Severe Pulmonary Arteriopathy Is Associated with Persistent Hypoxemia after Pulmonary Endarterectomy in Chronic Thromboembolic Pulmonary Hypertension.

Takayuki Jujo,Hatsue Ishibashi-Ueda,Masahisa Masuda,Toshihiko Sugiura,Nobuhiro Tanabe,Ayumi Sekine,Akira Naito,Koichiro Tatsumi,Fumiaki Kato,Seiichiro Sakao,Ayako Shigeta,Keiichi Ishida,Takao Takeuchi,Rintaro Nishimura,Masataka Kuwana

doi:10.1371/journal.pone.0161827

Takayuki Jujo, Hatsue Ishibashi-Ueda + Show 13 more

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https://doi.org/10.1371/journal.pone.0161827

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Abstract

BackgroundChronic thromboembolic pulmonary hypertension (CTEPH) is characterized by occlusion of pulmonary arteries by organized chronic thrombi. Persistent hypoxemia and residual pulmonary hypertension (PH) following successful pulmonary endarterectomy (PEA) are clinically important problems; however, the underlying mechanisms remain unclear. We have previously reported that residual PH is closely related to severe pulmonary vascular remodeling and hypothesize that this arteriopathy might also be involved in impaired gas exchange. The purpose of this study was to evaluate the association between hypoxemia and pulmonary arteriopathy after PEA.Methods and ResultsBetween December 2011 and November 2014, 23 CTEPH patients underwent PEA and lung biopsy. The extent of pulmonary arteriopathy was quantified pathologically in lung biopsy specimens. We then analyzed the relationship between the severity of pulmonary arteriopathy and gas exchange after PEA. We observed that the severity of pulmonary arteriopathy was negatively correlated with postoperative and follow-up PaO2 (postoperative PaO2: r = -0.73, p = 0.0004; follow-up PaO2: r = -0.66, p = 0.001), but not with preoperative PaO2 (r = -0.373, p = 0.08). Multivariate analysis revealed that the obstruction ratio and patient age were determinants of PaO2 one month after PEA (R2 = 0.651, p = 0.00009). Furthermore, the obstruction ratio and improvement of pulmonary vascular resistance were determinants of PaO2 at follow-up (R2 = 0.545, p = 0.0002). Severe pulmonary arteriopathy might increase the alveolar-arterial oxygen difference and impair diffusion capacity, resulting in hypoxemia following PEA.ConclusionThe severity of pulmonary arteriopathy was closely associated with postoperative and follow-up hypoxemia.

Highlights

Chronic thromboembolic pulmonary hypertension (CTEPH) is characterized by occlusion of pulmonary arteries by organized chronic thrombi [1,2]
We analyzed the relationship between the severity of pulmonary arteriopathy and gas exchange after pulmonary endarterectomy (PEA)
We observed that the severity of pulmonary arteriopathy was negatively correlated with postoperative and follow-up PaO2, but not with preoperative PaO2 (r = -0.373, p = 0.08)

Summary

Introduction

Chronic thromboembolic pulmonary hypertension (CTEPH) is characterized by occlusion of pulmonary arteries by organized chronic thrombi [1,2]. Pulmonary endarterectomy (PEA) is a surgical procedure in which the organized pulmonary thrombi are removed. Following PEA, many patients experience persistent hypoxemia and residual pulmonary hypertension (PH). Hypoxemia and residual PH have been observed in 50–60% [7] and 5–35% [8] of CTEPH patients, respectively, following successful PEA and are closely related to poor functional capacity (NYHA functional class III-IV) [9]. Chronic thromboembolic pulmonary hypertension (CTEPH) is characterized by occlusion of pulmonary arteries by organized chronic thrombi. Persistent hypoxemia and residual pulmonary hypertension (PH) following successful pulmonary endarterectomy (PEA) are clinically important problems; the underlying mechanisms remain unclear.

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