Imbalanced Angiogenesis in Peripartum Cardiomyopathy　- Diagnostic Value of Placenta Growth Factor.

BACKGROUND: Concentrations of the anti-angiogenic factor soluble fms-like tyrosine kinase-1 (sFlt-1) are altered in peripartum cardiomyopathy (PPCM). In this study we investigated changes in the angiogenesis balance in PPCM.Methods and Results:Plasma concentrations of sFlt-1 and the pro-angiogenic placenta growth factor (PlGF) were determined in patients with PPCM during the post-partum phase (n=83), in healthy women at delivery (n=30), and in patients with acute heart failure (AHF; n=65). Women with cardiac failure prepartum or associated with any form of hypertension, including pre-eclampsia, were excluded. Compared with non-pregnant women, in women with AHF and PPCM, median PlGF concentrations were greater (19 [IQR 16-22] and 98 [IQR 78-126] ng/mL, respectively; P<0.001) and the sFlt-1/PlGF ratio was lower (9.8 [6.6-11.3] and 1.2 [0.9-2.8], respectively; P<0.001). The sFlt-1/PlGF ratio was lower in PPCM than in normal deliveries (1.2 [0.9-2.8] vs. 94.8 [68.8-194.1], respectively; P<0.0001). The area under the curve for PlGF (cut-off value: 50ng/mL) and/or the sFlt-1/PlGF ratio (cut-off value: 4) to distinguish PPCM from either normal delivery or AHF was >0.94. Median plasma concentrations of the anti-angiogenic factor relaxin-2 were lower in PPCM and AHF (0.3 [IQR 0.3-1.7] and 0.3 [IQR 0.3-1] ng/mL, respectively) compared with normal deliveries (1,807 [IQR 1,101-4,050] ng/mL; P<0.001). CONCLUSIONS: Plasma of PPCM patients shows imbalanced angiogenesis. High PlGF and/or low sFlt-1/PlGF may be used to diagnose PPCM.

Mechanisms of brain signaling during sepsis.

Brain signaling is a crucial event for the body to mount an appropriate response to invading microorganisms. Pro-inflammatory cytokines are released from infected tissues and reach key structures in the brain via the circumventricular organs, areas of damaged blood brain barrier or they cross actively the blood brain barrier using specific carriers. Alternately, cytokines may activate brain endothelial cells or microglial to produce prostaglandins which then diffuse into the brain to activate neurons. Finally, cytokines may activate the autonomic nervous system at the periphery. The following crosstalk between astrocytes and microglial precedes neuronal activation particularly within the hippocampus, amygdale and hypothalamus. The resulting release of neuro-hormones in the systemic circulation allows restoration of homeostasis. It is likely that an excess in nitric oxide and complement anaphylatoxin C5a contributes to DNA damage within neurons of the hippocampus and hypothalamus and subsequent brain dysfunction.

[Anesthetic management of patients with muscular disease?]. / Quelle prise en charge anesthésique pour les patients ayant une pathologie musculaire?

The past two decades has been characterized by important advances in symptomatic care to the muscular patient. In particular, the development of home mechanical ventilation was associated by a substantial improvement in life expectancy. The presence of a muscular disease is less frequently a contra-indication of surgery and subsequently the issue of anesthetizing these patients has become a routine question. A growing number of muscular disorders have been subjected to specific guidelines for anesthetic procedures.