The Association of Obstructive Sleep Apnea and Hypertension.

Avani R Patel,Shantanu Singh,Shivank Singh,Amar R Patel,Imran Khawaja

doi:10.7759/cureus.4858

Avani R Patel, Shantanu Singh + Show 3 more

Open Access

https://doi.org/10.7759/cureus.4858

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Journal: Cureus	Publication Date: Jun 7, 2019
Citations: 18	License type: cc-by

Affiliation: Kaiser Permanente, Marshall University

Abstract

Obstructive sleep apnea (OSA) is a condition characterized by recurrent episodes of partial or complete upper airway obstruction during sleep. Hypertension (HTN) is defined by the presence of a chronic elevation of systemic arterial pressure above a certain threshold value (≥140 mm Hg systolic or ≥90 mm Hg diastolic). On the surface, OSA and HTN appear very different from one another. Despite this, they share several common risk factors including obesity, male gender, and advancing age. In 2003, the Seventh Joint National Committee (JNC VII) recognized OSA as a secondary cause of HTN. As physicians, our goal is to understand the OSA-HTN association better through academic study regarding its epidemiology, its pathophysiology, and its treatment.

Highlights

There has been some overlap between patients of obstructive sleep apnea (OSA) and hypertension (HTN) with about 50% of HTN patients having concomitant OSA [1]
There is a theory that the two conditions may have a causal, bidirectional relationship [1]. This was proven when OSA was named a secondary cause of HTN by the 2003 Joint National Committee (JNC VII) on prevention, detection, evaluation, and treatment of high blood pressure (BP) [2]
The objective is to address the association between OSA and HTN, the epidemiological evidence that supports their causal relationship, the system-specific pathophysiology of OSA that can lead to HTN development, and the treatment of OSA and how it impacts HTN treatment

Summary

Introduction

There has been some overlap between patients of obstructive sleep apnea (OSA) and hypertension (HTN) with about 50% of HTN patients having concomitant OSA [1]. The fact that OSA is the most prevalent secondary cause of HTN, both share many pathophysiological mechanisms that link them together [18,19] By understanding these mechanisms as determined by previous research, the development of HTN in OSA cases, and the overall increased risk of cardiovascular disease can be better understood. Increased aldosterone caused by RAAS activation can contribute to fluid retention seen in HTN, which leads to more rostral fluid displacement and an increase in upper airway obstruction [1,35] This will, in turn, worsen the patient’s hypoxemia and the pathophysiological cycle will continue. The trial determined that the BP was reduced significantly after surgery in a select group of patients with moderate to severe OSA [44]

Conclusions

Disclosures

Findings

Chobanian AV