Heart Failure Relapses in Response to Acute Stresses - Role of Immunological and Inflammatory Pathways.

Cardiovascular diseases continue to be the most imminent health care problems in the western world, accounting for numerous deaths per year. Heart failure (HF), namely the reduction of left ventricular function, is one of the major cardiovascular disease entities. It is chronically progressing with relapsing acute decompensations and an overall grave prognosis that is little different if not worse than most malignant diseases.

[Pneumonia, endocarditis of two valves and pulmonary artery embolism in a 26-year-old male patient].

A 26-year-old male patient presented with left-sided pneumonia, endocarditis of the tricuspid and pulmonary valves and a pulmonary artery embolism. In 2004 a Ross operation was performed because of congenital aortic valve stenosis. There was an elevation of the antibody titer for Coxiella burnetii, the pathogen of Q fever.

Fibulin-6 regulates pro-fibrotic TGF-β responses in neonatal mouse ventricular cardiac fibroblasts.

Fibulin-6, an essential component of extracellular matrix determines the architecture of cellular junctions in tissues undergoing strain. Increased expression and deposition of fibulin-6 facilitates fibroblast migration in response to TGF-β, following myocardial infarction in mouse heart. The underlying mechanism still remains elusive.

Expression of fibulin-6 in failing hearts and its role for cardiac fibroblast migration.

Aims: The cardiac extracellular matrix (ECM) undergoes a dynamic transition following myocardial infarction. Fibulin-6 is expressed in cell junctions particularly in tissues subjected to significant mechanical stress. Fibulin-6 deficiency results in defective cell migration in nematodes and early embryonic lethality in mice.