We report here the cloning and the characterization of the Tetrahymena pyriformis chaperonin-containing-TCP1 theta gene (TpCCT theta), an orthologue of the mouse chaperonin gene CCT theta. TpCCT theta gene is interrupted by eight introns, ranging in size between 91 and 419 nucleotides, and encodes a protein consisting of 540 amino acid residues (59.1 kDa), with a putative pI of 5.73. The amino acid sequence of TpCCT theta reveals 39.4-46.0% identity with the sequences of Candida albicans and mouse CCT theta subunits and 28.0-32.6% identity with the other TpCCT subunits known so far. We have studied the expression of this gene in exponentially growing Tetrahymena cells and in cells treated with colchicine for different times. The steady-state levels of CCT theta mRNA rapidly decrease in the first 30 min of colchicine treatment. Interestingly, treatment for subsequent 60 min gives expression levels higher than those found in exponentially growing cells.
Fundamento: Embora a elevação não isquêmica da troponina seja frequentemente observada em pacientes admitidos no pronto-socorro (PS), não há consenso quanto ao seu manejo.Objetivos: Este estudo teve como objetivo caracterizar os pacientes admitidos no PS com elevação da troponina nãoisquêmica e identificar potenciais preditores de mortalidade nessa população. Métodos: Este estudo observacional retrospectivo incluiu pacientes do PS com resultado positivo no teste da troponina entre junho e julho de 2015. Pacientes com diagnóstico clínico de síndrome coronariana aguda (SCA) foram excluídos. Os dados demográficos dos pacientes e as variáveis clínicas e laboratoriais foram extraídos dos prontuários médicos. Os dados do seguimento foram obtidos por 16 meses ou até a ocorrência de morte. O nível de significância estatística foi de 5%. Resultados: A elevação da troponina sem SCA foi encontrada em 153 pacientes no PS. A mediana (IIQ) de idade dos pacientes foi de 78 (19) anos, 80 (52,3%) eram do sexo feminino e 59 (38,6%) morreram durante o seguimento. A mediana do período de seguimento (IIQ) foi de 477 (316) dias. Os sobreviventes eram significativamente mais jovens 76 (24) vs. 84 (13) anos; p=0,004) e apresentaram uma maior proporção de elevação da troponina isolada (sem elevação da creatina quinase ou mioglobina) em duas avaliações consecutivas: 48 (53,9%) vs. 8 (17,4%), p<0,001. Os sobreviventes também apresentaram menor taxa de tratamento antiplaquetário e internação no mesmo dia. Na regressão logística multivariada com ajuste para variáveis significativas na análise univariada, a elevação isolada da troponina em duas avaliações consecutivas mostrou hazard ratio = 0,43 (IC95% 0,17-0,96, p=0,039); hospitalização, tratamento antiplaquetário anterior e idade permaneceram independentemente associados à mortalidade.Conclusões: A elevação isolada da troponina em duas medidas consecutivas foi um forte preditor de sobrevida em pacientes no PS com elevação da troponina, mas sem SCA.
Introduction
Hypertrophic cardiomyopathy (HCM) is characterized by a heterogeneous clinical expression with increased risk of sudden cardiac death (SCD) from ventricular arrhythmias (VAs).Several studies have shown that patients with malignant arrhythmias have increased electrical dispersion and in homogeneity of intraventricular conduction. Strain by echocardiography is an excellent tool for assessing regional and global left ventricular (LV) function and mechanical dispersion reflects heterogeneous myocardial contraction. We aimed to explore the value of strain parameters in prediction of VAs in HCM with LV preserved systolic function.
Methods
Retrospective observational study including all patients with HCM and ICD implanted in setting of primary prevention in our centre. Patients with LVEF < 40% or coronary artery disease were excluded. LV GLS was defined as the average of peak longitudinal strains from a 16 LV segments model, obtained from three apical views. Time to peak strain was defined as the time from onset Q/R wave on ECG to peak negative longitudinal strain during the entire cardiac cycle. Mechanical dispersion was defined as the standard deviation of time to peak negative strain in 16 LV segments. Patients with VA (group1) and patients without VA (group2) were compared.
Results
The study population included 48 patients, 63.3% of male gender. A family history of HCM was present in 64 pts (43%). All patients were under anti arrhythmic therapy (BB in 95.6%, other anti-arrhythmic in 28.2%). VAs (sustained and non sustained) were documented in 27 (55%) patients. The study groups did not differ regarding to mean age (54 ± 12 vs 56 ± 12 years, p = 0.67), male gender (54% vs 56%, p = 0.87) and BB therapy (91% vs 96%,p = 0.07). Mean LVEF was 58% in group 1 and 61% in group 1, p = 0.56; a LVOT gradient >30mmHg was present in 52% of group 1 pts and 45% of group 2 pts, p = 0.06. Mean wall thickness was 22mm vs 18 mm, p = 0.03, respectively.
GLS was significantly lower in group 1 (- 13.9 ±3.4 vs -16.1 ±3.5, p = 0.02), mechanic dispersion was significantly higher in group 1(81 ± 14 vs 60 ± 12ms, respectively, p = 0.01. Using a multivariate logistic regression model including variables included in SCD HCM risk score proposed by ESC mechanical dispersion (OR: 1.54 (1.03–8.7), p = 0,03) was a strong and independent risk predictor of VA. Using optimal cut-off values from ROC analyses, patients with mechanical dispersion >67 ms (AUC = 0.82, p= 0.02) had more VAs.
Conclusions
Mechanical dispersion and GLS may help to identify HCM patients with high risk of VAs and SCD.
Abstract P1541 Figure 1
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