Results from cardiac imaging exams, New York Heart Association (NYHA) classification and quality of life measurements.

<p>*This row represents left ventricular ejection fraction (LVEF) by magnetic resonance imaging (MRI) or, if the latter result was not available at both baseline and follow-up, LVEF by echocardiography (E/D, N = 18). ^† p < 0.05 for difference between baseline and follow-up. CI: confidence interval; EDV: end diastolic left ventricular internal volume; ESV: end systolic left ventricular internal volume; NT-proBNP: N-terminal pro-B-type natriuretic peptide; LDL: low density lipoprotein; MLHFQ: Minnesota Living with Heart Failure Questionnaire; VAS: visual analogue scale.</p

Baseline data stratified according to treatment allocation.

<p>NYHA: New York Heart Association; TIA: transient ischemic attack; ACEI: angiotensin converting enzyme inhibitor; ARB: angiotensin receptor blocker.</p

Results of blood tests.

<p>* p < 0.05 for difference between baseline and follow-up. CI: confidence interval; LDL: low density lipoprotein; HDL: high density lipoprotein; NT-proBNP: N-terminal pro-B-type natriuretic peptide; sTNF-R1: soluble tumour necrosis factor receptor 1; MCP-1: monocyte chemotactic protein-1; gp130: Soluble glycoprotein 130; MMP-9: matrix metalloproteinase-9; PINP: procollagen type I N-terminal pro-peptide; PIIINP: procollagen type III N-terminal pro-peptide.</p

Correlation between left ventricular ejection fraction as measured by echocardiography and as measured by magnetic resonance imaging.

<p>Data from baseline and follow-up are pooled. The Pearson correlation coefficient between results obtained by magnetic resonance imaging (MRI) and results obtained by echocardiography was 0.82 (p < 0.001).</p

Trial flow chart.

<p>Trial flow chart.</p

Changes in markers of inflammation and extracellular matrix turnover.

<p>Changes in C-reactive protein (CRP), soluble tumor necrosis factor receptor type 1 (sTNF-R1), and procollagen type I and III N-terminal pro-peptides (PINP and PIIINP) stratified by treatment allocation. p-values for between-group differences in changes were computed by independent group t-tests. While PINP increased more in patients treated with rosuvastatin as compared to patients treated with placebo (p  =  0.03), treatment did not affect any of the other markers of inflammation or matrix remodeling. Boxes: 25–75 percentiles; whiskers: 5–95 percentiles.</p

Increased expression of IL-9 and IL-9R in human atherosclerotic carotid plaques.

<p>mRNA levels of IL-9 (<b>A</b>) and IL-9R (<b>B</b>) in patients with asymptomatic (n = 13) and symptomatic (n = 55) carotid stenosis and in non-atherosclerotic vessels obtained from organ donors (common iliac artery, n = 10) were quantified by real-time RT-PCR. No IL-9R transcripts were detected in control samples. Levels of IL-9 and IL-9R expression are related to reference gene β-actin. Data are presented as mean±SEM. ***p<0.0001 versus controls.</p

IL-9 promotes IL-17 release in PBMCs.

<p>PBMCs from healthy controls (Ctr, n = 5) and patients with unstable angina (UAP, n = 5) were stimulated with IL-9 (100 ng/ml) with and without co-stimulation with PHA (20 µg/ml). Panel <b>A</b> shows the absolute release of IL-17 after culturing for 72 hours as assessed by EIA measurements in cell-free supernatants (controls to the left, patients to the right). Panel <b>B</b> shows the percentage change in IL-17 release when adding IL-9 to unstimulated cells from healthy controls (left) and patients (right). Panel <b>C</b> shows the percentage change in IL-17 release when adding IL-9 to PHA-stimulated cells from healthy controls (left) and patients (right). Data are given as mean±SEM. *p<0.05 versus comparative condition without IL-9 (unstimulated and PHA stimulated, respectively). #p<0.05 versus healthy controls.</p

Increased plasma levels of IL-9 in patients with carotid and coronary atherosclerosis.

<p>Panel <b>A</b> shows plasma levels of IL-9 in patients with asymptomatic (n = 56) and symptomatic (n = 88) carotid plaques and in healthy controls (n = 28). Panel <b>B</b> shows plasma levels of IL-9 in patients with STEMI (n = 42) at admission and at different time points after PCI (2, 7 and 60 days). For comparison, levels were also measured in healthy controls (n = 10). Data are presented as mean±SEM. *p<0.05, **p<0.01 and ***p<0.0001 versus controls. #p<0.05 and ##p<0.01 versus levels at admission.</p

Increased expression of IL-9 and IL-9R in immune cells from patients with coronary atherosclerosis.

<p>mRNA levels of IL-9 and IL-9R were quantified by real-time RT-PCR in CD3⁺ T cells (<b>A</b> and <b>B</b>) and in monocytes (<b>C</b>) from healthy controls (n = 11) and from patients with stable (SAP, n = 11) and unstable (UAP, n = 17) angina. mRNA levels are related to the reference gene 18S (T cells) and β-actin (monocytes) and normalized to levels in healthy controls. For monocyte analyses, only samples from 9 of the controls and 13 of the patients with unstable angina were available. No IL-9R transcripts were detected in patients or controls in these cells. Bars represent mean±SEM. #p<0.05 versus stable angina, *p<0.05 and **p<0.01 versus controls.</p