Background-Pregnancy provides a unique model to study the adaptation of the heart in a physiological situation of transient load changes. The aim of this study was to assess the performance of the left ventricle (LV) in normal, uncomplicated pregnancies while considering the actual LV load and shape. Methods and Results-Serial echocardiographic examinations were performed in 51 women in each pregnancy trimester and 3 to 6 months after delivery. Data from 10 nulliparous, age-matched women were used as the control. Conventional parameters of LV function (ejection fraction) as well as myocardial deformation (strain) were interpreted, taking into consideration maternal hemodynamics and LV shape. Cardiac output increased during pregnancy because of a higher stroke volume in early pregnancy and a late increase in heart rate, whereas total vascular resistance decreased. Progressive development of eccentric hypertrophy was observed, which subsequently recovered postpartum. Sphericity index decreased from the first to the third trimester (1.92Ϯ0.17 versus 1.71Ϯ0.17) and returned postpartum to values comparable to the control. Although higher LV stroke work was noted toward the third trimester (5.9Ϯ1.1 versus 5.3Ϯ1.0 Newton meter, PϽ0.001), ejection fraction showed no significant changes. LV strain decreased significantly in late pregnancy (Ϫ19.5Ϯ2% to Ϫ17.6Ϯ1.6%, PϽ0.001) and returned to baseline values after delivery (Ϫ19.5Ϯ2%). Conclusions-Pregnancy is a physiological process associated with increased cardiac performance and progressive LV remodeling. These changes are not directly reflected by parameters traditionally considered to describe systolic function, such as ejection fraction and longitudinal deformation. While ejection fraction was insensitive to the functional changes, the transient decrease in longitudinal deformation becomes only plausible when considering the changes in LV geometry. (Circ Cardiovasc Imaging. 2012;5:289-297.)

IntroductionHuman Wharton’s jelly (WJ) has become a preferred source of mesenchymal stem cells (MSCs) whose clinical applications are limited by the use of adequate xeno-free (XF), in vitro manipulation conditions. Therefore, the objective of our study was to characterize WJ-derived MSCs (WJ-MSCs), isolated by different methods and cultured in a commercially available, MSC XF medium, not least of all by investigating their endothelial differentiation capacity.MethodsWJ explants and enzymatically dissociated WJ cells were cultured in a defined, XF medium for MSCs. Adherent cells at passages 2 and 5 were characterized as MSCs by flow cytometry, MTT, real-time quantitative reverse transcription PCR, and functional multipotent differentiation assays. The endothelial differentiation capacity of MSCs isolated and expanded until passage 2 in the MSC XF medium, and then subcultured for five passages in a commercially available endothelial growth medium (group A), was assessed over serial passages, as compared to adherent WJ-derived cells isolated and expanded for five consecutive passages in the endothelial medium (group B).ResultsThe MSC phenotype of WJ explant- and pellet-derived cells, isolated and expanded in the MSC XF medium, was proven based on the expression of CD44/CD73/CD90/CD105 surface markers and osteo-/adipo-/chondrogenic multipotent differentiation potential, which differed according to the isolation method and/or passage number. Upon exposure to endothelial differentiation cues, cells belonging to group A did not exhibit endothelial cell characteristics over serial passages; by contrast, WJ pellet-derived cells belonging to group B expressed endothelial characteristics at gene, protein and functional levels, potentially due to culture conditions favoring the isolation of other stem/progenitor cell types than MSCs, able to give rise to an endothelial progeny.ConclusionsThe use of defined, MSC XF media for isolation and expansion of human WJ-MSCs is a prerequisite for the establishment of their real endothelial differentiation capacity, as candidates for clinical therapy applications. Thus, the standardization of WJ-MSCs isolation and culture expansion techniques in defined, MSC XF media, for their accurate characterization, would be a priority in the stem cell research field.

Objectives To investigate maternal hemodynamic changes following laser therapy and amnioreduction in twin-totwin transfusion syndrome (TTTS). Methods (Ht) and protein levels were also measured. Cases were retrospectively divided into groups according to treatment: Group A had laser therapy followed by amnioreduction > 1000 mL (n = 25); Group B had laser therapy followed by amnioreduction < 1000 mL (n = 14). (range, 16-26) weeks. The mean amniotic fluid withdrawal was 1700 (range, 1000-3000) and 300 (range, 150-800) Results The mean gestational age at inclusion was 21

Objective To monitor changes in the maternal renin-angiotensinaldosterone system following laser therapy and amnioreduction in severe twin-to-twin transfusion syndrome (TTTS).Design Observational prospective study.Setting Single university hospital in Poissy, France.Population Sixty cases of TTTS at 16-26 weeks of gestation.Method Maternal blood sampling before, 6 and 24 hours following the procedure.Main outcome measures Plasma levels of aldosterone, renin, angiotensin II (AII), atrial natriuretic peptide (ANP), vasopressin, sodium, potassium and plasma proteins together with full blood count were measured before, 6 and 24 hours following the procedure.Results TTTS is associated with maternal hyperaldosteronism dissociated from renin-angiotensin changes. Correcting TTTS by placental surgery and amnioreduction triggers incomplete correction of hyperaldosteronism, as early as 6 hours following the procedure, without changes in AII but an increase in the levels of ANP in plasma. Electrolyte concentrations remained stable despite haemodilution, while vasoactive hormone levels such as that of vasopressin remained unchanged.Conclusion Mechanisms involved in marked fluid retention in TTTS are rapidly corrected by laser therapy followed by amnioreduction while maintaining electrolyte homeostasis.

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