Editorial Type:
Article Category: Research Article
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Online Publication Date: 01 Aug 2009

Pulmonary Hypertension in Obstructive Sleep Apnea Syndrome

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Page Range: 131 – 140
DOI: 10.21693/1933-088X-8.3.131
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Keywords: obstructive sleep apnea; pulmonary hypertension; right heart failure; right ventricular hypertrophy
AP Chua, MD. AP Chua, MD. AP Chua, MD.
AP Chua, MD

Citation: Advances in Pulmonary Hypertension 8, 3; 10.21693/1933-088X-8.3.131

OA Minai, MD. OA Minai, MD. OA Minai, MD.
OA Minai, MD

Citation: Advances in Pulmonary Hypertension 8, 3; 10.21693/1933-088X-8.3.131

Introduction

Cor pulmonale has a well-described association with chronic respiratory diseases such as chronic obstructive pulmonary disease (COPD) and interstitial lung diseases.1 This association is felt to be the result of chronic hypoxic pulmonary vasoconstriction as well as a complex interaction of molecular pathways culminating in pulmonary vascular remodeling. The WHO clinical classification of pulmonary hypertension (PH) includes these patients in WHO Class III (PH associated with lung diseases and/or hypoxemia), which also incorporates patients with sleep disordered breathing.2 Obstructive sleep apnea (OSA)/hypopnea syndrome is the most widely studied of all sleep disordered breathing syndromes, occurring in approximately 10% of adult men and 5% of middleaged women.3 It is becoming increasingly clear that, in addition to excessive daytime sleepiness and snoring, OSA is associated with a variety of chronic cardiovascular sequelae, including hypertension, stroke, coronary artery disease, and sudden death.4 Pulmonary hypertension is a less appreciated complication of the physiologic changes associated with OSA.5–8 Patients with OSA have been shown to have transient, sometimes severe, elevations in pulmonary arterial pressures (PAP) during sleep;9 however, daytime, fixed PH has received less attention. Several factors associated with OSA may produce PH,5–8 including chronic hypoxia, left ventricular systolic dysfunction, left ventricular diastolic dysfunction, intermittent intrathoracic pressure changes, and associated comorbidities. This review is devoted to permanent, daytime PH in patients with OSA.

Definition of Pulmonary Hypertension in Obstructive Sleep Apnea

Pulmonary hypertension is defined by the presence of resting mean PAP (mPAP) >25 mmHg during right heart catheterization (RHC).1011 However, previous studies on PH in patients with COPD and OSA have defined PH as mPAP >20 mm Hg. Pulmonary arterial hypertension (PAH) is a subgroup further defined by the presence of pulmonary capillary wedge pressure (PCWP) ≤15 mm Hg and both PAH (PCWP ≤15 mm Hg) and pulmonary venous hypertension (PVH; PCWP >15 mm Hg) have been reported in patients with OSA.71213 Severe PH remains poorly defined and the suggested definition of resting mPAP ≥40 mm Hg has several limitations.714

Pulmonary Hemodynamics in Sleep

Several hemodynamic alterations have been described in association with normal sleep, including a decrease in systemic blood pressure and heart rate.15 However, limited data suggest that normal sleep has minimal impact on pulmonary hemodynamics.1617 This relationship is dramatically altered during episodes of apnea. 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).1618–21 These acute changes are more pronounced during rapid eye movement (REM) sleep than in non-REM sleep,91820–22 and are felt to be related to acute changes in intrathoracic pressure, hypoxia, and reflex mechanisms. Repeated apneic episodes with attendant hypoxia can produce a sustained augmentation of the pressor response of the pulmonary arterial system, which escalates progressively during the night.91823 It may be that the marked oxygen desaturation in REM sleep augments progressive increase in PAP without time to recover to baseline in the event of consecutive prolonged apneic episodes with short interapneic intervals.17

Epidemiology of Awake Pulmonary Hypertension in Obstructive Sleep Apnea

Similar to patients with chronic lung diseases, PH in the setting of OSA generally appears to be mild to moderate,2425 with severe PH being less common.72425 Largely as a result of concern over the invasive nature of RHC, the true prevalence of PH in OSA is not known due to a lack of large, population-based studies. Prevalence data on resting, awake PH in OSA is based primarily on retrospective case series or prospective cohort studies with poorly defined entry criteria (Table 1).712131822–37 This literature is further confounded by several limitations—the most important among which are a lack of consistency in defining PH, the varying methods used to detect its presence, and the lack of exclusion of other secondary causes with proper evaluation. It is generally accepted that measurement of PH in obese patients with OSA is especially prone to error when performed by Doppler echocardiography (DE),5103839 and although DE estimates of right ventricular systolic pressure (RVSP) correlate strongly with systolic PAP measured by RHC, there is large variation among individual patients (Figure 1).7 Despite these limitations of DE in making a diagnosis of PH in this population,57 several studies have used this methodology (Table 1). In addition, several comorbidities including left-sided cardiac disease, COPD, and obesity may have an impact on the occurrence of PH and were not always excluded.

Table 1. Prevalence of Resting, Awake Pulmonary Hypertension in Obstructive Sleep Apea
Table 1.
Figure 1:. Correlation between pulmonary artery systolic pressure (PASP) measured by RHC and RVSP measured by transthoracic echocardiography (A) in a cohort of 83 patients with OSA. (B) Degree of agreement in individual patients showing inaccuracy of RVSP from TTE compared to PASP by RHC. Adapted from Minai et al7 with permission.Figure 1:. Correlation between pulmonary artery systolic pressure (PASP) measured by RHC and RVSP measured by transthoracic echocardiography (A) in a cohort of 83 patients with OSA. (B) Degree of agreement in individual patients showing inaccuracy of RVSP from TTE compared to PASP by RHC. Adapted from Minai et al7 with permission.Figure 1:. Correlation between pulmonary artery systolic pressure (PASP) measured by RHC and RVSP measured by transthoracic echocardiography (A) in a cohort of 83 patients with OSA. (B) Degree of agreement in individual patients showing inaccuracy of RVSP from TTE compared to PASP by RHC. Adapted from Minai et al7 with permission.
Figure 1: Correlation between pulmonary artery systolic pressure (PASP) measured by RHC and RVSP measured by transthoracic echocardiography (A) in a cohort of 83 patients with OSA. (B) Degree of agreement in individual patients showing inaccuracy of RVSP from TTE compared to PASP by RHC. Adapted from Minai et al7 with permission.

Citation: Advances in Pulmonary Hypertension 8, 3; 10.21693/1933-088X-8.3.131

The prevalence of PH determined by RHC or DE in patients with OSA, in studies excluding cardiopulmonary disease, ranges from 17% to 41% (Table 1). In the largest series published to date, 17% of a sample of 220 patients with OSA met diagnostic criteria for PH.1024 The true gender distribution of PH in OSA patients is unknown. Female preponderance has been described in several other forms of PH and has been attributed to genetic predisposition, the role of estrogen, and higher prevalence of autoimmune disease in females.10 Two recent studies of PH in patients with OSA have reported a higher prevalence of PH among females than males.724 The accuracy and significance of this finding, if any, requires larger studies in view of the predominantly male nature of the OSA population.

Coexistence of underlying chronic lung disease increases the risk of developing PH, and most studies showing a >50% prevalence of PH in patients with OSA have not excluded patients with chronic cardiopulmonary disease.7182228 Studies have indicated that the presence of obstructive82840 or restrictive7 ventilatory defects on spirometry indicate a group at higher risk. On the other hand, even studies of patients without significant cardiopulmonary disease have included patients with small airway abnormalities35 or mild hypoxemia.1232 In a European population with lower body mass index (BMI) (32±6 kg/m2),30 a lower prevalence of PH was reported than an Australian population with a higher BMI (37 [range 24–54 kg/m2]).25 Other studies have reported no association between the prevalence or severity of PH and BMI in patients with OSA.733

Exercise-induced PH has also been described in patients with OSA.18244142 In a cohort of 49 consecutive patients with OSA, Hetzel et al41 found that 6 (12%) patients had resting PH (mPAP >20 mm Hg), whereas 39 (80%) patients had PH during exercise (mPAP >30 mm Hg). All patients had normal pulmonary vascular resistance, and the main contributors to PH were elevated BMI, total lung capacity, and elevated PCWP.

Right Ventricular Hypertrophy and Right Heart Failure in Obstructive Sleep Apnea

Early studies in patients with OSA reported on the occurrence of clinical cor pulmonale.2843 However, it is not clear that cor pulmonale equates to RV systolic failure in this population since RV diastolic dysfunction and solute and water retention may produce similar clinical findings. O'Hearn et al and Whyte et al4445 found lower extremity edema to be a highly specific indicator of right heart failure in OSA patients with a BMI >40 kg/m2. Unlike patients with PAH who have chronic RV pressure overload and markedly elevated pulmonary vascular resistance, OSA patients may have chronic volume overload with milder elevation in pulmonary vascular resistance, suggesting that these patients may not have a large decrease in the cross-sectional area of the pulmonary vasculature.4446

Cineradiographic observation in humans has demonstrated a progressive enlarging of the heart size throughout apnea.47 Thus, RV hypertrophy and dilation could stem from the mechanical effect of long-term, recurrent upper airway obstruction.48 The Framingham Heart Study found a small but significant increase in RV wall thickness using DE, suggestive of elevated PAP, in patients with severe OSA.48 Thickness of the RV wall was independently and positively correlated with the severity of OSA. The prevalence of RV abnormalities has varied widely between 0% and 71% among studies (Table 2).28434449–55 The validity and clinical significance of this observation remains poorly defined given the obvious limitations of DE in imaging the RV in morbidly obese patients with OSA.

Table 2. Prevalence of Right Ventricular Dysfunction and Right Ventricular Hypertrophy in Obstructive Sleep Apnea
Table 2.

Following the Framingham Heart Study, several studies reported decreased RV contractility and RV failure in patients with severe OSA.56–58 Right ventricular dysfunction, however, appears to be less common compared to PH alone and is frequently associated with coexisting left heart or chronic lung diseases with daytime hypoxemia.445455 Echocardiographic studies in OSA patients without significant pulmonary comorbidities found elevated awake arterial partial pressure of carbon dioxide (PaCO2), apnea-hypopnea index (AHI) >40,55 and obesity to be important risk factors for reduced RV ejection fraction.59 Mild abnormalities in RV function have been reported in the absence of daytime, resting PAH and may presumably occur as a consequence of the nocturnal hypoxia and attendant hemodynamic alterations. Current evidence, however, suggests that the occurrence of RV systolic failure in OSA requires the presence of additional comorbidities such as chronic lung disease or left ventricular dysfunction.244360

Pathogenesis and Pathophysiology (Figure 2)

The role of apnea and hypoxia

Figure 2:. Pathophysiology of pulmonary hypertension in obstructive sleep apnea.Figure 2:. Pathophysiology of pulmonary hypertension in obstructive sleep apnea.Figure 2:. Pathophysiology of pulmonary hypertension in obstructive sleep apnea.
Figure 2: Pathophysiology of pulmonary hypertension in obstructive sleep apnea.

Citation: Advances in Pulmonary Hypertension 8, 3; 10.21693/1933-088X-8.3.131

Patients with OSA have normal gas exchange when awake and only become hypoxemic during sleep.61 Animal experiments have shown that intermittent hypoxia (4–8 hours per day) is sufficient to induce a sustained rise in PAP and RV hypertrophy.62–66 Coccagna and colleagues20 have demonstrated occurrence of PAP elevation with sleep-related hypoxemia, and acute rise in PAP during obstructive events has been shown to correlate inversely with the degree of oxygen desaturation.91665 The mild increase in PAP during a respiratory event is due to an interplay of multiple factors including hypoxic pulmonary vasoconstriction, mechanically induced negative intrathoracic pressure from heightened inspiratory muscle response against an occluded airway, and direct effect on the vasculature from reflex mechanisms inducing variations in heart rate, cardiac output, and increased left-sided filling pressures. However, most studies have reported no association between severity of OSA (as measured by AHI) and the presence or severity of PH.374866–68

It is well established that chronic daytime hypoxia can lead to PH and cor pulmonale.69 Hypoxic pulmonary vasoconstriction improves ventilation-perfusion matching by shunting blood to betterventilated lung zones and induces a rise in PAP.70 The deleterious effects of episodic hypoxia on pulmonary hemodynamics have been extensively described;62–6471 however, the mechanisms by which chronic hypoxia leads to pulmonary vascular remodeling are complex and poorly understood. In addition to causing vasoconstriction and shear stress, chronic hypoxia exerts its effect on the vascular endothelium and smooth muscle cells (mainly the small muscular pulmonary arteries and nonmuscular precapillary arterioles) to release vasoconstrictive, pro-proliferative, and mitogenic mediators. Several mediators including endothelin-1, vascular endothelial growth factor, angiotensin II, nitric oxide, endothelial apoptotic factors, angiotensin converting enzyme, inflammatory mediators (IL-8, IL-6), reactive oxygen species, and various transcription factors such as hypoxia-inducible factor-1 have been implicated in this process.72 These events lead to angiogenesis, promote muscle and fibroblast proliferation, produce extension of smooth muscle into nonmuscularized vessels, and increase vascularity.72 The pathologic features of hypoxic vasculopathy include concentric intimal thickening secondary to proliferation of endothelial cells, smooth muscle cells, and myofibroblasts, medial hypertrophy with longitudinally oriented smooth muscle bundles of the muscular pulmonary arteries, adventitial proliferation, and abnormal extracellular matrix deposition.72–74 There is muscularization of the arterioles, with well-developed distinct elastic laminae and medial muscle layer extending to the smaller vessels. Extreme capillary proliferation may also be seen in some patients with severe OSA and RV hypertrophy.72

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. Individual variation in ventilatory responsiveness to hypoxia demonstrated in awake OSA patients75 could also modulate the magnitude of PAP changes,17 although its role in PH remains controversial. So far it has not been convincingly demonstrated that a reduced chemosensitivity, possibly secondary to repetitive nighttime hypoxemic and hypercapnic episodes, can lead to daytime hypoxemia or PH.3076 Although hypercapnia is known to potentiate the hypoxic response, evidence does not support it being a major factor for OSA-associated PAP changes. Whether the repetitive upper airway collapse and large intrathoracic negative pressure swings with nocturnal oxygen desaturation and hypercapnia leading to marked variation in PAP underlies the chronic PAP elevation in OSA requires further study.182021232777

The hypothesis that isolated nocturnal hypoxemia may lead to permanent PH is supported by studies demonstrating PH in patients with normal daytime PaO225 or very slight hypoxemia.33 A decrease in PAP after 3–6 months of nighttime continuous positive airway pressure (CPAP) therapy without an associated improvement in spirometry or awake blood gases323778 further strengthens this hypothesis.

The role of comorbidities

Several studies have shown that OSA patients with PH often have concomitant cardiac or pulmonary disease, leading to the speculation that such comorbidities are a prerequisite for the development of significant PH and RV failure in OSA. It has been suggested that PH in association with OSA is mainly precapillary in nature;8 however, given the prevalence of morbid obesity, hypertension, and left ventricular systolic and diastolic dysfunction in this population, it is likely that postcapillary factors37505679–82 play an important role. Diastolic dysfunction and left ventricular hypertrophy with elevated PCWP have been demonstrated in OSA patients without any other evidence of underlying cardiac disease and may contribute to the diagnosis of PH during rest and exercise.5883–85 Diastolic dysfunction can produce elevated PCWP in severely obese OSA patients with normal left ventricular function.414454 Chaouat et al24 demonstrated a rise in mPAP from 26.0±5.8 to 46.7±12 mm Hg during submaximal steady-state exercise, partly explained by an exercise-induced rise in PCWP. Two other studies have reported similar findings, suggesting that PVH due to diastolic dysfunction is an important factor in patients with OSA.1842 Whether exercise-induced PH identifies a subgroup of OSA patients at higher risk of developing resting PH requires further study.

Patients with both COPD and OSA (also known as “overlap syndrome”) are at a higher risk of developing PH than patients with either condition alone. Chronic obstructive pulmonary disease is often the primary cause of alveolar hypoventilation in OSA.8 Studies have clearly demonstrated that presence of airway obstruction predicts hypoxemia-hypercapnia and PH.78142428408687 In these patients with PH, bronchial obstruction is usually mild-moderate, and the degree of blood gas disturbances may not be severe.8

The role of obesity

The likelihood of PH in morbid obesity is increased considerably when OSA is present.3444 Bady et al demonstrated that the severity of obesity and the associated changes in lung function play an important role in the pathogenesis of PH in patients with OSA.12 Another study showed that greater age and increased BMI distinguished OSA patients with mild PH from those without PH.32 However, other studies72533 have not found a significant difference in body weight in OSA patients with and without PH. Discrepancies in the findings among the series in the literature could be accounted for by the differences in the prevalence of severe obesity in each series and across continents where these studies were conducted.8 Obesity hypoventilation syndrome, which is defined by a clinical triad of obesity, awake chronic hypercapnia, and OSA, is associated with a higher prevalence of PH and greater PAP levels.8889 Whether obesity confers an added risk for PH over and above that due to OSA and the associated comorbidities needs to be better defined.

Role of humoral factors

The effect of humoral factors on awake PAP remains speculative. Increased natriuretic peptides and decreased nitric oxide have been found in OSA patients90 and levels improved with CPAP treatment.91 Both circulating humoral substances and genetic factors could influence individual responsiveness to hypoxia and therefore the levels of PAP reached after obstructive events causing similar degree of oxygen desaturations.17

Clearly we are in need of studies to better define the role of pulmonary vasoconstriction, vascular remodeling, and preclinical changes in pulmonary circulation and the impact of genetic factors on changes in pulmonary hemodynamics due to OSA.

Predictors of Pulmonary Hypertension in Obstructive Sleep Apnea

The presence of comorbidities such as COPD and left-sided cardiac disease increases the likelihood of PH in patients with OSA. Studies have shown that the development of PH is correlated with lower daytime baseline arterial oxygen tension (PaO2) and longer duration of nocturnal hypoxemia (SaO2 <90%), which are important surrogate markers of severity in OSA.12132433 In a recent study, younger age, female gender, obesity, and increased duration of nocturnal desaturation were found to be associated with the presence of PH.7 However, presumably because of the small sample size and the relatively low prevalence of PH in this population, no prediction models based on demographics and polysomnographic variables had been reported until recently.

Clinical Significance of Pulmonary Hypertension in Obstructive Sleep Apnea

Pulmonary hypertension can lead to functional decline and poor prognosis in several diseases, including connective tissue diseases, pulmonary fibrosis, and COPD.92 Previous studies of PH in patients with OSA have not addressed this association, largely because of the small numbers of patients with PH and the shortterm nature of these studies.5 A recent report found that OSA patients with PH had lower functional capacity (as measured by 6-minute walk distance) and more dyspnea compared to OSA patients without PH.7 This association did not reach statistical significance largely due to the small sample size. This study further showed that mortality was increased in patients with PH (Figure 3) and that in addition to factors such as age, forced expiratory volume in 1 second, diffusion capacity for carbon monoxide, and AHI, pulmonary hemodynamics were important correlates of increased mortality in patients with OSA.7 The only other report to examine the hemodynamic predictors of mortality in OSA did not find resting mPAP to be a predictor of mortality on multivariate analysis.93

Figure 3:. Kaplan-Meier survival estimates in 83 patients with OSA (A) with and without PH and (B) those without PH compared to those with PAH and PVH. Adapted from Minai et al7 with permission.Figure 3:. Kaplan-Meier survival estimates in 83 patients with OSA (A) with and without PH and (B) those without PH compared to those with PAH and PVH. Adapted from Minai et al7 with permission.Figure 3:. Kaplan-Meier survival estimates in 83 patients with OSA (A) with and without PH and (B) those without PH compared to those with PAH and PVH. Adapted from Minai et al7 with permission.
Figure 3: Kaplan-Meier survival estimates in 83 patients with OSA (A) with and without PH and (B) those without PH compared to those with PAH and PVH. Adapted from Minai et al7 with permission.

Citation: Advances in Pulmonary Hypertension 8, 3; 10.21693/1933-088X-8.3.131

Management of Obstructive Sleep Apnea – Pulmonary Hypertension

The American College of Chest Physicians consensus panel has recommended that patients with PH should be evaluated for OSA but did not recommend routine screening for PH in patients with OSA.5

Given the likelihood of comorbidities, an important initial step should be to look for and manage comorbidities, including diastolic dysfunction and COPD. In addition, exertional and nocturnal hypoxia should be corrected with oxygen supplementation or CPAP therapy as appropriate. Oxygen supplementation has been shown to reduce PAP in patients with COPD and nocturnal hypoxemia.94 In dog models of artificially-induced recurrent episodes of obstructive apnea, blunting of PAP elevation results from restoration of arterial oxygen saturation following O2 supplementation.9596 Tracheostomy has also been shown to cause a dramatic reduction in PAP in OSA patients with sleep-related oxygen desaturation.2097

Treatment of OSA with CPAP has been shown to lower systolic blood pressure, improve quality of life, and improve arterial oxygen saturation in patients without concomitant COPD. It is unclear whether the mild PH found among OSA patients without concomitant cardiopulmonary diseases requires treatment. In addition to relieving the upper airway obstruction and minimizing the intrathoracic pressure swings, long-term treatment with CPAP can produce significant improvement in daytime arterial oxygenation,98 raising the expectation of improvement or stabilization of PH, similar to that seen in COPD patients receiving long-term oxygen supplementation.94 Studies examining the effect of nasal CPAP treatment on PH in patients with OSA are sparse and have reported conflicting results (Table 3).323755597890919899 Prevention of high PAP peak through application of CPAP during sleep was first demonstrated by Marrone et al.100 Studies by Sforza et al and Chaouat et al5999 did not demonstrate a change in PAP following nasal CPAP use for 1 and 5 years respectively. These studies were limited by the very small subset of patients with PH in the OSA group (N=8 and 4 respectively). Two small, uncontrolled studies addressed the positive impact of CPAP therapy on pulmonary hemodynamics in OSA patients with PH. Collop and coworkers98 showed that treatment of OSA with nasal CPAP reverses PH in morbidly obese women without clinically significant lung disease. A prospective, uncontrolled, single-center case series by Sajkov et al78 showed significant decrease in the daytime PAP and pulmonary vascular response to hypoxia after 4 months of nasal CPAP treatment in 5 of the 20 OSA patients with mild PH. These were followed by larger prospective, controlled trials. Alchanatis et al,32 in a study of OSA patients (N=29) without other pulmonary or cardiac disease, reported a reduction in mPAP in both groups of OSA patients with (N=6) and without PH (N=23) after 6 months of CPAP treatment. Arias and colleagues37 demonstrated a reduction in systolic PAP after CPAP therapy in 10 obese patients in the first placebo-controlled trial of OSA treatment in PH.

Table 3. Effects of Pulmonary Arterial Pressure Therapy in Obstructive Sleep Apnea on Pulmonary Hemodynamics and Biochemical Markers
Table 3.

Based on the current limited data, we can conclude that CPAP therapy has a modest role in improving pulmonary hemodynamics in OSA and is less likely to normalize the more severe elevations in PAP.5 The role of additional vasomodulatory agents in this setting requires further study. It had been reported that the response of RV function to OSA treatment is better than that of PAP.2855101 Right ventricular ejection fraction has been shown to improve significantly after long-term CPAP treatment in both pediatric and adult populations.2855101

Dramatic weight reduction brought about by surgical options may also play a role in improving pulmonary hemodynamics in OSA. Matilde et al102 showed a significant improvement in pulmonary hemodynamics following a marked reduction in body weight and resolution of OSA following bariatric surgery. In their study, the PAP completely normalized in 4 out of 28 patients with mPAP ranging from 31 to 80 mm Hg. There was also a significant reduction in mean systolic PAP in the group of obese patients in whom OSA resolved post-surgery (mean systolic PAP 61±16 mm Hg before to 43±9 mm Hg after surgery).

Summary

Obstructive sleep apnea modestly increases the risk of PH and causes mild elevation of PAP as compared to PAH. Development of PH is likely multifactorial, involving both precapillary and postcapillary processes. Due to a lack of population-based studies, the true prevalence of PH is not known; however, it is clear that patients with comorbidities are at higher risk. In patients with milder elevations in PAP, CPAP therapy has the potential to improve pulmonary hemodynamics, although the role of adjunctive vasomodulatory therapy should be explored in those with more significant elevations. Longer-term studies of various treatment options with an emphasis on functional improvement, quality of life, and survival are required to properly assess their role.

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Copyright: © 2009 Pulmonary Hypertension Association
AP Chua, MD
AP Chua, MD

OA Minai, MD
OA Minai, MD

Figure 1:
Figure 1:

Correlation between pulmonary artery systolic pressure (PASP) measured by RHC and RVSP measured by transthoracic echocardiography (A) in a cohort of 83 patients with OSA. (B) Degree of agreement in individual patients showing inaccuracy of RVSP from TTE compared to PASP by RHC. Adapted from Minai et al7 with permission.

Figure 2:
Figure 2:

Pathophysiology of pulmonary hypertension in obstructive sleep apnea.

Figure 3:
Figure 3:

Kaplan-Meier survival estimates in 83 patients with OSA (A) with and without PH and (B) those without PH compared to those with PAH and PVH. Adapted from Minai et al7 with permission.

Contributor Notes

Address for reprints and other correspondence: minaio@ccf.org
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