Troponin I elevation after elective percutaneous coronary interventions: Prevalence and risk factors.

Troponin elevation after coronary angioplasty is a prognostic marker associated with significant morbidity and mortality, although its prevalence varies according to clinical and procedural characteristics. We analyzed the frequency of post-procedural enzyme elevation among 112 elective interventions between 2013 and 2014 in a private hospital in Brazil. Troponin increase was observed in 62.5% of the procedures, and was related to age, female sex, low pre-procedural hemoglobin, prior angiotensin converting enzyme inhibitor or angiotensin receptor blocker use and multivessel angioplasty. PCI is not a risk free procedure and these results underscore the importance of a careful clinical assessment before its utilization.

Troponin I elevation and all-cause mortality after elective percutaneous coronary interventions.

BACKGROUND/PURPOSE: Although troponin I (TnI) elevation and myocardial injury after percutaneous coronary interventions (PCI) are frequent findings, their prognoses remain controversial. We aimed to determine the association between any or ≥5 times TnI elevation after elective PCI and subsequent one year mortality rates and long term survival. METHODS: Consecutive patients admitted for elective PCI between January 2013 and December 2014 were retrospectively analyzed by chart review in two hospitals in Rio de Janeiro. Only patients with post-PCI TnI measurements were included. Clinical, angiographic and procedural characteristics were correlated with any or ≥5 times TnI elevation, as well as 1year mortality and long term survival. RESULTS: A total of 407 interventions were included in the analysis. Post-PCI TnI elevation was observed in 74.7% of cases and ≥5 times elevations occurred in 41.3%. Age≥70years, female gender and multistenting were predictors of enzyme elevation. Prior aspirin or hypoglycemic therapy were protective factors. One year mortality was significantly associated with any TnI elevation (6.6% vs 1.05%, p=0.035) and values ≥5 times above the normal limit predicted the highest mortality rates (8.13% vs 3.14%, p=0.031). Survival of patients with single vessel disease was also adversely affected by ≥5 times enzyme elevation (log-rank: p=0.039). CONCLUSION: Troponin I elevation after elective PCI is frequent and associated with progressively higher mortality rates at 1year. A cutoff value ≥5 times the 99th percentile, currently defined as myocardial injury, appears to be an even more significant predictor of this outcome, even in lower risk subgroups.

Dasatinib Reduces Lung Inflammation and Fibrosis in Acute Experimental Silicosis.

Silicosis is an occupational lung disease with no effective treatment. We hypothesized that dasatinib, a tyrosine kinase inhibitor, might exhibit therapeutic efficacy in silica-induced pulmonary fibrosis. Silicosis was induced in C57BL/6 mice by a single intratracheal administration of silica particles, whereas the control group received saline. After 14 days, when the disease was already established, animals were randomly assigned to receive DMSO or dasatinib (1 mg/kg) by oral gavage, twice daily, for 14 days. On day 28, lung morphofunction, inflammation, and remodeling were investigated. RAW 264.7 cells (a macrophage cell line) were incubated with silica particles, followed by treatment or not with dasatinib, and evaluated for macrophage polarization. On day 28, dasatinib improved lung mechanics, increased M2 macrophage counts in lung parenchyma and granuloma, and was associated with reduction of fraction area of granuloma, fraction area of collapsed alveoli, protein levels of tumor necrosis factor-α, interleukin-1ß, transforming growth factor-ß, and reduced neutrophils, M1 macrophages, and collagen fiber content in lung tissue and granuloma in silicotic animals. Additionally, dasatinib reduced expression of iNOS and increased expression of arginase and metalloproteinase-9 in silicotic macrophages. Dasatinib was effective at inducing macrophage polarization toward the M2 phenotype and reducing lung inflammation and fibrosis, thus improving lung mechanics in a murine model of acute silicosis.