Surgical repair of Tetralogy of Fallot (ToF) is usually performed in the first months of life with low early postoperative mortality. During long-term follow-up, however, both right (RV) and left... Show moreSurgical repair of Tetralogy of Fallot (ToF) is usually performed in the first months of life with low early postoperative mortality. During long-term follow-up, however, both right (RV) and left ventricular (LV) performances may deteriorate. Tissue Doppler imaging (TDI) and speckle tracking echocardiography (ST) can unmask a diminished RV and LV performance. The objective of the current study was to assess the cardiac performance before and shortly after corrective surgery in ToF patients using conventional, TDI and ST echocardiographic techniques. Thirty-six ToF patients after surgery were included. Transthoracic echocardiography including TDI and ST techniques was performed preoperatively and at hospital discharge after surgery (10 days to 4 weeks after surgery). Median age at surgery was 7.5 months [5.5-10.9]. Regarding the LV systolic function there was a significant decrease in interventricular septum (IVS) S ' at discharge as compared to preoperatively (pre IVS S ' = 5.4 +/- 1.4; post IVS S ' = 3.9 +/- 1.2; p < 0.001) and in global longitudinal peak strain (GLS) (pre = - 18.3 +/- 3.4; post = - 14.2 +/- 4.1; p = 0.003); but not in the fractional shortening (FS). Both conventional and TDI parameters showed a decrease in diastolic function at discharge. Tricuspid Annular Plane Systolic Excursion and RV S ' were significantly lower before discharge. When assessing the RV diastolic performance, only the TDI demonstrated a RV impairment. There was a negative correlation between age at surgery and postoperative LV GLS (R = - 0.41, p = 0.031). There seems to be an impairment in left and right ventricle performance at discharge after ToF corrective surgery compared to preoperatively. This is better determined with TDI and ST strain imaging than with conventional echocardiography. Show less
The central cell type within vascular development is the endothelial cell (EC). It forms during (lymph)vasculogenesis, proliferates during angiogenesis and instructs medial cells during... Show moreThe central cell type within vascular development is the endothelial cell (EC). It forms during (lymph)vasculogenesis, proliferates during angiogenesis and instructs medial cells during arteriogenesis. The venous population also gives rise to a subset of the lymphatic endothelium and the endocardium is instructive in formation of the primitive heart. We show that endothelial plasticity is very high in the developing embryo/fetus and that its outcome is dependent on the VEGF, Notch and PDGF-signaling pathways. Alterations in VEGF and Notch-signaling abrogate endocardial and endothelial differentiation, cardiac development and coronary maturation. Alterations in these pathways are most likely also involved in abnormal lymphatic development as seen in fetuses with increased nuchal translucency. In this thesis, lymphatic endothelial plasticity is particularly underscored, as lymphatic ECs gain arterial characteristics in certain pathological situations. Additionally, we show that impaired VEGF, Notch and PDGF-B/PDGFR-_-signaling in ECs and/or vSMCs severely impairs coronary arteriogenesis. In conclusion, many growth factors either influencing the EC (such as VEGF) or produced by the EC (such as PDGF) play a role in regulating and fine-tuning these processes. Increasing our knowledge on how these factors influence (ab)normal vascular development will improve our understanding of many pathological conditions and might increase therapeutic approaches. Show less
