Beyond the immediate respiratory consequences of OSA, the condition exerts a significant impact on cardiovascular physiology and contributes to a variety of cardiac conditions ranging from hypertension and coronary artery disease to stroke and congestive heart failure[1,2]. OSA increases the risk for cardiovascular disease (CVD) regardless of individual demographics or risks such as smoking[1]. In patients with CVD, it’s estimated 40-60% also have OSA[3]. Studies report that OSA increases the risk of heart failure by 140%, stroke by 60%, and coronary heart disease by 30%[1].
Whilst the underlying mechanisms that link the two are not completely understood, the linkage is evident by the improvement in cardiac health upon treatment of OSA with CPAP therapy[1]. Events identified as possible mechanisms include sustained activation of the sympathetic system, changes in intrathoracic pressure, and oxidative stress[1].
The sympathetic nervous system is an important modulator of the heart, however when over-activated it can cause detrimental effects on cardiac health. Sympathetic effects on the heart include increased heart rate, increased strength of contraction, and peripheral vasoconstriction, which in turn increase blood pressure[4]. When these effects are sustained over long periods of time, the heart is vulnerable to cardiomyocyte death, abnormal vascular and ventricular remodeling, and onset of arrhythmia[5]. In patients with OSA, sympathetic activity has been seen to be elevated not only during sleep but also during the day[2].
The intrathoracic pressure swings involved in OSA have been shown to contribute to the onset of premature atrial beats and atrial fibrillation[5]. Atrial fibrillation is a serious condition that increases the risk of blood clots, stroke, and heart failure. Oxidative stress in OSA corresponds with high blood pressure, endothelial function and thickness of the intima-media, which are all surrogate markers of cardiovascular disease[6]. CPAP therapy reverses oxidative stress in patients with OSA and is important in management of not only OSA but in preventing the onset of cardiac conditions that may arise as a result.
References:
- Jean-Louis G, Zizi F, Clark LT, Brown CD, McFarlane SI. Obstructive sleep apnea and cardiovascular disease: role of the metabolic syndrome and its components. J Clin Sleep Med. 2008;4(3):261-272.
- Somers VK, Dyken ME, Clary MP, Abboud FM. Sympathetic neural mechanisms in obstructive sleep apnea. J Clin Invest. 1995;96(4):1897-1904. doi:10.1172/JCI118235
- Tietjens, J. R., Claman, D., Kezirian, E. J., De Marco, T., Mirzayan, A., Sadroonri, B., Goldberg, A. N., Long, C., Gerstenfeld, E. P., & Yeghiazarians, Y. (2019). Obstructive sleep apnea in cardiovascular disease: A review of the literature and proposed multidisciplinary clinical management strategy. AM Heart J, 8(1). https://doi.org/10.1161/jaha.118.010440
- Zhang DY, Anderson AS. The sympathetic nervous system and heart failure. Cardiol Clin. 2014;32(1):33-vii. doi:10.1016/j.ccl.2013.09.010
- Borovac JA, D’Amario D, Bozic J, Glavas D. Sympathetic nervous system activation and heart failure: Current state of evidence and the pathophysiology in the light of novel biomarkers. World J Cardiol. 2020;12(8):373-408. doi:10.4330/wjc.v12.i8.373
- Eisele HJ, Markart P, Schulz R. Obstructive Sleep Apnea, Oxidative Stress, and Cardiovascular Disease: Evidence from Human Studies. Oxid Med Cell Longev. 2015;2015:608438. doi:10.1155/2015/608438
