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Objective: Dilated cardiomyopathy (DCM) is characterised by systolic dysfunction and simultaneous dilatation of the left or both ventricles. Besides other causes, the innate immune system plays a major role in the development and progression of the disease. To uncover links between molecular mechanisms and disease progression our group has focused on the toll like receptor 4 (TLR-4)/ myeloid differentiation factor-2 (MD-2) system.

Purpose: We already reported that soluble MD-2 (sMD-2) is a risk factor for survival in patients with DCM. In the current study, we determined levels of lipopolysaccharide (LPS) and high mobility group box protein 1 (HMGB1) in serum/plasma as main interaction partners of MD-2.

Methods: We included 136 patients (age 53.9 years [23.4–81.1]; female n=22) with reduced left ventricular ejection fraction (LVEF <40%) due to DCM and elevated left ventricular end-diastolic diameter (LVEDD) according to Henry (>117%). Mortality was monitored up to 13 years after first hospital admission. During the follow-up period 37 patients died. Within the first four years (mean 1.57 [0.02–3.46]) 20 patients died (DCM1) (age 55.5 years [23.4–77.9]; female n=2). A second group (n=17) died later, after four years (mean 6.4 [4.0–13.1]) (DCM2) (age 57.2 years [29.5–73.9]; female n=2). The third group (n=99) survived the follow-up period (DCM3) (age 53.0 years [24.1–81.1]; female n=18). MD-2, HMGB1 and LPS were quantified by means of ELISA. Statistical analysis was performed using a linear regression model.

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