%0 Journal Article
%T Etiopathogenetic Mechanisms of Pulmonary Hypertension in Sleep-Related Breathing Disorders
%A Ayodeji Adegunsoye
%A Siva Ramachandran
%J Pulmonary Medicine
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/273591
%X Obstructive sleep apnea syndrome is a common disorder with significant health consequences and is on the rise in consonance with the obesity pandemic. In view of the association between sleep-disordered breathing and pulmonary hypertension as depicted by multiple studies, current clinical practice guidelines categorize obstructive sleep apnea as a risk factor for pulmonary hypertension and recommend an assessment for sleep disordered breathing in evaluating patients with pulmonary hypertension. The dysregulatory mechanisms associated with hypoxemic episodes observed in sleep related breathing disorders contribute to the onset of pulmonary hypertension and identification of these potentially treatable factors might help in the reduction of overall cardiovascular mortality. 1. Introduction In consonance with the obesity pandemic, there is an increasing awareness of sleep-related breathing disorders (SRBDs) as a potentially treatable factor in reducing overall cardiovascular mortality. The spectrum of SRBD ranges from habitual snoring to obstructive sleep apnea (OSA) and increasing evidence shows that improved cardiovascular function may be obtained by early recognition and treatment of these disorders [1]. Over the past three decades, the pathophysiology of sleep-related breathing disorders (SRBDs) has been better understood and though the exact contributory pathways are still not clearly defined several studies allude to multi-factorial mechanisms being involved in the development of pulmonary hypertension in relation to SRBD [1]. Sleep apnea occurs in about 12 million US adults in their 4th to 6th decades of life and about a quarter of all those are over the age of 65£¿yrs. Nearly half of all nursing home residents have sleep apnea and 38,000 deaths annually are directly attributed to SRBD. With the prevalence of SRBD currently exceeding that of asthma in adults, the cardiovascular consequences of its associated comorbidities especially pulmonary hypertension (PH) have been of significant interest in recent years [1]. The most recent classification system of pulmonary hypertension was published in the 2009 European Society of Cardiology Guidelines where the definition of PH was based on an increased mean pulmonary arterial pressure >£¿25£¿mmHg at rest. This broadly encompasses all clinical subgroups of PH as outlined by the 4th World Symposium on Pulmonary Hypertension in Dana Point, California, in 2008. This update classifies Group 1 as pulmonary arterial hypertension (PAH) due to idiopathic, heritable, or drug- and toxin-induced causes; it also includes
%U http://www.hindawi.com/journals/pm/2012/273591/