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Background: High-sensitivity cardiac troponin T (hs-cTnT) assay is used in the diagnosis and risk assessment of patients with symptoms of myocardial infarction. This study was undertaken to establish an age-specific 99th percentile cutoff value for hs-cTnT in Chinese population, and to evaluate its potential for early prediction of non-ST-segment elevation myocardial infarction (NSTEMI) in middle-aged patients., Methods: Troponin T levels in blood obtained from healthy Chinese adults were assayed using hs-cTnT. The distribution was plotted and 99th percentiles were determined by nonparametric statistics. Prediction performance at the conventional cutoff (14 ng/L) recommended by the Roche company was compared with the age-specific cutoff for NSTEMI in 100 middle-aged patients (40-60 years of age) with acute chest pain., Results: The 99th percentile for hs-cTnT was 14 ng/L for patients ≥60 years of age and 11 ng/L for those <60. Fifty of the 100 patients were finally diagnosed with NSTEMI. The age-specific 99th percentile cutoff value of 11 ng/L identified a higher number of patients with NSTEMI than the conventional 14 ng/L cutoff (46 vs. 40 patients), although the difference was not statistically significant (P = 0.084). In addition, the sensitivity of hs-cTnT increased from 80 to 92% and the negative predictive values increased from 82.4 to 91.8%., Conclusion: Using 11 ng/L as a decision-making cutoff point for hs-cTnT facilitated earlier prediction of NSTEMI in middle-aged patients than the conventional 14 ng/L cutoff. Further studies are needed to confirm this finding in larger group of patients., (© 2013 Wiley Periodicals, Inc.)

Background and Purpose: Sirtuin 6 (SIRT6) is involved in regulation of glucose and fat metabolism. However, its possible contribution to cardiac dysfunction remains to be determined. In the present study, the effect of SIRT6 on cardiac hypertrophy induced by angiotensin II (AngII) and the underlying molecular mechanisms were investigated., Experimental Approach: The expression and deacetylase activity of SIRT6 were measured in hypertrophic cardiomyocytes induced by AngII. After SIRT6 overexpression by transfection, or depletion by RNA interference in neonatal rat cardiomyocytes, cellular hypertrophy was monitored by measuring cell surface area and the mRNA levels of hypertrophic biomarkers. Further, the interaction between SIRT6 and the transcription factor NF-κB was investigated by co-immunoprecipitation, confocal immunofluorescence microscopy and luciferase reporter gene assay. The expression and deacetylase activity of SIRT6 were measured in vivo, using the abdominal aortic constriction (AAC) model of cardiac hypertrophy in rats., Key Results: In AngII-induced hypertrophic cardiomyocytes and also in AAC-induced hypertrophic hearts, the expression of SIRT6 protein was upregulated, while its deacetylase activity was decreased. Overexpression of wild-type SIRT6 but not its catalytically inactive mutant, attenuated AngII-induced cardiomyocyte hypertrophy. We further demonstrated a physical interaction between SIRT6 and NF-κB catalytic subunit p65, whose transcriptional activity could be repressed by SIRT6 overexpression., Conclusions and Implications: Our findings suggest that SIRT6 suppressed cardiomyocyte hypertrophy in vitro via inhibition of NF-κB-dependent transcriptional activity and that this effect was dependent on its deacetylase activity., (© 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society.)