score these as snore arousals.


Micro arousals on sleep tracing

There is a report of improved deep sleep in patients following a reduction in their snoring. A disease called upper airway resistance syndrome has been proposed to classify these patients who complain of sleepiness but do not have apnea or hypopnea. However, they do snore and have disturbed sleep.


Percentage sleep period time (SPT) in all sleep stages before and after treatment

Snoring is also one of the most frequent complaints associated with sleep apnea. In these patients, snoring is associated with collapse of the airway resulting in loss of airflow in sleep for up to 600 or more times per night. In sleep apnea there are repeated episodes of hypoxemia (low oxygen) and hypercapnia (high CO2) resulting from apnea that lasts from 10 to 150 seconds.

In addition there are significant physiological disturbances in their cardiovascular system and sleep structure that results in multiple problems. These include an increased risk for heart attack, angina, stroke and hypertension. These patients also complain of excessive daytime sleepiness, have more automobile accidents, and are more irritable, depressed and intellectually impaired than normals. They often function poorly at work and are somewhat dysfunctional in their social life. They mumble in their sleep, drool on their pillows, awaken with headaches, experience sweating in sleep, toss and turn through the night and make frequent nocturnal trips to the bathroom. They fall asleep rapidly at night and make sleep for their spouse difficult if not impossible. They represent a more severely symptomatic subset of loud snoring individuals.

In the loud snoring patient with sleep apnea (obstruction of their airway), there is usually major sleep disruption. In a typical patient, there is anywhere from 10 to 70 events per hour across the night. Often deeper sleep stages are absent and in severe cases, sleep may be restricted to a few dream episodes with largely S-1 NREM (transitional) sleep through the night. They are usually very sleepy the next day and understandably so. Sleep latencies on a daytime nap series for normal individuals is about 13 minutes. For apneic patients, falling asleep in less than 10 minutes is common but some do so in less than 60 seconds. Loud snoring is thought to increase daytime sleepiness by disturbing sleep processes that refresh us nightly. This ranges from subtle snore arousals to frank disruption of sleep the entire night.

The increased risk for cardiovascular disease in this group of patients is well-documented. These can be summarized as a vagally mediated slowing of heart rate, generation of ectopic beats, acute pulmonary and systemic vasoconstriction resulting in acute pulmonary and systemic hypertension and possibly stimulation of erythropoiesis. Profound bradycardia and ventricular ectopic beats are the most serious of these events. Fortunately these are usually only associated with severe oxygen loss. Instead of the progressive decrease in both systolic and diastolic pressures across the night, many patients experience a rise in both values. Also, there is an increase in both diastolic and systolic pressure during each apnea but each apnea has a different time course. Systolic blood pressure rises at the end of apnea and diastolic pressure rises during apnea. The greater the hypoxemia, the greater the hypertensive response to sleep we note. Mean increases in systolic and diastolic pressures te nd to be on the order of 25%. In general, cardiac arrhythmias tend to be more prevalent in sleep apnea patients. With severe desaturation, there can be a marked increase in arrhythmias. It should also be noted that cases of sudden death in sleep have been reported in untreated sleep apnea patients with known arrhythmias.

There are significant swings in intrathoracic pressure which can cause major shifts in stroke volume for both the right and left sides of the heart. These can cause rises in blood pressure also. The connection between snoring and strokes is readily understood in the sleep apnea patient. With elevated blood pressure and large swings in pressure associated with apnea, the probability for rupture of a cerebral vessel is increased. Lastly, the connection to angina or chest pain is rather obvious. This pain comes when the heart is inadequately supplied with oxygen. With each apneic episode there is some hypoxemia induced. At the end of the apnea when oxygen levels are at their lowest, there is a sudden demand for an increase in heart performance with a sympathetic surge resulting in tachycardia. The patient is roused and may be vaguely aware of the hypoxemia, adding further to the sympathetic surge. It is not unusual for sleep apnea patients to present at the emergency room with a complaint that they awakened with angina but corroboration is never made once the patient is awake.

The best discussion of how snoring alone increases cardiovascular disease is presented by Dr. Lugaresi et al in Principles and Practice of Sleep Medicine. They point out that during snoring there is an associated increase in intercostal muscle activity and a larger negative pressure in the thorax (lungs). (Fig 3a below) This increased negative pressure provokes a downward traction of the trachea and the attached larynx. This results in a stretching of the oropharynx and a narrowing of its diameter during inspiration. (Fig 3b below)

Fig 3a. Intercostal muscle activity and endoesophageal negative pressure
Fig 3b. Upper airway collapse due to negative endothoracic pressure

Pulmonary artery pressure increases during snoring. This is the diastolic side of the heart. This could be the result of mild hypoxemia. Also, in heavy and habitual snorers there is an increase in systemic arterial pressure at night instead of the usual progressive decline during sleep. This is thought to be a mechanical response related to changes associated with cardiac filling because of higher endothoracic pressures during snoring. (figure below)

They conclude that for male subjects between the ages of 30 and 60 years, snoring represents a risk factor for the heart and circulation. However, the mechanism of these negative effects of snoring remains elusive.

Snoring as a risk factor can be summarized as follows:

  • Habitual snorers suffer significantly more hypertension than non-snorers. All epidemiological studies have confirmed this finding.
  • A prospective study of twins revealed that snorers were more often affected by angina pectoris (chest pain) and heart attack or stroke.
  • Hypertensive subjects tend to have a higher incidence of sleep apnea than normals.
  • The distribution of snoring in the population and its associated problems is best illustrated by a large epidemiological study conducted in the San Ramino Republic of Northeastern Italy. There are 20,000 people in this state with free national health service. Questionnaires about sleep disorders, snoring and vital statistics were collected on 5,713 individuals over a 3-year period. These data showed the following distribution by age and sex:

Snoring Level:

Age effect on chronic snoring


















Hypertension was more frequent among chronic snorers than among non-snorers. This difference was more apparent after age 40. (see below)

Because obesity (>15% above ideal body weight) is associated with hypertension, the data were analyzed for weight, snoring and hypertension relationships.


Chronic Snoring


Conclusion: Weight is associated with an increase in snoring and hypertension.
1. Overweight



2. Normal Wt