Suspected etiologies of newly diagnosed non-ischemic cardiomyopathy in our study population.

<p>Values are n (%).</p><p>HNCM – hypertrophic non-obstructive cardiomyopathy, HOCM – hypertrophic obstructive cardiomyopathy.</p

Patients` baseline characteristics.

<p>Values are n (%) or mean±standard deviation. BNP – brain natriuretic peptide, CMR – cardiac magnetic resonance imaging, CRP – C-reactive protein, CK – creatinkinase, DCM –dilated cardiomyopathy, HCM – hypertrophic cardiomyopathy, LGE – late gadolinium enhancement, LVEDD – left ventricular enddiastolic diameter, LVEF - left ventricular ejection fraction, NYHA – New York Heart Association, SD – standard deviation, TnI –troponin I, y – years.</p

Kaplan-Meier-curves for prediction of the composite endpoint stratified by presence of late gadolinium enhancement, left ventricular ejection fraction, serum levels of brain natriuretic peptide and troponin I.

<p>Kaplan-Meier-curves for prediction of the composite endpoint stratified by presence of late gadolinium enhancement, left ventricular ejection fraction, serum levels of brain natriuretic peptide and troponin I.</p

Baseline characteristics of patients with and without late gadolinium enhancement.

<p>Values are n (%) or mean±standard deviation. BNP – brain natriuretic peptide, CMR – cardiac magnetic resonance imaging, CRP – C-reactive protein, CK – creatinkinase, LGE – late gadolinium enhancement, LVEDD – left ventricular enddiastolic diameter, LVEF - left ventricular ejection fraction, NYHA – New York Heart Association, SD – standard deviation, TnI – troponin I, y – years.</p

Late gadolinium-enhanced (LGE) cardiac magnetic resonance imaging in short-axis orientation of the left ventricle in three different patients.

<p>Different types of LGE can be found, characteristic for entity of non-ischemic cardiomyopathy. (a) Epicardial LGE in a patient suspected of having (sub)acute myocarditis. (b) Non-ischemic cardiomyopathy with diffuse midwall stripe pattern of the septum, indicating idiopathic dilated cardiomyopathy. (c) Typical patchy LGE/fibrosis of the septal as well as the free lateral wall segments seen in hypertrophic cardiomyopathy.</p

Clinical outcome during follow-up.

<p>Values are n (%).</p>*<p>all-cause death, heart transplantation, aborted sudden death, sustained ventricular tachycardia, hospitalization due to decompensated heart failure.</p><p>HF – heart failure, LGE – late gadolinium enhancement, VT – ventricular tachycardia.</p

Results of univariate analysis of covariance (ANCOVA) for MIF and possible confounders in symptomatic CAD.

†<p>Hyperlipidemia was defined as triglycerides ≥175 mg/dl and/or LDL-cholesterol≥100 mg/dl and/or taking any of lipid lowering drugs.</p><p>ASA: aspirin.</p

Boxplots showing MIF-levels according to acuity of CAD compared with healthy volunteers.

<p>Boxplots showing MIF-levels according to acuity of CAD compared with healthy volunteers.</p

Patients with ACS due to plaque rupture showed higher plasma levels of MIF than patients with flow limiting stenotic lesions in coronary angiography.

<p>Patients with ACS due to plaque rupture showed higher plasma levels of MIF than patients with flow limiting stenotic lesions in coronary angiography.</p

Association of inflammatory markers IL-6, RANTES, MCP-1 and CRP with MIF levels in the study cohort.

<p>Association of inflammatory markers IL-6, RANTES, MCP-1 and CRP with MIF levels in the study cohort.</p