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Controversy remains over whether intermittent hypoxia (such as that produced by apneic events during sleep) is adequate to produce pulmonary vascular remodeling resulting in awake, resting PH.
Obstructive sleep apnea modestly increases the risk of PH and causes mild elevation of PAP as compared to PAH.
Fletcher EC, Luckett RA, Miller T, Costarangos C, Kutka N, Fletcher JG Pulmonary vascular hemodynamics in chronic lung disease patients with and without oxyhemoglobin desaturation during sleep.
Several studies have described significant increases in PAP from the middle of the apnea to the end of the apnea, which reaches a maximum during the first few breaths once the obstruction is relieved (postapneic hyperventilation).24 25 26 27 28 These acute changes are more pronounced during rapid eye movement (REM) sleep than in non-REM sleep,29 30 31 32 33 and are felt to be related to acute changes in intrathoracic pressure, hypoxia, and reflex mechanisms.
It has been suggested that PH in association with OSA is mainly precapillary in nature;168 however, given the prevalence of morbid obesity, hypertension, and left ventricular systolic and diastolic dysfunction in this population, it is likely that postcapillary factors169 170 171 172 173 174 175 play an important role.
Pulmonary artery hypertension and sleep-disordered breathing: ACCP evidence-based clinical practice guidelines. Frequency and impact of pulmonary hypertension in patients with obstructive sleep apnea syndrome. Pulmonary hypertension in the obstructive sleep apnoea syndrome: Prevalence, causes and therapeutic consequences. Screening, early detection, and diagnosis of pulmonary arterial hypertension: ACCP evidence-based clinical practice guidelines.
Continuous recording of the pulmonary and systemic arterial pressure during sleep in syndromes of hypersomnia with periodic breathing.
Manifestation of pulmonary hypertension during REM sleep in obstructive sleep apnea syndrome. Time course of pulmonary artery pressure during sleep in sleep apnoea syndrome: role of recurrent apnoeas. Frequency and mechanism of daytime pulmonary hypertension in patients with obstructive sleep apnoea syndrome. Daytime pulmonary hypertension in patients with obstructive sleep apnea: the effect of continuous positive airway pressure on pulmonary hemodynamics.
Daytime pulmonary hemodynamics in patients with obstructive sleep apnea without lung disease.


Diagnostic strategies for suspected pulmonary arterial hypertension: a primer for the internist. Pulmonary hemodynamics in obstructive sleep apnea: frequency and causes of pulmonary hypertension. Pulmonary circulation at rest and during exercise in patients with obstructive sleep apnea before and after one year of treatment with CPAP Pneumonol Alergol Pol. Role of daytime hypox emia in the pathogenesis of right heart failure in the obstructive sleep apnea syndrome. Lower extremity edema and pulmonary hypertension in morbidly obese patients with obstructive sleep apnea. Echocardiographic features of the right heart in sleep-disordered breathing: The Framingham heart study Am J Respir Crit Care Med.
Left ventricular hypertrophy independent of hypertension in patients with obstructive sleep apnoea. Right ventricular hypertrophy detected by echocardiography in patients with newly diagnosed obstructive sleep apnea. Right ventricular dysfunction in obstructive sleep apnoea: reversal with nasal continuous positive airway pressure. Comparison of cardiac structural and functional changes in obese otherwise healthy adults with versus without obstructive sleep apnea. Impact of obstructive sleep apnea on right ventricular global function: sleep apnea and myocardial performance index.
Long-term effects of treatment with nasal continuous positive airway pressure on daytime lung function and pulmonary hemodynamics in patients with obstructive sleep apnea. Pulmonary hypertension and right ventricular hypertrophy caused by intermittent hypoxia and hypercapnia in the rat. Transient hypoxemia during sleep in chronic obstructive pulmonary disease is not a sleep apnea syndrome.
The cardiovascular effects of obstructive sleep apnoeas: analysis of pathogenic mechanisms.


Continuous positive airway pressure treatment improves pulmonary hemodynamics in patients with obstructive sleep apnea. Left ventricular function in patients with obstructive sleep apnoea syndrome before and after treatment with nasal continuous positive airway pressure.
Evidence for left ventricular dysfunction in patients with obstructive sleep apnoea syndrome. Left ventricular hypertrophy is a common echocardiographic abnormality in severe obstructive sleep apnea and reverses with nasal continuous positive airway pressure. Prevalence of left ventricular hypertrophy in persons with and without obstructive sleep apnea.
The nocturnal secretion of cardiac natriuretic peptides during obstructive sleep apnoea and its response to therapy with nasal continuous positive airway pressure. Decreased plasma levels of nitric oxide derivatives in obstructive sleep apnoea: response to CPAP therapy. Comparison of baseline characteristics and survival between patients with idiopathic and connective tissue disease-related pulmonary arterial hypertension. Cardiopulmonary hemodynamics during sleep in subjects with chronic obstructive pulmonary disease. Five-year effects of nasal continuous positive airway pressure in obstructive sleep apnoea syndrome. Effect of bariatric surgery on obstructive sleep apnea and hypopnea syndrome, electrocardiogram, and pulmonary arterial pressure.



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