Sleep Apnea HealthQM

Does Sleep Apnea Cause Cardiovascular Diseases?

Obstructive sleep apnea (OSA) can cause cardiovascular diseases through the following mechanisms:

  • Sympathetic activation
  • Intrathoracic pressure changes
  • Oxidative stress
  • Abnormalities in coagulation factors
  • Endothelial damage
  • Inflammatory mediators

Approximately 34% of middle-aged men and 17% of middle-aged women are diagnosed with OSA [1]. The prevalence of OSA is estimated at 40% to 80% in patients with hypertension, coronary artery disease, heart failure (HF), atrial fibrillation (AF), pulmonary hypertension (PH), and stroke [2].

What Is Sleep Apnea?

Sleep apnea is a sleep disorder that is characterized by pauses in breathing or shallow breaths during sleep. These pauses can last for several seconds to minutes and can occur 30 times or more per hour.

Each pause in breathing reduces the amount of oxygen that reaches the brain, which can lead to snoring, interrupted sleep, and excessive daytime sleepiness. Sleep apnea is a serious medical condition that can significantly impact the quality of life.

1- Sympathetic activation

The sympathetic nervous system is a part of the autonomous nervous system responsible for the fight-or-flight response. Its repetitive activation by apnea results in increased systolic blood pressure that leads to hypertension and its complication with time [3]. Repetitive apnea may also lead to an autonomic imbalance and reduced heart rate variability [4].

Treatment with nasal continuous positive airway pressure (CPAP) has been shown to reduce blood pressure during the day and night. CPAP treatment of patients with sleep apnea and heart failure or congestive heart failure resulted in the reduction of systolic blood pressure and an improvement of the left ventricular systolic function [5]

2- Intrathoracic pressure changes

Due to the anatomical location of the heart and lungs in the thoracic cage, the interactions between the two are frequent.

Although both heart and lungs occupy limited spaces within the thoracic cage, the breathing dynamic of the lungs results in changes in the space it occupies, and therefore, affects the space occupied by the heart.

These breathing dynamics result in changes in the external constraint of the heart function, blood volume redistribution, direct systolic ventricular interaction (increased pressure by the pericardium), and afterload of the left ventricular.

An increased intrathoracic pressure limits the ventricular diastolic loading resulting in increased direct ventricular interaction, which may limit the filling of the left ventricle [6]. This interaction between the heart and the lungs may explain the association between sleep apnea and cardiovascular morbidity.

3- Oxidative Stress, Inflammatory Mediators, and Endothelial Damage

Hypoxia is a condition associated with a decrease in the level of oxygen available to the body’s tissues. This condition is commonly observed in patients with sleep apnea [7].

Hypoxia triggers an inflammatory response and an increase in innate immune cells such as neutrophils. These cells secrete reactive oxygen species (ROS) or destructive proteinases that are responsible for tissue damage, including damage to the tissues of the cardiovascular system [8].

Neutrophils also activate the transcription factor HIF-1 (Hypoxia Inducible Factor 1) which promotes the activation of endothelial cells, which are essential for the formation of the blood vessels. However, during hypoxia, endothelial cells express adhesion molecules and proinflammatory cytokines that result in endothelial damage leading to defects in vascular formation [9].

4- Abnormalities in coagulation factors

Blood platelets play an essential role in coagulation, thrombosis, and wound healing. During hypoxia, HIF-1 can promote the activation of platelets, and therefore, increase their blood content [9].

Several studies have shown a strong correlation between the increase in platelets, thromboembolic complications, and worse outcomes of cardiovascular events. It was also reported that blood viscosity due to platelet reactivity is increased in patients with OSA in the morning [10].

5- Potential Factors Influencing the Relationship Between Sleep Apnea and Cardiovascular Diseases

Metabolic syndrome comprises related diseases such as obesity, hypertension, diabetes, and dyslipidemia (abnormal cholesterol or triglyceride levels). Having one of these conditions significantly increases the risk of serious disease, including cardiovascular morbidity and mortality from coronary heart disease and stroke.

Several studies investigated the relationship between sleep apnea and diseases related to metabolic syndrome [5].

A study investigated the correlation between obesity and apnea and found that 60% of obese men had sleep-disordered breathing and 27% had obstructive sleep apnea. Another study reported that 60% to 90% of patients with sleep apnea are obese.

Regarding the relationship between sleep apnea and hypertension, a study found that about 40% of patients with sleep apnea suffer from hypertension.

An association between diabetes and sleep apnea was investigated by a study that found that patients with sleep apnea have increased glucose levels and increased insulin resistance.

Although dyslipidemia is a known factor contributing to cardiovascular diseases, a relationship between sleep apnea and dyslipidemia has not yet been established and future studies will certainly investigate a potential association.


Due to the complexity of the factors involved in the relationship between sleep apnea and cardiovascular diseases, the management of patients with OSA requires the involvement of several healthcare professionals including a sleep specialist, cardiologist, primary provider, otolaryngologist, dietitian, neurologist, and pulmonologist. 

Treatments also exist and include CPAP, auto-titrating PAP, bilevel PAP, adaptive servo-ventilation, positional therapy, lifestyle intervention (e.g., weight loss), upper airway surgery, upper airway neurostimulation, oral appliances, and bariatric surgery. Unfortunately, these treatments may prevent OSA but cannot treat some of the underlying causes that require other types of treatments.


[1] Peppard, P.E., Young, T., Barnet, J.H., Palta, M., Hagen, E.W. and Hla, K.M., 2013. Increased prevalence of sleep-disordered breathing in adults. American journal of epidemiology177(9), pp.1006-1014.

[2] Javaheri, S., Barbe, F., Campos-Rodriguez, F., Dempsey, J.A., Khayat, R., Javaheri, S., Malhotra, A., Martinez-Garcia, M.A., Mehra, R., Pack, A.I. and Polotsky, V.Y., 2017. Sleep apnea: types, mechanisms, and clinical cardiovascular consequences. Journal of the American College of Cardiology69(7), pp.841-858.

[3] Fletcher, E.C., 2003. Sympathetic over activity in the etiology of hypertension of obstructive sleep apnea. Sleep26(1), pp.15-19.

[4] Guzzetti, S., Piccaluga, E., Casati, R., Cerutti, S., Lombardi, F., Pagani, M. and Malliani, A., 1988. Sympathetic predominance in essential hypertension: a study employing spectral analysis of heart rate variability. Journal of hypertension6(9), pp.711-717.

[5] Jean-Louis, G., Zizi, F., Clark, L.T., Brown, C.D. and McFarlane, S.I., 2008. Obstructive sleep apnea and cardiovascular disease: role of the metabolic syndrome and its components. Journal of Clinical Sleep Medicine4(3), pp.261-272.

[6] Verhoeff, K. and Mitchell, J.R., 2017. Cardiopulmonary physiology: why the heart and lungs are inextricably linked. Advances in physiology education41(3), pp.348-353.

[7] Friedman, M., Landsberg, R. and Ascher-Landsberg, J., 2001. Treatment of hypoxemia in obstructive sleep apnea. American journal of rhinology15(5), pp.311-313.

[8] Williams, A.E. and Chambers, R.C., 2016. Neutrophils and tissue damage: is hypoxia the key to excessive degranulation?.

[9] Lavie, L., 2003. Obstructive sleep apnoea syndrome–an oxidative stress disorder. Sleep medicine reviews7(1), pp.35-51.

[10] Toraldo, D.M., Peverini, F., De Benedetto, M. and De Nuccio, F., 2013. Obstructive sleep apnea syndrome: blood viscosity, blood coagulation abnormalities, and early atherosclerosis. Lung191(1), pp.1-7.

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