Snoring is a common disorder that affects 20%-40% of the general population. The mechanism of snoring is the vibration of anatomical structures in the pharyngeal airways. The flutter of the soft palate explains the harsh aspect of the snoring sound, which occurs during natural sleep or drug-induced sleep. The presentation of snoring may vary throughout the night or between nights, with a subjective, and therefore inconsistent, assessment of its loudness.
Objective evaluation of snoring is important for clinical decision-making and predicting the effect of therapeutic interventions. It also provides information regarding the site and degree of upper airway obstruction. Snoring is one of the main features of sleep-disordered breathing, including hypopnea events, which reflect partial upper airway obstruction.
Obstructive sleep apnea (OSA) is characterized by episodes of complete (apnea) or partial (hypopnea) collapse of the upper airways with associated oxygen desaturation or awakening from sleep. Most patients with OSA snore loudly almost every night. However, in the Sleep Heart Health Study, one third of participants with OSA reported no snoring, while one third of snoring participants did not meet the criteria for OSA. Therefore, subjective assessments of snoring (self-reported) may not be sufficiently reliable to assess its potential impact on cardiovascular (CV) health outcomes.
CV Effects
OSA has been hypothesized as a modifiable risk factor for CV diseases (CVD), including hypertension, coronary artery disease (CAD), atrial fibrillation, heart failure, and stroke, primarily because of the results of traditional observational studies. Snoring is reported as a symptom of the early stage of OSA and has also been associated with a higher risk for CVD. However, establishing causality based on observational studies is difficult because of residual confounding from unknown or unmeasured factors and reverse causality (ie, the scenario in which CVD increases the risk for OSA or snoring). A Mendelian randomization study, using the natural random allocation of genetic variants as instruments capable of producing results analogous to those of randomized controlled trials, suggested that OSA and snoring increase the risk for hypertension and CAD, with associations partly driven by body mass index (BMI). Conversely, no evidence was found that CVD causally influenced OSA or snoring.
Snoring has been associated with multiple subclinical markers of CV pathology, including high blood pressure, and loud snoring can interfere with restorative sleep and contribute to the risk for hypertension and other adverse outcomes in snorers. However, evidence on the associations between snoring and CV health outcomes remains limited and is primarily based on subjective assessments of snoring or small clinical samples with objective assessments of snoring for only 1 night.
Snoring and Hypertension
A study of 12,287 middle-aged patients (age, 50 years) who were predominantly males (88%) and generally overweight (BMI, 28 kg/m2) determined the prevalence of snoring and its association with the prevalence of hypertension using objective evaluation of snoring over multiple nights and multiple daytime blood pressure measurements. The findings included the following observations:
An increase in snoring duration was associated with a 3-mmHg increase in systolic (SBP) and a 4-mmHg increase in diastolic blood pressure (DBP) in patients with frequent and regular snoring, compared with those with infrequent snoring, regardless of age, BMI, sex, and estimated apnea/hypopnea index.The association between severe OSA alone and blood pressure had an effect size similar to that of the association between snoring alone and blood pressure. In a model where OSA severity was classified and snoring duration was stratified into quartiles, severe OSA without snoring was associated with 3.6 mmHg higher SBP and 3.5 mmHg higher DBP, compared with the absence of snoring or OSA. Participants without OSA but with intense snoring (4th quartile) had 3.8 mmHg higher SBP and 4.5 mmHg higher DBP compared with participants without nighttime apnea or snoring.Snoring was significantly associated with uncontrolled hypertension. There was a 20% increase in the probability of uncontrolled hypertension in subjects aged> 50 years with obesity and a 98% increase in subjects aged ≤ 50 years with normal BMI.Duration of snoring was associated with an 87% increase in the likelihood of uncontrolled hypertension.
Implications for Practice
This study indicates that 15% of a predominantly overweight male population snore for> 20% of the night and about 10% of these subjects without nighttime apnea snore for> 12% of the night.
Regular nighttime snoring is associated with elevated blood pressure and uncontrolled hypertension, regardless of the presence or severity of OSA.
Physicians must be aware of the potential consequences of snoring on the risk for hypertension, and these results highlight the need to consider snoring in clinical care and in the management of sleep problems, especially in the context of managing arterial hypertension.
This story was translated from Univadis Italy, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
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