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

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

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

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

Trial flow chart.

<p>Trial flow chart.</p

Myocardial collagen content and MMP activity following pressure overload.

<p>(<b>A</b>) Myocardial collagen content measured by quantitative analysis of tissue hydroxyproline by HPLC in left ventricles from wild type (WT) and CCR7^−/− mice three weeks after sham-operation and aorta banding. (<b>B</b>) Total left ventricular MMP-2 activity measured in wild type (WT) and CCR7^−/− mice three weeks after aorta banding by zymography. Data are mean±SEM. *p<0.05 vs. sham operated in same genotype.</p

Circulating CCL21 levels in patients with AS and associations with clinical features and myocardial function.

<p>(<b>A</b>) Plasma levels of CCL21 in 136 patients with symptomatic aortic stenosis compared to healthy controls (n = 20). (<b>B</b>) Plasma levels of CCL21 in the aortic stenosis patients with and without coronary artery disease (CAD). Data in A and B are shown as a box and whisker plot with median (Q1, Q3) in the box and the whiskers representing the 5 and 95 percentile. Outliers are shown as filled circles. (<b>C</b>) Scatter plots showing associations between plasma CCL21 and aortic valve area, cardiac output, N-terminal pro-brain natriuretic peptide (NT-proBNP) and troponin T (TnT). (<b>D</b>) Association between plasma CCL21 and all-cause mortality in patients with symptomatic aortic stenosis. Receiver-operating characteristics curve analysis (area under the curve) for the predictive value of CCL21(left panel) and Kaplan–Meier curves showing the cumulative incidence of all-cause mortality according to median CCL21 (low, high) levels at enrolment (right panel).</p

Myocardial CCL21 and CCR7 mRNA and CCL21 protein expression in experimental LV pressure overload.

<p>Left ventricular expression of (<b>A</b>) CCL21 mRNA, (<b>B</b>) CCL21 protein levels and (C) CCR7 mRNA in mice with compensated (n = 7) and de-compensated (n = 7) hypertrophy three weeks after aortic banding, compared to sham operated mice (n = 7). mRNA levels were quantified by real-time RT-PCR and are presented relative to the gene expression of GAPDH. CCL21 protein levels were quantified by Western blotting. Data are mean±SEM. *p<0.05, **p<0.01 and ***p<0.001 vs. controls/sham.</p

Patient characteristics and association (Pearsson) with plasma CCL21 levels in 136 patients with symptomatic AS.

<p>Data are given as mean ±SD, ^†median (1. and 3. quartiles) or percentage of total number.</p><p>BMI, Body Mass Index; CAD, coronary artery disease; DM, Diabetes Mellitus; ARB, angiotensin receptor blocker; CO, cardiac output. To convert NT-proBNP values from <i>pM</i> to <i>pg</i>/<i>ml</i> multiply by 8.47.</p><p>*p<0.05,</p><p>**p<0.01,</p><p>***p<0.001.</p><p>Patient characteristics and association (Pearsson) with <u>plasma</u> CCL21 <u>levels</u> in 136 patients with symptomatic AS.</p