Obstructive Sleep Apnea (OSA) And Cardiovascular Diseases
Obstructive sleep apnea (OSA) is a very common sleep disorder affecting about 33% per cent of the US population, with mild OSA accounting for 19% (more than half of the cases). It is characterized by obstruction of the airway and intermittent cessation of breathing during sleep. Unlike central sleep apnea (CSA) which occurs due to a lack of signals to the respiratory muscles by the brain, OSA sets in due to relaxation of throat muscles and consequent blockage of the airway indicated by snoring; a hallmark of OSA. A shutdown in ventilation causes a drop in oxyhemoglobin levels which in turn triggers ventilatory efforts. This eventually leads to arousal from sleep.1
Other symptoms of sleep apnea subsume:
- Excessive daytime sleepiness due to irregular awakenings during night
- Headaches early in the morning
- Decreased concentration throughout the day
- Mood fluctuations
- An increased blood pressure
Obstructive sleep apnea has also been linked with increased risk for cardiovascular diseases and high morbidity and mortality.2
OSA and Hypertension
Many studies have been carried out on the association between OSA and increased blood pressure (hypertension). These studies suggest that obstructive sleep apnea does contribute to an increased blood pressure. However, whether OSA is an independent risk factor for hypertension is not yet established as many risk factors for hypertension are also seen in people with OSA such as age, gender, body mass index (BMI), smoking and alcohol intake etc.
A recent study called ‘The Wisconsin Sleep Cohort Study’ was done to observe direct association between OSA and hypertension, if any. The study subjects were divided into two groups and followed up for ten years and revealed that People with OSA were 2.9 times more likely to develop hypertension.
Similarly, another study revealed a linear relationship between obstructive sleep apnea and hypertension. The relation between OSA and hypertension is often attributed to an increased sympathetic outflow in these patients. Increased stimulation of sympathetic nervous system leads to an elevated heart rate with raised vascular resistance and resultant high blood pressure. Moreover, it has also been seen that people with OSA have relatively greater renal reabsorption of sodium as compared to people without OSA. High retention of sodium leads to increased blood volume (hypervolemia) which adds to hypertension.3
Heart Disease and OSA
OSA has also been linked to an increased incidence of heart diseases such as coronary heart disease. One study revealed that obstructive sleep apnea is a risk factor equivalent to smoking, obesity and high blood pressure in causing myocardial infarction.4 Others suggest that people with severe OSA are more likely to develop ischemic heart disease with manifestations such as nocturnal angina (attacks of angina during night). Also in these patients, nocturnal ST segment changes are observed. This is explained by the fact that during the apneic episodes, there is a rise in heart rate and blood pressure post apnea. The change in myocardial oxygen requirements post apnea causes the observed changes in ST segment in such patients.5
Congestive Heart Failure (CHF)
It has been observed that people who have congestive heart failure often have obstructive sleep apnea. The process behind OSA in such people is the elevation of venous pressure leading to cardiac failure. Increased venous pressure forces the blood out of the vessels causing edema and involvement of pharyngeal/airway vasculature results in an obstructed lumen which in turn results is obstructive sleep apnea. Similarly, OSA reciprocally increases the risk for congestive heart failure. Hypoxia induced by the cessation of ventilation negatively impacts the function of heart’s left ventricle predisposing the person to CHF. A study carried out to evaluate the risk revealed that; in people with OSA, the risk of developing CHF is 2.38 times more than other diseases of cardiovascular origin.6
Obstructive sleep apnea is also associated with altered rhythms of cardiac contractions. It sets in both types of arrhythmias including bradyarrhythmias (or slow heart rhythms) and tachyarrhythmias (fast rhythms such as fibrillation and flutter). However, bradyarrhythmias occur more frequently in people who suffer from obstructive sleep apnea. Moreover, there is an increased likelihood of such people developing an AV block. The pathogenesis behind this is; an increased vagal tone after such apneic episodes. Increased vagal stimulation slows down the conduction between heart fibers and the incidence of such bradyarrhythmias is directly related to the severity of obstructive sleep apnea.7
Mechanics Behind OSA and Cardiovascular Diseases
Normally during sleep, there is a decrease in heart rate due to a drop in sympathetic activity. However, in OSA, there is a rise in sympathetic outflow from the brain that leads to both increased heart rate and blood pressure. The hypoxemia induced by OSA decreases oxygen supply to heart increasing myocardial oxygen demand. This happens right after apnea and results in ventilatory efforts and arousal from sleep. The increased sympathetic signaling as a compensatory response causes vasoconstriction and elevated blood pressure.
Research studies reveal that people with obstructive sleep apnea have an increased predisposition to endothelial damage and atherosclerosis. These changes are explained by the presence of certain mediators of vascular endothelial inflammation and by the damage that is found in greater amounts in people with OSA. Two of them are C-reactive protein (CRP) and interleukin 6 (both play a significant role in atherosclerosis).
Thus, people with OSA have overall different hemodynamics that predispose them to cardiovascular diseases.2
- A. M. Osman, S. G. Carter, J. C. Carberry, and D. J. Eckert, “Obstructive sleep apnea: current perspectives,” Nat. Sci. Sleep, vol. 10, pp. 21–34, Jan. 2018, doi: 10.2147/NSS.S124657.
- J. Collen, C. Lettieri, E. Wickwire, and A. Holley, “Obstructive sleep apnea and cardiovascular disease, a story of confounders!,” Sleep Breath., vol. 24, no. 4, pp. 1299–1313, 2020, doi: 10.1007/s11325-019-01945-w.
- R. Tamisier and P. Lévy, “Management of hypertension in obstructive sleep apnoea: predicting blood pressure reduction under continuous positive airway pressure,” Eur. Respir. J., vol. 50, no. 4, p. 1701822, Oct. 2017, doi: 10.1183/13993003.01822-2017.
- A. V. Benjafield, N. T. Ayas, P. R. Eastwood, R. Heinzer, S.M. Ip, M. J.Morrell, C. M. Nunez, S. R. Patel, T. Penzel, J. L. Pépin, P.E. Peppard, S. Sinha, S. Tufik, K. Valentine, & A. Malhotra, (2019). Estimation of the global prevalence and burden of obstructive sleep apnoea: a literature-based analysis. The Lancet. Respiratory medicine, 7(8), 687–698. https://doi.org/10.1016/S2213-2600(19)30198-5
- M. Marin-Oto, E. E. Vicente, and J. M. Marin, “Long term management of obstructive sleep apnea and its comorbidities,” Multidiscip. Respir. Med., vol. 14, no. 1, p. 21, 2019, doi: 10.1186/s40248-019-0186-3.
- H. K. Khattak, F. Hayat, S. V Pamboukian, H. S. Hahn, B. P. Schwartz, and P. K. Stein, “Obstructive Sleep Apnea in Heart Failure: Review of Prevalence, Treatment with Continuous Positive Airway Pressure, and Prognosis,” Texas Hear. Inst. J., vol. 45, no. 3, pp. 151–161, Jun. 2018, doi: 10.14503/THIJ-15-5678.
- A. S. Hersi, “Obstructive sleep apnea and cardiac arrhythmias,” Ann. Thorac. Med., vol. 5, no. 1, pp. 10–17, Jan. 2010, doi: 10.4103/1817-1737.58954.
|25th January 2022
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