C hronic thromboembolic pulmonary hypertension (CTEPH) is defined as a progressive disease of increasing pulmonary vascular resistance because of chronic thromboembolism in the pulmonary arteries that leads to pulmonary hypertension (PH), right-sided heart failure, and a grave prognosis. [1][2][3][4][5][6][7][8][9] Several studies have demonstrated the efficacy of medical therapies using anticoagulation and pulmonary vasodilators, including several newly developed agents. 1,10,11 The most powerful conventional therapeutic strategy for CTEPH is invasive surgical pulmonary endarterectomy (PEA).12-16 Surgical therapy is indicated when the thromboembolic lesions are located in the proximal pulmonary arteries or lobar branches.9 Thus, there are some patients in whom PEA is not indicated; furthermore, some patients continue to suffer from severe PH despite treatment with PEA. Editorial see p 744A few reports have demonstrated the efficacy of balloon pulmonary angioplasty. In 1988, 1 case report demonstrated the efficacy of pulmonary angioplasty after acute pulmonary embolism.17 In 2001, Feinstein et al 18 showed that pulmonary hemodynamics were markedly improved by pulmonary angioplasty in 18 patients with CTEPH, and that 11 of 18 patients developed reperfusion pulmonary edema. However, this therapy has not been developed further since then, and is rarely performed now. Thus, it is important to take into account the experiences of this therapy and the data regarding its complications, to consider the possibility of pulmonary angioplasty as an alternative therapy for selected patients with CTEPH.Therefore, the objectives of this study were (1) to investigate the clinical efficacy of percutaneous transluminal pulmonary Background-Chronic thromboembolic pulmonary hypertension leads to pulmonary hypertension and right-sided heart failure. The purpose of this study was to investigate the efficacy of percutaneous transluminal pulmonary angioplasty (PTPA) for the treatment of chronic thromboembolic pulmonary hypertension. Methods and Results-Twenty-nine patients with chronic thromboembolic pulmonary hypertension underwent PTPA. One patient had a wiring perforation as a complication of PTPA and died 2 days after the procedure. In the remaining 28 patients, PTPA did not produce immediate hemodynamic improvement at the time of the procedure. However, after follow-up (6.0 ± 6.9 months), New York Heart Association functional classifications and levels of plasma B-type natriuretic peptide significantly improved (both P<0.01). Hemodynamic parameters also significantly improved (mean pulmonary arterial pressure, 45.3 ± 9.8 versus 31.8 ± 10.0 mm Hg; cardiac output, 3.6 ± 1.2 versus 4.6 ± 1.7 L/min, baseline versus followup, respectively; both P<0.01). Twenty-seven of 51 procedures in total (53%), and 19 of 28 first procedures (68%), had reperfusion pulmonary edema as the chief complication. Patients with severe clinical signs and/or severe hemodynamics at baseline had a high risk of reperfusion pulmonary edema. Conclusions-PTPA imp...

Pulmonary Flow Grade score is useful in determining therapeutic efficacy, and PEPSI is highly supportive to reduce the risk of RPE after PTPA. Using these 2 indexes, PTPA could become a safe and common therapeutic strategy for CTEPH.

Overnight fluid shift from the legs to the neck and lungs may contribute to the pathogenesis of obstructive sleep apnoea (OSA) and central sleep apnoea (CSA). We hypothesised that exercise training will decrease the severity of OSA and CSA in patients with coronary artery disease (CAD) by decreasing daytime leg fluid accumulation and overnight rostral fluid shift.Patients with CAD and OSA or CSA (apnoea-hypopnoea index >15 events per h) were randomised to 4 weeks of aerobic exercise training or to a control group. Polysomnography, with measurement of leg, thoracic and neck fluid volumes and upper-airway cross-sectional area (UA-XSA) before and after sleep, was performed at baseline and follow-up.17 patients per group completed the study. Apnoea-hypopnoea index decreased significantly more in the exercise group than in the control group (31.1±12.9 to 20.5±9.4 versus 28.1±13.5 to 27.0±15.1 events per h, p=0.047), in association with a greater reduction in the overnight change in leg fluid volume (579±222 to 466±163 versus 453±164 to 434±141 mL, p=0.04) and by a significantly greater increase in the overnight change in UA-XSA in the exercise group (p=0.04).In patients with CAD and sleep apnoea, exercise training decreases sleep apnoea severity via attenuation of overnight fluid shift and an increase in UA-XSA.