Journal of Clinical and Preventive Cardiology

: 2016  |  Volume : 5  |  Issue : 1  |  Page : 29--30

Hypertension with obstructive sleep apnea

Bornali Datta, Ashish Kumar Prakash 
 Department of Respiratory and Sleep Medicine, Medanta The Medicity, Gurgaon, Haryana, India

Correspondence Address:
Bornali Datta
Senior Consultant, Department of Respiratory and Sleep Medicine, Medanta - The Medicity, Sector 38, Gurgaon - 122 001

How to cite this article:
Datta B, Prakash AK. Hypertension with obstructive sleep apnea.J Clin Prev Cardiol 2016;5:29-30

How to cite this URL:
Datta B, Prakash AK. Hypertension with obstructive sleep apnea. J Clin Prev Cardiol [serial online] 2016 [cited 2022 May 26 ];5:29-30
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Full Text

Hypertension is one of the most common diseases encountered by the general physicians. On the contrary, obstructive sleep apnea (OSA) and other sleep disordered breathing (SDB) are not so common and are often underdiagnosed. Hypertension when combined with OSA has a poor outcome and it is very difficult to manage if OSA is not managed properly. There are common risk factors for both the diseases which can lead to problems such as aging, obesity (i.e., body mass index), gender, smoking, and dyslipidemia, either together or alone. Overall, they both have a bidirectional effect. [1],[2]

Two entities have been described as follows: [3],[4]

OSA definitions, as described, have been markedly influenced by hypertension itself. OSA is defined as apnea-hypopnea index (AHI) of at least 10-14 events/h or AHI between 5 and 14 events/h with documented hypertension, ischemic heart disease, history of stroke, or symptoms of excessive daytime sleepiness, impaired cognition, mood disorders, or insomnia that existOSA syndrome is defined by the AHI as the number of apneas and hypopneas per hour of sleep ≥5 events/h and persistent complaints of excessive daytime somnolence, unrefreshing sleep, or fatigue.The evidence now clearly demonstrates that hypertensive patients with OSA are at an increased risk of developing resistant hypertension. The presentation which is first reported to general practitioner can be confusing and the patient needs to be evaluated by a sleep specialist.

In OSA patients, it is the fragmented sleep and intermittent hypoxemia with or without CO 2 retention which alter the autonomic and hemodynamic responses to sleep. Sympathetic nerve activation and high serum catecholamine levels are the functions of periodic hypercapnia and hypoxemia due to apnea-hypopnea episodes. Impaired baroreflex sensitivity and the continuous activation of the renin-angiotensin-aldosterone axis also contribute to OSA-associated cardiovascular disorders. 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. Research has demonstrated that patients with both OSA and primary hyperaldosteronism are more likely to develop drug-resistant hypertension. Most importantly, sleep deprivation from OSA is associated with endothelial dysfunction and arterial stiffness, both of which initiate and accelerate the development of hypertension. There are specific categories of hypertension related to OSA; the most common and clinically relevant categories are resistant hypertension, nocturnal hypertension, and masked hypertension. [5],[6]

The management of OSA with hypertension is by giving antihypertensive and proper management of the OSA component. The diagnostic tool is polysomnography which can differentiate SDB such as OSA, central sleep apnea, and others. The gold standard for the diagnosis of SDB is in laboratory-attended polysomnography. It is a diagnostic test where the patient is made to sleep under observation, and comprehensive recording of biophysical changes during sleep is performed with the help of various parameters. There are both attended and unattended sleep studies. There is a debate regarding cost-effectiveness and compliance with respect to home sleep testing (HST), which is unattended versus laboratory polysomnography, as more compliance is found with HST. [7],[8] Once OSA is diagnosed, its severity is graded on the basis of AHI (mild: 6-15/moderate: 16-30/severe: >30). [4]

The treatment includes conservative management such as weight reduction, avoidance of alcohol and sleeping pills, and good sleep hygiene. Other interventions such as uvulo-palato-pharyngoplasty and mandibular appliances are also advised in specific cases.

The treatment of choice for OSA is positive airway pressure (PAP) either Bilevel PAP or continuous. Continuous PAP (CPAP) therapy has been found to be successful for reducing OSA. However, the four available meta-analyses have found that the effect of prolonged CPAP therapy on ambulatory blood pressure is small (1-2 mmHg reduction). [9],[10],[11] The compliance of CPAP is a major concern, and the poor results of meta-analysis may be attributed to that. Recently, two prospective studies have reported that (i) normotensive subjects with OSA were characterized over a 12-year follow-up by a significant increase in the risk of developing hypertension and (ii) the risk of new-onset hypertension was lower in subjects treated with CPAP, although the benefit seemed restricted to those with daytime sleepiness. [12],[13]


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