Cardiac Troponin T:Smaller Molecules in Patients with End-Stage Renal Disease than after Onset of Acute Myocardial Infarction

BACKGROUND: We have found previously that in acute myocardial infarction (AMI), cardiac troponin T (cTnT) is degraded in a time-dependent pattern. We investigated whether cTnT forms differed in patients with chronic cTnT increases, as seen with renal dysfunction, from those in the acute phase of myocardial infarction. METHODS: We separated cTnT forms by gel filtration chromatography (GFC) in end-stage renal disease (ESRD) patients: prehemodialysis (pre-HD) and post-HD (n = 10) and 2 months follow-up (n = 6). Purified (cTnT) standards, quality control materials of the clinical cTnT immunoassay (Roche), and AMI patients' sera also were analyzed. Immunoprecipitation and Western blotting were performed with the original cTnT antibodies from the clinical assay and antibodies against the N-and C-terminal end of cTnT. RESULTS: GFC analysis revealed the retention of purified cTnT at 27.5 mL, identical to that for cTnT in quality controls. For all ESRD patients, one cTnT peak was found at 45 mL, pre- and post-HD, and stable over time. Western blotting.illustrated that this peak corresponded to cTnT fragments CONCLUSIONS: We found that cTnT forms in ESRD patients are small

Cardiac troponin in ischemic cardiomyocytes: Intracellular decrease before onset of cell death

Aim: Cardiac troponin I (ant) and T (cTnT) are the most important biomarkers in the diagnosis of acute myocardial infarction (AMI). Nevertheless, they can be elevated in the absence of AMI. It is unclear if such elevations represent irreversible cardiomyocyte-damage or leakage from viable cardiomyocytes. Our objective is to evaluate whether cTn is released from viable cardiomyocytes in response to ischemia and to identify differences in the release of cTn and its molecular forms. Methods and results: HL-1 cardiomyocytes (mouse) were subjected to ischemia (modeled by anoxia with glucose deprivation). The total contents and molecular forms of cTn were determined in culture media and cell lysates. Cell viability was assessed from the release of lactate dehydrogenase (LDH). Before the release of LDH, the intracellular cTn content in ischemic cells decreased significantly compared to control (52% for cTnI; 23% for cTnT) and was not matched by a cTn increase in the medium. cTnI decreased more rapidly than cTnT, resulting in an intracellular cTnT/cTnI ratio of 25.5 after 24 h of ischemia. Western blots revealed changes in the relative amounts of fragmented cTnI and cTnT in ischemic cells. Conclusions: HL-1 cardiomyocytes subjected to simulated ischemia released cTnl and cTnT only in combination with the release of LDH. We find no evidence of cTn release from viable cardiomyocytes, but did observe a significant decrease in cTn content, before the onset of cell death. Intracellular decrease of cTn in viable cardiomyocytes can have important consequences for the interpretation of cTn values in clinical practice

The development of physical characteristics and kinetic abilities of 3-6 years old children

Název: Vývoj tělesných znaku a motorických schopností dětí ve věku 3-61et The development of physical characteristics and kinetic abilities of 3-6 years old children Cíle práce: Roční antropometrické sledování somatického vývoje a tělesné zdatnosti ve vybrané skupině dětí 3-6 let. Metoda: U souboru 53 dětí ve věku 3-6 let byly ve 4 měsíčních intervalech během jednoho kalendářního roku měřeny vybrané somatické znaky a byla testována tělesná zdatnost. Rodičům dětí byl dán k vyplnění dotazník pro zjištění sociálního zázemí dětí. Výsledky: Osvětlují korelace antropometrických charakteristik s tělesnou zdatností dětí ve věku 3-6 let. Hodnotí průměrné přírůstky sledovaných somatických znaku. Klíčová slova: antropometrické charakteristiky, tělesná zdatnost, přírůstky, normativní soubor, předškolní věk, motorický vývo

Adjusted multivariable linear regression analysis for the influence of CT and echocardiographic parameters and eGFR on hs-cTn concentrations (N = 549/1864).

<p>Almost identical standardized β values (stβ) for eGFR were observed when comparing adjusted multivariable models 1, 3 and 5, indicating the independent influence of eGFR on hs-cTn concentrations beyond echocardiographic parameters.</p

Cox proportional regression analysis for the association of hs-cTnT and hs-cTnI with adverse events in all patients or when stratified for eGFR ≥or <90mL/min/1.73m².

<p>Cox proportional regression analysis for the association of hs-cTnT and hs-cTnI with adverse events in all patients or when stratified for eGFR ≥or <90mL/min/1.73m².</p

Univariable and multivariable linear regression analysis, demonstrating the independent influence of eGFR on hs-cTn concentrations beyond CCTA parameters.

<p>Univariable and multivariable linear regression analysis, demonstrating the independent influence of eGFR on hs-cTn concentrations beyond CCTA parameters.</p

Cardiac Troponin T and i Release after a 30-km Run

Prolonged endurance-type exercise is associated with elevated cardiac troponin (cTn) levels in asymptomatic recreational athletes. It is unclear whether exercise-induced cTn release mirrors a physiological or pathological underlying process. The aim of this study was to provide a direct comparison of the release kinetics of high-sensitivity cTnI (hs-cTnI) and T (hs-cTnT) after endurance-type exercise. In addition, the effect of remote ischemic preconditioning (RIPC), a cardioprotective strategy that limits ischemia-reperfusion injury, was investigated in a randomized controlled crossover manner. Twenty-five healthy volunteers completed an outdoor 30-km running trial preceded by RIPC (4 × 5 min 220 mm Hg unilateral occlusion) or control intervention. hs-cTnT, hs-cTnI, and sensitive cTnI (s-cTnI) concentrations were examined before, immediately after, 2 and 5 hours after the trial. The completion of a 30-km run resulted in a significant increase in circulating cTn (time: all p <0.001), with maximum hs-cTnT, hs-cTnI, and s-cTnI levels of 47 ± 27, 69 ± 62, and 82 ± 64 ng/L (mean ± SD), respectively. Maximum hs-cTnT concentrations were measured in 60% of the participants at 2 hours after exercise, compared with maximum hs-cTnI and s-cTnI concentrations at 5 hours in 84% and 80% of the participants. Application of an RIPC stimulus did not reduce exercise-induced cTn release (time × trial: all p >0.5). In conclusion, in contrast to acute myocardial infarction, maximum hs-cTnT levels after exercise precede maximum hs-cTnI levels. Distinct release kinetics of hs-cTnT and hs-cTnI and the absence of an effect of RIPC favors the concept that exercise-induced cTn release may be mechanistically distinct from cTn release in acute myocardial infarction