Background: Distal-type chronic thromboembolic pulmonary hypertension (CTEPH) is a fatal disease for which a new therapeutic strategy needs to be developed. We examined the effects of percutaneous transluminal pulmonary angioplasty (PTPA). Methods and Results:We prospectively enrolled 12 patients with distal-type CTEPH. After stabilizing their condition with pulmonary vasodilators, we then performed PTPA, which markedly improved pulmonary hemodynamics and pulmonary artery structure, as confirmed by angiography and optical coherence tomography, and also significantly improved their long-term prognosis compared with 39 historical controls.Conclusions: PTPA is a promising therapeutic option for distal-type CTEPH. (Circ J 2012; 76: 485 - 488)

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These results indicate that the occurrences of all types of CVDs and pneumonia were increased in somewhat different time courses after the Earthquake, including the first observation of the marked and prolonged increase in HF, emphasizing the importance of intensive medical management of all types of CVDs after great earthquakes.

C ytokines/chemokines and growth factors regulate pulmonary endothelial function and influence the development of pulmonary arterial hypertension (PAH).1 PAH is characterized by pulmonary vascular remodeling and perivascular inflammation, leading to right ventricular (RV) failure and premature death. [2][3][4][5] Endothelial dysfunction is a crucial pathogenic status that triggers a variety of vascular disorders, such as PAH. 6,7 Endothelial dysfunction is also considered a key underlying feature in most forms of clinical and experimental PAH, which is enhanced by inflammatory cytokines/ chemokines and growth factors.1,8 Indeed, we experience rapid progression and worsening of PAH, especially when complicated with infectious diseases, such as pneumonia and catheter-related infection.8 Pulmonary endothelial dysfunction in patients with PAH enhances pulmonary vascular remodeling through impaired release of vasodilators, such as nitric oxide (NO) and prostacyclin. [9][10][11] AMP-activated protein kinase (AMPK) is a heterotrimeric complex consisting of a catalytic subunit α and 2 regulatory subunits β and γ, and it is expressed in various tissues and Molecular Medicine© 2016 American Heart Association, Inc. ). In contrast, development of hypoxia-induced PH was accelerated in eAMPK -/-mice compared with controls. Furthermore, the exacerbation of PH in eAMPK -/-mice was accompanied by reduced endothelial function, upregulation of growth factors, and increased proliferation of pulmonary artery smooth muscle cells. Importantly, conditioned medium from endothelial cells promoted pulmonary artery smooth muscle cell proliferation, which was further enhanced by the treatment with AMPK inhibitor. Serum levels of inflammatory cytokines, including tumor necrosis factor-α and interferon-γ were significantly increased in patients with PAH compared with healthy controls. Consistently, endothelial AMPK and cell proliferation were significantly reduced by the treatment with serum from patients with PAH compared with controls. Importantly, long-term treatment with metformin, an AMPK activator, significantly attenuated hypoxiainduced PH in mice. Conclusions:

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