|
 
 |
| BRIEF REVIEW |
|
| Year : 2016 | Volume
: 5
| Issue : 1 | Page : 25-28 |
|
Hypertension and sleep apnea: The Deadly Duo
Navneet Wadhwa MD (Pharmacology) 1, Neeraj Tewari MBBS 2
1 AUW Global, New Delhi, India
2 Medicare, Lucknow, Uttar Pradesh, India
| Date of Web Publication | 14-Jun-2016 |
Correspondence Address:
Navneet Wadhwa
Physician Scientist, AUW Global, New Delhi
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2250-3528.184012
Obstructive Sleep Apnea is one of the most common cause of the secondary cause of consistent raised blood pressure. Evidence, consistently demonstrates that sleep apnea is a major modifiable risk factor of hypertension. Resistant hypertension has a strong correlation with OSA. There needs to be a strong emphasis for the effective therapeutic strategies to simultaneously improve the management of OSA and hypertension. Keywords: Hypertension, polysomnography, resistant hypertension, sleep apnea
How to cite this article:
Wadhwa N, Tewari N. Hypertension and sleep apnea: The Deadly Duo. J Clin Prev Cardiol 2016;5:25-8 |
| Introduction | |  |
Obstructive sleep apnea (OSA) is one of the most common causes of the secondary cause of consistent raised blood pressure (BP). The evidence now clearly demonstrates that hypertensive patients with OSA are at increased risk of developing resistant hypertension. [1] Moreover, there are higher chances of cardiovascular events in hypertensive patients with OSA as compared to hypertensives without OSA.
Hypertensive patients with OSA need specific screening and identification for diagnosis and management. Innumerable experimental and clinical studies demonstrate pathophysiological interactions between OSA and hypertension. [2],[3],[4]
It is pertinent to understand the general pathophysiological effects OSA has on cardiovascular systems, explore the underlying mechanisms by which OSA contributes to the pathogenesis of arterial hypertension and other categories of OSA-associated hypertension. [5]
| Definition of Obstructive Sleep Apnea | | |
The OSA is defined on the basis of the apnea-hypopnea index with typical clinical symptoms of OSA including daytime sleepiness and fatigue, frequent awakening during sleep, snoring, nocturia, reduced concentration and impaired memory are also important clues for clinical diagnosis. [5]
Diagnosis of OSA requires polysomnography to assess key variables such as arterial oxygen saturation, chest, and abdomen respiratory movement, electroencephalogram findings and quantified air flow. OSA occurs during nocturnal sleep. [6],[7] It is important to note the significance of apnea-hypopnea index. [7],[8] It is the total number of episodes of apnea (complete blockade of airflow for >10 s) and hypopnea (450% reduction in respiratory airflow accompanied by 43% reduction in arterial oxygen saturation for >10 s) per sleep hour. The three categories of with OSA are categorized as mild, moderate, and severe.
| Risk Factors for Obstructive Sleep Apnea | | |
It is interesting to note the certain sensitive predictors that are useful to identify high-risk population like the patients with pharyngeal collapse due to macroglossia and adenotonsillar hypertrophy tongue displacement and pharynx narrowing due to retrognathia. [9] Various epidemiological studies have shown that males are predisposed to OSA, and the chances are increased with the advancing age and weight gain. There are certain other risk factors like smoking, alcohol abuse, hormone depletion in postmenopausal women and nasal congestion due to allergic rhinitis which predispose to OSA. [10]
It is important for the timely identification of the unrecognized OSA population and the proper use of polysomnography is helpful to accurately diagnose and evaluate the severity of OSA.
| Pathophysiological Mechanisms of Obstructive Sleep Apnea and Association with Hypertension | | |
There are multi-varied pathophysiological effects on the cardiovascular system through a variety of mechanisms in which OSA is directly or indirectly implicated.
Sympathetic nerve activation and serum catecholamine elevation are a function of periodic hypercapnia and hypoxemia due to apnea-hypopnea episodes. [11] The frequent arousals and sleep deprivation due to periodic asphyxia also result in sympathetic nerve activation and contribute to tachycardia and hypertension. Hemodynamic changes ultimately lead to left ventricular hypertrophy and heart failure. Hypoxemia promotes oxidative stress, systemic inflammation and endothelium dysfunction, all of which can contribute to the development of atherosclerotic cardiovascular diseases. To counteract the narrowing pharynx, negative intrathoracic pressure is generated and it increases the mechanical stress on the ventricles and atria. Left ventricle hypertrophy and left atrial enlargement, occurs and these maladaptive changes can manifest ultimately as overt cardiovascular diseases such as diastolic heart failure and atrial fibrillation. [12],[13] Impaired baroreflex sensitivity and the continuous activation of the renin-angiotensin-aldosterone axis also contribute to OSA-associated cardiovascular disorders. The overall picture reflects that, OSA has a central role in the pathogenesis of cardiovascular disease; it is clinically important to effectively control OSA, to reduce the adverse effects OSA imparts on the cardiovascular system.
| The Strong Relationship between the Obstructive Sleep Apnea and Hypertension | | |
There is ample and compelling evidence to indicate that there is a dose-effect relationship between the severity of in the OSA and degree of hypertension. The pathophysiological mechanisms by which OSA contributes to BP elevation are multi-factorial. On the other hand, the periodic hypoxemia, frequent arousals and sleep deprivation all cause sympathetic nerve activation that leads to increased cardiac output and peripheral vessel constriction, and thereby promotes BP elevation [9] It has been reported that patients with OSA have a higher prevalence of isolated diastolic hypertension and the underlying mechanism might be due to the tachycardia and shortening of cardiac diastole. [14],[15] Research has demonstrated that patients with both OSA and primary hyperaldosteronism are more likely to develop drug-resistant hypertension. Importantly, sleep deprivation from OSA is associated with endothelial dysfunction and arterial stiffness, both of which initiate and accelerate the development of hypertension. Collectively, the pathophysiological effects of OSA on hypertension are multi-factorial and they are due to the high prevalence of OSA in hypertensive subjects. [12]
It seems beyond doubt that improving OSA should result in profound benefits in hypertension management.
There are specific categories of hypertension related to OSA; the most common and clinically relevant categories are resistant hypertension, nocturnal hypertension and masked hypertension.
| Obstructive Sleep Apnea and Resistant Hypertension | | |
Resistant hypertension, which is defined as BP that remains higher than 140/90 mmHg despite treatment with three different classes of anti-hypertensive medicines (including diuretics) at their optimal doses, is a common secondary effect of OSA. About 90% of male patients and 77% of female patients have been shown to have resistant hypertension with OSA. [16]
| Mechanistic Insights | | |
A substantial number of mechanisms contribute to OSA-related resistant hypertension. In addition to the aforementioned pathophysiological effects of OSA that can lead to BP elevation, primary hyperaldosteronism is also believed to be responsible for these phenomena. It has been reported that primary hyperaldosteronism is highly prevalent in patients with concomitant OSA and resistant hypertension, as evidenced by the finding that both the urine and plasma levels of aldosterone were significantly higher in this population. On the one hand, sodium and water retention caused by hyperaldosteronism can lead to volume overload and BP elevation. On the other hand, parapharyngeal edema induced by fluid retention could exacerbate OSA and thereby promote further BP elevation. Previous studies have suggested that this vicious cycle can be interrupted by treatment with aldosterone antagonists and continuous positive airway pressure (CPAP) therapy. [8]
Nocturnal hypertension is substantially higher in subjects with OSA. Approximately 84% of patients with OSA have been demonstrated to have experienced nocturnal hypertension. Data from the Wisconsin Sleep Cohort Study indicated that there was a dose-effect relationship between the severity of OSA and the risk of night time BP elevation. The main mechanism contributing to night time BP elevation is the sympathetic over-activation caused by hypoxemia, frequent arousals and sleep deprivation. Treatment of OSA with CPAP therapy reversed the night time BP elevation. It is clinically important to screening for OSA in patients with nondipping or difficult-to-treat hypertension.
| Obstructive Sleep Apnea and Masked Hypertension | | |
Masked hypertension is the term used to describe the condition when the BP measured in the office is within the target range but the BP assessed at home or by 24-h ambulatory BP monitoring is above the normal range. The incidence of masked hypertension in subjects with newly diagnosed OSA was nearly 30%. Another study revealed that among 61 male participants who were identified as normotensive by a clinic BP evaluation, one-third had masked hypertension and the patients with OSA had a higher incidence of masked hypertension than those without OSA. These data suggest a potential association between OSA and masked hypertension; however, large, prospective studies are needed to corroborate these findings and to help physician identify those patients who are at increased risk of incident masked hypertension. Moreover, experimental and clinical studies are needed to elucidate the mechanisms.
| Management Approaches for Obstructive Sleep Apnea associated Hypertension | | |
In addition to anti-hypertensive drugs, there are some other highly effective nonpharmacologic modalities for treating OSA-associated hypertension. Effective control of the co-morbidities that contribute to OSA and hypertension, such as obesity, smoking, and alcohol abuse, is considered to be the most cost-effective strategy. Surgical correction of the anatomical abnormalities of the upper airway is also a highly effective and efficient method. In addition, the use of oral appliances and CPAP therapy can also decrease BP in hypertensive patients with OSA. Clinical studies have revealed that oral appliance therapy was not only beneficial for OSA improvement but also for BP reduction. [17]
Treatment in prehypertensive or hypertensive patients with OSA substantially reduced the daytime systolic blood and the night time systolic BP (SBP) and diastolic BP (DBP), when compared with the control group. Meta-analysis have shown that CPAP therapy was significantly associated with 24-h ambulatory SBP and DBP reduction. Moreover, CPAP seemed more beneficial for decreasing nocturnal SBP than for diurnal SBP, and patients with resistant hypertension seemed to benefit most from CPAP therapy. In brief, the benefits derived from CPAP treatment may be associated with amelioration of hypoxemia and decreased nocturnal sympathetic nervous activation, and the resulting improvements in arterial oxygen saturation could mitigate the systemic inflammation and oxidative stress. [12] Moreover, reduced negative intra-thoracic pressure caused by the positive pressure ventilation could also result in beneficial hemodynamic changes. All of these favorable effects of CPAP treatment simultaneously improve hypertension control. For physicians considering which anti-hypertensive drugs to prescribe, there is no solid evidence to support the use of one specific drug class over another. There is no solid evidence of apnea-hypopnea index improvement with the commonly used anti-hypertensive medicines, including angiotensin-converting enzyme inhibitor or angiotensin receptor blocker, calcium channel blocker, diuretic, β-blocker and α-receptor antagonist. Nonetheless, in patients with hyperaldosteronism, aldosterone antagonists should be the first choice agents. Moreover, diuretics especially spironolactone may have a greater role in BP control by improving para-pharyngeal edema.
| Summary | | |
It is important to screen for OSA in hypertensive patients, especially those patients who exhibit predominant DBP elevation, difficult to control BP and nocturnal BP elevation.
Increasing our understanding of the interplay of the mechanisms of OSA and hypertension is critical for the effective management of OSA-associated hypertension.
More studies, are warranted to investigate effective therapeutic strategies to improve the management of OSA and hypertension.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Prejbisz A, Florczak E, Pregowska-Chwala B, Klisiewicz A, Kusmierczyk-Droszcz B, Zielinski T, et al. Relationship between obstructive sleep apnea and markers of cardiovascular alterations in never-treated hypertensive patients. Hypertens Res 2014;37:573-9.  |
| 2. | Silverberg DS, Oksenberg A, Iaina A. Sleep-related breathing disorders as a major cause of essential hypertension: Fact or fiction? Curr Opin Nephrol Hypertens 1998;7:353-7. |
| 3. | Fletcher EC, DeBehnke RD, Lovoi MS, Gorin AB. Undiagnosed sleep apnea in patients with essential hypertension. Ann Intern Med 1985;103:190-5. |
| 4. | Sleep-related breathing disorders in adults: Recommendations for syndrome definition and measurement techniques in clinical research. The report of an American Academy of sleep medicine task force. Sleep 1999;22:667-89. |
| 5. | Ryan CM, Bradley TD. Pathogenesis of obstructive sleep apnea. J Appl Physiol 2005;99:2440-50. |
| 6. | Li KK, Kushida C, Powell NB, Riley RW, Guilleminault C. Obstructive sleep apnea syndrome: A comparison between Far-East Asian and white men. Laryngoscope 2000;110 (10 Pt 1):1689-93. |
| 7. | Young T, Skatrud J, Peppard PE. Risk factors for obstructive sleep apnea in adults. JAMA 2004;291:2013-6. |
| 8. | Peppard PE, Young T, Palta M, Dempsey J, Skatrud J. Longitudinal study of moderate weight change and sleep-disordered breathing. JAMA 2000;284:3015-21. |
| 9. | Buxbaum SG, Elston RC, Tishler PV, Redline S. Genetics of the apnea hypopnea index in Caucasians and African Americans: I. Segregation analysis. Genet Epidemiol 2002;22:243-53. |
| 10. | Parati G, Lombardi C, Hedner J, Bonsignore MR, Grote L, Tkacova R, et al. Position paper on the management of patients with obstructive sleep apnea and hypertension: Joint recommendations by the European Society of Hypertension, by the European Respiratory Society and by the members of European COST (COoperation in Scientific and Technological research) ACTION B26 on obstructive sleep apnea. J Hypertens 2012;30:633-46. |
| 11. | Somers VK, Dyken ME, Clary MP, Abboud FM. Sympathetic neural mechanisms in obstructive sleep apnea. J Clin Invest 1995;96:1897-904. |
| 12. | Konecny T, Kara T, Somers VK. Obstructive sleep apnea and hypertension: An update. Hypertension 2014; 63:203-9. |
| 13. | Niroumand M, Kuperstein R, Sasson Z, Hanly PJ. Impact of obstructive sleep apnea on left ventricular mass and diastolic function. Am J Respir Crit Care Med 2001;163:1632-6. |
| 14. | Kato M, Roberts-Thomson P, Phillips BG, Haynes WG, Winnicki M, Accurso V, et al. Impairment of endothelium-dependent vasodilation of resistance vessels in patients with obstructive sleep apnea. Circulation 2000;102:2607-10. |
| 15. | McNicholas WT. Obstructive sleep apnea and inflammation. Prog Cardiovasc Dis 2009;51:392-9. |
| 16. | Young T, Peppard P, Palta M, Hla KM, Finn L, Morgan B, et al. Population-based study of sleep-disordered breathing as a risk factor for hypertension. Arch Intern Med 1997;157:1746-52. |
| 17. | Querejeta Roca G, Shah AM. Sleep disordered breathing: Hypertension and cardiac structure and function. Curr Hypertens Rep 2015;17:91. |
|
Search Pubmed for