4 research outputs found

    Korelacja odsetka hemoglobiny glikowanej z ciężkością choroby wieńcowej występująca u młodych osób niezależnie od tradycyjnych czynników ryzyka

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    Introduction: In this study, we aimed to investigate the relationship between glycated haemoglobin (HbA1c) levels and the severity of coronary artery disease (CAD) in < 40 years old patients. Material and methods: The study population consisted of 211 premature coronary atherosclerotic patients (pCAP) (aged 36.4 &#177; 2.5 years) and 160 control subjects (36.4 &#177; 2.4 years). The severity of CAD was evaluated by the Gensini scoring system. HbA1c levels and the other basic biochemical parameters were analysed, and relations with severity of CAD were evaluated. Results: There were statistically significant differences in serum HbA1c levels between the two groups (pCAP = 6.1 &#177; 1.8%, control = 4.7 &#177; 1.2%, p < 0.001). HbA1c levels significantly positively correlated with the Gensini score in pCAP (r = 0.662, p < 0.001). In linear multivariate regression analysis (including age, sex, HbA1c, smoking, diabetes mellitus and hypertension as dependent parameters), only HbA1c was found to be an independent risk factor for the presence of severe CAD (Beta = 0.374, p < 0.001). In ROC curve analysis, the optimal cut-off value of HbA1c to predict severe CAD was 6.52%, with 74.4% sensitivity and 75.1% specificity (area under the curve 0.781, 95% confidence interval 0.661 to 0.901, p < 0.001). Conclusions: HbA1c levels were found to be correlated with the Gensini score in pCAP with and without diabetes. In this respect, glucose metabolism abnormalities, indicated by HbA1c, may play an important role in premature CAD. (Endokrynol Pol 2012; 63 (5): 367-371)Wstęp: Niniejsze badanie przeprowadzono w celu oceny zależności między odsetkiem hemoglobiny glikowanej (HbA1c) a ciężkością choroby wieńcowej (CAD) u chorych w wieku < 40 lat. Materiał i metody: Badana populacja składała się z 211 chorych z przedwczesną miażdżycą tętnic wieńcowych (pCAP) (w wieku 36,4 &#177; 2,5 roku) i 160 osób stanowiących grupę kontrolną (36,4 &#177; 2,4 roku). Ciężkość CAD określano na podstawie wartości wskaźnika Gensiniego. Przeanalizowano odsetek HbA1c oraz inne wyjściowe parametry biochemiczne i oceniono ich zależności z ciężkością CAD. Wyniki: Stwierdzono statystycznie istotne różnice między grupami w zakresie stężeń HbA1c w surowicy (pCAP = 6,1 &#177; 1,8%, grupa kontrolna = 4,7 &#177; 1,2%; p < 0,001). Wartości HbA1c były istotnie skorelowane z wartościami wskaźnika Gensiniego u chorych z pCAP (r = 0,662; p < 0,001). W wieloczynnikowej analizie regresji liniowej (w której uwzględniono wiek, płeć, stężenie HbA1c, palenie tytoniu, cukrzycę i nadciśnienie tętnicze jako zmienne zależne) jedynie stężenie HbA1c okazało się niezależnym czynnikiem ryzyka wskazującym na występowanie ciężkiej CAD (Beta = 0,374; p < 0,001). Jak wykazano w analizie krzywych ROC, optymalny punkt odcięcia wartości HbA1c pozwalający prognozować ciężką CAD wynosi 6,52%, przy czułości metody 74,4% i swoistości 75,1% (pole pod krzywą 0,781, 95-proc. przedział ufności 0,661&#8211;0,901; p < 0,001). Wnioski: U osób z pCAP, zarówno chorych na cukrzycę, jak i bez tej choroby, stwierdzono korelacje między wartościami HbA1c i wskaźnikiem Gensiniego. Jak wynika z powyższych obserwacji, zaburzenia metabolizmu glukozy, których wyznacznikiem jest odsetek HbA1c, mogą odgrywać ważną rolę w rozwoju przedwczesnej CAD. (Endokrynol Pol 2012; 63 (5): 367-371

    The Effects of Ivabradine on Left Ventricular Synchronization and Tei Index in Patients with Systolic Heart Failure

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    WOS: 000392042800008PubMed: 28115808Background: The aim of our study was to evaluate in stable outpatients with systolic heart failure (HF) the 3 months effect of ivabradine on LV synchronization and Tei index in stable outpatients with systolic HF. Methods: We evaluated prospectively 40 (30 males, 10 females) patients with HF. All patients were evaluated before and after treatment by transthoracic M mode, two dimensional (2D), pulsed-wave (PW), continuous wave (CW), color flow and tissue Doppler imaging (TDI) and tissue synchronization imaging (TSI). Standard deviation of Ts of the 12 LV segments (Ts-SD-12) is the most widely used parameter of intra-LV asynchrony. Results: Thirty men and 10 women with mean +/- SD age of 64.7 +/- 9.9 years were included in this study. Most of the patients benefitted from some degree of clinical improvement, 12/16 (75.0%) from NYHA III to II and 18/24 (75.0%) from II to I, respectively. Resting heart rate was significantly reduced after ivabradine treatment (84.3 +/- 11.4 vs. 66.5 +/- 11.5 bpm, p <0.001). E/E' and Tei index were significantly changed after ivabradine treatment (17.3 +/- 9.0 vs. 14.8 +/- 7.1, p = 0.02 and 0.86 +/- 0.74 vs. 0.81 +/- 0.69, p = 0.02). Intra-LV synchrony parameters Ts-SD-12 and Ts-12 were significantly reduced after ivabradine (46.8 +/- 13.6 vs. 42.7 +/- 13.1, p = 0.01 and 142.5 +/- 44.0 vs. 128.5 +/- 45.2, p = 0.009). Conclusions: The present study demonstrated that adding ivabradine to the standard therapy reduced HR and significantly improved LV ventricular asynchrony and Tei index in systolic HF patients

    The percentage of ALK-positive cells and the efficacy of first-line alectinib in advanced non-small cell lung cancer: is it a novel factor for stratification? (Turkish Oncology Group Study)

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    Introduction Alectinib is an effective second-generation ALK tyrosine kinase inhibitor (TKI) used in the first-line treatment of patients with advanced ALK-positive NSCLC. Recent studies demonstrated that the percentage of ALK-positive tumor cells in patient groups receiving crizotinib might affect outcomes. This study aimed to investigate whether the percentage of ALK-positive cells had a predictive effect in patients with advanced NSCLC who received first-line Alectinib as ALK-TKI. Materials and methods This retrospective study included patients with advanced-stage NSCLC who received alectinib as a first-line ALK-TKI and whose percentage of ALK-positive cells was determined by FISH at 27 different centers. Patients who received any ALK-TKI before alectinib were not included in the study. Patients were separated into two groups according to the median (40%) value of the percentage of ALK-positive cells (high-positive group >= 40% and low-positive group = 60%, the median PFS was 4.5, 17.1, and 26 months, respectively, and could not be reached in the >= 60% group. Conclusion Our study demonstrated that the efficacy of alectinib varies significantly across patient subgroups with different percentages of ALK-positive cells. If these findings are prospectively validated, the percentage of ALK-positive cells may be used as a stratification factor in randomized trials comparing different ALK-TKIs
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