Masahiro Kohzuki, MD, PhD
Department of Internal Medicine and Rehabilitation Science Tohoku University Graduate School of Medicine 1-1, Seiryo-cho, Aoba-ku Sendai, Japan; Tel. 022-717-7351; Fax: 022-717-7355; E-mail: kohzuki@med.tohoku.ac.jp
Chronic thromboembolic pulmonary hypertension (CTEPH) has a poor prognosis because of increased pulmonary arterial pressure (PAP) causing pulmonary hypertension and progressive right-sided heart failure.1,2 Typical symptoms are dyspnea on exertion, fatigability, and reduced quality of life.3 Balloon pulmonary angioplasty (BPA) has been reported to improve hemodynamics and functional capacity in patients with CTEPH who are not candidates for pulmonary endarterectomy.4,5 However, the effect of BPA on respiratory function in patients with CTEPH is unclear.
Recently, Akizuki et al3 investigated how BPA affects hemodynamics, ventilatory efficiency, and gas exchange in patients with CTEPH using right heart catheterization, respiratory function testing, and cardiopulmonary exercise testing (CPX).3 They enrolled patients with inoperable CTEPH who underwent BPA primarily in lower lobe arteries and upper and middle lobe arteries. They compared changes in hemodynamics and respiratory function between different BPA fields.
They showed differences in the effect of BPA on respiratory function in different BPA fields in patients with CTEPH. Mean PAP and pulmonary vascular resistance significantly improved. Oxygenation at rest and during exercise improved regardless of the BPA field.
However, the time course of changes in the percent predicted diffusion capacity of lung for carbon monoxide (% DLCO), The ventilation/CO2 production (VE/VCO2) slope, and FETCO2 was significantly different between lower and upper/middle lung BPA fields. %DLCO decreased after BPA in the lower lung field with no recovery. However, %DLCO increased after BPA in the upper middle lung field and continued to improve during the follow-up. VE/VCO2 slope significantly improved after BPA in the lower lung field and continued to improve during the follow-up. However, the VE/VCO2 slope remained unchanged after BPA in the upper/middle lung field. Therefore, the effect of BPA on respiratory function in patients with CTEPH differed depending on the lung field.3
Based on their results, they suggested that BPA in the lower lung field improves oxygenation and respiratory function parameters during exercise, such as VE/VCO2 slope and FETCO2, because of remarkable improvement in hemodynamics. They also suggested that BPA in the upper/middle lung field may improve oxygenation and respiratory function parameters at rest, such as %DLCO, caused by improvement in V/Q mismatch.3
However, reduced DLCO in CTEPH reflects not only the effect of low V/Q but also dead space ventilation (deadspace/tidal volume [VD/VT]) in regions with high V/Q.6 Further, one hypothesis suggests that in patients with CTEPH, a decrease in DLCO also indicates microvascular remodeling.6 Results of previous reports that DLCO remained unchanged even after successful pulmonary endarterectomy and BPA supported the hypothesis.7,8
These points of view suggest that reduced DLCO in patients with CTEPH may be caused by low V/Q, high V/Q and microvascular remodeling.6 Therefore, it is important to distinguish the effects of these three components when discussing DLCO in CTEPH. To obtain further evidence to support their hypothesis, Takei et al6 suggest analyzing the VD/VT and shunt fraction (Qs/Qt) to distinguish the amelioration of high V/Q and deterioration of low V/Q in different lung lobes.6
The goal of effective CTEPH management is to relieve symptoms, slow disease progression, improve exercise tolerance, prevent and treat complications, and improve prognosis and overall quality of life. The clinical presentation of CTEPH is similar to pulmonary arterial hypertension (PAH) with nonspecific symptoms. Further studies are required to elucidate to noninvasively examine the severity of CTEPH and to noninvasively distinguish CTEPH from PAH, for example, by respiratory function or ventilator gas analysis in different postures.
1. Hoeper MM, Mayer E, Simonneau G, Rubin LJ. Chronic thromboembolic pulmonary hypertension. Circulation. 2006; 113(16): 2011-2020. doi: 10.1161/CIRCULATIONAHA.105.602565
2. Jenkins D, Mayer E, Screaton N, Madani M. State-of-the-art chronic thromboembolic pulmonary hypertension diagnosis and management. Eur Respir Rev. 2012; 21(123): 32-39. doi: 10.1183/09059180.00009211
3. Akizuki M, Serizawa N, Ueno A, Adachi T, Hagiwara N. Effect of balloon pulmonary angioplasty on respiratory function in patientswith chronic thromboembolic pulmonary hypertension. Chest. 2017; 151(3): 643-649. doi: 10.1016/j.chest.2016.10.002
4. Mizoguchi H, Ogawa A, Munemasa M, Mikouchi H, Ito H, Matsubara H. Refined balloon pulmonary angioplasty for inoperable patients with chronic thromboembolic pulmonary hypertension. Circ Cardiovasc Interv. 2012; 5(6): 748-755. doi: 10.1161/ CIRCINTERVENTIONS.112.971077
5. Sugimura K, Fukumoto Y, Satoh K, et al. Percutaneous transluminal pulmonary angioplasty markedly improves pulmonary hemodynamics and long-term prognosis in patients with chronic thromboembolic pulmonary hypertension. Circ J. 2012; 76(2): 485-488. doi: 10.1253/circj.CJ-11-1217
6. Takei M, Kawakami T, Kuwahira I, Fukuda K. Elucidating the ventilation/perfusion mismatch and reduction of diffusing capacity for carbon monoxide in chronic thromboembolic pulmonary hypertension. Chest. 2017; 151(3): 725-726. doi: 10.1016/j.chest.2016.12.032
7. Takei M, Kataoka M, Kawakami T, et al. Respiratory function and oxygenation after balloon pulmonary angioplasty. Int J Cardiol. 2016; 212: 190-191. doi: 10.1016/j.ijcard.2016.03.061
8. Kapitan KS, Clausen JL, Moser KM. Gas exchange in chronic thromboembolism after pulmonary thromboendarterectomy. Chest. 1990; 98(1): 14-19. doi: 10.1378/chest.98.1.14
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