Deceleration capacity: A novel predictor for total mortality in patients with non-ischemic dilated cardiomyopathy.

OBJECTIVES: We hypothesized that deceleration capacity (DC), a novel marker of cardiac autonomic modulation, is an independent predictor for mortality in patients with non-ischemic dilated cardiomyopathy (NICM). BACKGROUND: NICM is associated with a high risk for sudden cardiac death (SCD). However there are no clinically established parameters available for risk stratification beyond LVEF. DC has been previously shown to be a strong independent predictor for total mortality in patients after myocardial infarction. METHODS: Holter-ECG recordings of 201 patients NICM (83.1% male, mean age: 61.4years, mean LVEF: 33.3%) were analyzed by the method of phase-rectified-signal-averaging (PRSA) to obtain DC. RESULTS: During a minimum follow-up of 40month 59 patients died. Kaplan Meyer Analysis showed a significantly higher mortality in patients with a DC below 4.5ms (log rank p=0.012) irrespective to the presence of atrial fibrillation. CONCLUSIONS: Impaired DC is a powerful independent predictor for mortality in patients with NICM.

Effects of aflibercept on primary RPE cells: toxicity, wound healing, uptake and phagocytosis.

BACKGROUND/AIM: Anti-VEGF treatment is the therapy of choice in age-related macular degeneration, and is also applied in diabetic macular oedema or retinal vein occlusion. Recently, the fusion protein, aflibercept, has been approved for therapeutic use. In this study, we investigate the effects of aflibercept on primary RPE cells. METHODS: Primary RPE cells were prepared from freshly slaughtered pigs' eyes. The impact of aflibercept on cell viability was investigated with MTT and trypan blue exclusion assay. The influence of aflibercept on wound healing was assessed with a scratch assay. Intracellular uptake of aflibercept was investigated in immunohistochemistry and its influence on phagocytosis with a phagocytosis assay using opsonised latex beads. RESULTS: Aflibercept displays no cytotoxicity on RPE cells but impairs its wound healing ability. It is taken up into RPE cells and can be intracellularly detected for at least 7 days. Intracellular aflibercept impairs the phagocytic capacity of RPE cells. CONCLUSIONS: Aflibercept interferes with the physiology of RPE cells, as it is taken up into RPE cells, which is accompanied by a reduction of the phagocytic ability. Additionally, it impairs the wound healing capacity of RPE cells. These effects on the physiology of RPE cells may indicate possible side effects.