What is more affected in patients wit obstructive sleep apnea: the right or the left heart?

Abstract

EDITORIAL What is more affected in patients with obstructive sleep apnea: the right or the left heart? 217 diameter, suggesting that severe OSA may cause pulmonary artery dilation.Taken these original and interesting studies together, we have observed a common limitation, likely due to an ethical issue. Indeed, both papers did not evaluate pulmonary arterial pressure by right cardiac catheterization, nor evaluated the left ventricular alterations, so we could not clarify the exact associations among the severity of OSA, pulmonary artery dilation, and pulmonary artery pressure. In addition, these studies found a positive linear correlation between the pulmonary artery dimension and severity of OSA, without considering the role of the body mass index (BMI) in OSA, since the body fat distribution and BMI have been invariably recognized to be strongly correlated to the apnea-hypopnea index, and thus to the severity of OSA. 8 OSA typically causes only mild PH, which generally does not require treatment. However, these patients often present with more severe degrees of PH when they have comorbid conditions contributing to hypoxemia, such as obesity hypoventilation syndrome.9 In addition, cardiomyopathy characterized by eccentric ventricular hypertrophy and diastolic heart failure is a well-recognized condition in severely obese patients. The chronically elevated left ventricular filling pressure might be transmitted into the pulmonary venous system, leading to elevated pulmonary venous pressures, arteriolar remodeling, and ultimately to persistent elevated pulmonary vascular resistance.10 The interplay between OSA, insulin resistance, and elevated left ventricular filling is likely responsible for endothelial dysfunction, with consequent PH in obese individuals. Thus, obesity may promote endothelial pulmonary dysfunction, while the coexistence with OSA might accelerate progression to PH. 11,12Obstructive sleep apnea (OSA) is a chronic disease, which, in predisposed subjects, causes repeated episodes of upper airway collapse, apnea, and arousals during sleep. Intraluminal airway pressure and pharyngeal muscle activity are widely recognized as major determinants of the size and collapsibility of the upper airways.1 Excessively negative intrathoracic pressure, generated during inspiratory efforts against the collapsed upper airway, chronically occurs during sleep. The pulmonary artery, being an elastic low pressure system, may be easily stretched by the repetitive negative intrathoracic pressure. 2 The persistent mechanical stress during sleep may be likely responsible for pulmonary artery dilation in OSA. 3Furthermore, repetitive hypoxia-induced pulmonary arterial vasoconstriction, occurring during obstructive sleep apneas, may promote remodeling of pulmonary vasculature, resulting in pulmonary artery dilation, with consequent pulmonary hypertension (PH). 4 The study of Dobrowolski et al 5 clearly demonstrates the existing relationship between pulmonary artery dilation and the presence of newly diagnosed severe OSA in p...

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