18 research outputs found

    Study design and signs of STEMI.

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    <p>A) Thrombolysis was performed during proinflammatory reaction launched by ischemic condition. PCI and injection followed 40–77 hours (mean time presented in the figure) after onset of symptoms and cytokine sampling was performed 2 and 4 days after that. B) Troponin level were measured immediately after onset of symptoms and 2 and 4 days later. As a sign of STEMI, the levels increased similarly in both study groups but declined 2 days later. No statistically significant differences existed (control N = 12; BMMNC n = 14; p = 0.71). C) Contrast opacification of left ventricular angiograms was used to analyse EF at the baseline and after 6 months to evaluate effect of BMMNC transplantation on cardiac function. There was grater absolute increase in EF in BMMNC treated patients. However, the difference was not statistically significant possibly due to small sample size (control n = 11; BMMNC n = 13; p = 0.15).</p

    Cytokine levels of single patients.

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    <p>Due to high variability among cytokine concentrations of the single patients, no clear trend in levels existed in either study groups. This illustrates the complexity of cytokine network and systemic factors contributing on inflammation process and cardiac repair.</p

    Baseline characteristics of the study subjects (n = 958) according to the presence or absence of NAFLD.

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    <p>The values are means ± SD, absolute numbers with percentages or percentages alone. The medication data is expressed as number of subjects and percentages. Differences were tested by the ANOVA test for continuous variables and Pearson Chi-Squared test for categorical variables. ANP, atrial natriuretic peptide; hs-CRP, high-sensitive C-reactive protein; γ-GT, gamma-glutamyl transpeptidase; ALT, alanine aminotransferase; ACE, angiotensin converting enzyme.</p><p>Baseline characteristics of the study subjects (n = 958) according to the presence or absence of NAFLD.</p

    Association between NAFLD (n = 958) and risk of AF during follow-up.

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    <p>Values are expressed as ORs (95% CIs) as assessed by multivariate Cox regression analyses. Independent predictors of AF are highlighted in bold type. BMI, body mass index; ALT, alanine transferase; CAD, coronary artery disease; ANP, atrial natriuretic peptide; LVMI, left ventricular mass index; hs-CRP, high-sensitive C-reactive protein.</p><p>Association between NAFLD (n = 958) and risk of AF during follow-up.</p

    The left atrial diameter (mm) by transient elastography tertiles.

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    <p>The mean LAD in the first TE tertile (n = 21) was 39mm (SD ±7mm), in the second tertile (n = 28) 45mm (SD ± 7mm) and in the third tertile (n = 26) 48mm (SD ± 8mm) (p<0.001). After adjustments (BMI, age, gender, amount of alcohol intake (g/week), smoking (pack years), Quick index, systolic blood pressure) the statistical significance prevailed (p = 0.012). Abbreviations: LAD, left atrial diameter; TE, transient elastography; BMI, body mass index.</p

    Association of genetic variants with the MI phenotypes and the LD structure at 1p13.3 (GRCh37 Chromosome 1:111,397,480–111,863,701).

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    <p>The P-values for both imputed and genotyped variants are depicted, while the LD is calculated from the genotyped SNPs only. Known genes from the RefSeq database are shown together with potential regulatory regions marked by histone 3 lysine 27 acetylation (Layered H3K27Ac) and DNase I hypersensitivity clusters from the Encode consortium.</p

    Summary of the genome-wide significant association results on chromosome 1p13.3.

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    <p><sup>a</sup> Major/minor</p><p><sup>i</sup> Imputed variant</p><p>MAF, minor allele frequency;</p><p>OR, odds ratio;</p><p>MI, myocardial infarction;</p><p>STEMI, ST elevation myocardial infarction;</p><p>NSTEMI, non-ST elevation myocardial infarction</p><p>Statistical significance tested using logistic regression setting age, sex, and the first ten genomic principal components as covariates. The 95% confidence interval is reported in parentheses for the OR estimates.</p><p>Summary of the genome-wide significant association results on chromosome 1p13.3.</p
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