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Objectives The aim of this study was to assess the prognostic impact of post-procedural troponin T increase and mortality in patients undergoing percutaneous coronary intervention (PCI) for chronic total occlusion (CTO) to define the threshold at which procedure-related myocardial injury drives mortality. Background Coronary CTO recanalization represents the most technically challenging PCI. The complexity harbors a significant increased risk for complications with CTO PCI with compared with non-CTO PCI. However, there are evidenced biomarker cutoff levels that help identify those patients at risk for unfavorable clinical outcomes. Methods A total of 3,712 consecutive patients undergoing PCI for at least 1 CTO lesion were enrolled, and comprehensive troponin T measurements were performed 6, 8, and 24 h after the procedure. All-cause mortality was defined as the primary study endpoint. Results Using spline curve analysis, a more than 18-fold increase of troponin above the upper reference limit was significantly associated with mortality. In a Cox regression analysis, the crude hazard ratio was 2.32 (95% confidence interval: 1.83 to 2.93; p Conclusions This large-scale outcome study demonstrates for the first time the prognostic value of post-procedural troponin T elevation after PCI in patients with CTOs. A threshold was defined for procedure-related myocardial injury in patients with CTOs to differentiate them from those without CTOs that may help guide post-procedural clinical care in this high-risk patient population.

Drs. Yacob and Garcia-Garcia address an issue of great importance, namely the impact of complications during percutaneous coronary intervention (PCI) in chronic total occlusions (CTOs) and the impact of complications on our proposed definition of periprocedural myocardial injury after CTO-PCI. We

Objective Chronic thromboembolic pulmonary hypertension (CTEPH) is characterized by one or more of the following features: intraluminal thrombus organization, fibrous stenosis, and complete obliteration of major pulmonary arteries, amenable to significant improvement by pulmonary endarterectomy (PEA) or balloon pulmonary angioplasty, and medical treatments with vasodilators. Because treatment practices and outcomes differ in Europe versus Japan, we hypothesized that population-based characteristics of pulmonary vascular phenotypes may exist in Austria compared with Japan. The objectives of this study were to analyze clinical characteristics, hemodynamics, and PEA specimens in consecutive patients with CTEPH undergoing PEA in Austria and Japan. Methods Clinical features, hemodynamics, and PEA specimens were collected and analyzed in patients with CTEPH undergoing PEA, and clinical features and hemodynamics were collected and analyzed in patients with not-operated CTEPH and in patients with nonthromboembolic pulmonary arterial hypertension. Results Apart from key differences between Austrian and Japanese patients regarding body size, lung function vital capacity, cardiac output, and serum high-density lipoprotein levels, Austrian patients were more likely to be obese, have greater hematocrits and greater white blood cells counts, greater C-reactive protein levels, and significantly elevated serum myeloperoxidase levels compared with Japanese patients with CTEPH. Analysis of PEA specimens demonstrated more proximal thrombus and more fresh red thrombus components in Austrian patients. Conclusions This study documents an inflammatory thrombotic phenotype in Austrian compared with Japanese patients with CTEPH that may be a determinant of differential treatment outcomes.

Malignant pleural mesothelioma (MPM) is a malignant neoplasm arising from mesothelial cells existing in pleura. It is difficult to identify a crucial symptom in patients with MPM, and there is no standard curative therapy for this malignancy. The incidence of MPM is increasing worldwide, and many patients can not survive more than one year after diagnosis. MPM is an asbestos-related disease, and it is believed that the incidence is closely related to the amount and time of exposure to asbestos. Since the latency period after exposure to asbestos is very long, the incidence may increase over the next two decades. Therefore, it is important to understand the biology of MPM, and to find a molecular target for its therapy. Three of human malignant pleural mesothelioma (MPM) cell lines (NCIH28, NCI-H2052, NCI-H2452) and a human pleural mesothelial cell line (MeT-5A) were analyzed by proteomics with the use of twodimensional gel electrophoresis (2-DE) and liquid chromatographytandem mass spectrometry (LC-MS/MS). From the results of 2-DE between MeT-5A and three MPM cell lines, 9 protein spots showed increased expression levels in MPM cells compared to MeT-5A. These spots were analyzed by LC-MS/MS analysis, and identified by a peptide sequence tag. Identified increased spots included 78 kDa glucose regulated protein (GRP78), heat shock 70 kDa protein (HSP70), protein disulfide isomerase A3, annexin A3, peroxiredoxin-2 and 14 kDa phosphohistidine phosphatase. Western blotting using specific antibodies against GRP78 and HSP70 confirmed the elevated expression level of GRP78 and HSP70 in MPM cell lines compared to MeT-5A cells. These results suggest that GRP78 and HSP70 expression is likely to be associated with the tumorigenesis of MPM, and they may be expectable as biomarkers or therapeutic targets for MPM. Disclosure: All authors have declared no conflicts of interest.