Retrograde transfemoral catheterization of the left ventricle in children with aortic valve stenosis

1986 ◽  
Vol 7 (2) ◽  
pp. 79-82 ◽  
Author(s):  
Kai-Chiu Lau ◽  
Maurice Ping Leung ◽  
Roxy N. S. Lo
2020 ◽  
Vol 73 (11) ◽  
pp. 961-964
Author(s):  
María Bastos Fernández ◽  
Diego López Otero ◽  
Javier López Pais ◽  
Virginia Pubul Núñez ◽  
Carmen Neiro Rey ◽  
...  

Author(s):  
Jordi S. Dahl ◽  
Jacob E. Møller ◽  
Lars Videbæk ◽  
Mikael K. Poulsen ◽  
Torsten R. Rudbæk ◽  
...  

2019 ◽  
Vol 35 (10) ◽  
pp. S116
Author(s):  
M. Asaadi ◽  
W. Mawad ◽  
A. Djebbari ◽  
Z. Keshavarz-Motamed ◽  
L. Kadem ◽  
...  

2002 ◽  
Vol 283 (4) ◽  
pp. H1609-H1615 ◽  
Author(s):  
A. Van der Toorn ◽  
P. Barenbrug ◽  
G. Snoep ◽  
F. H. Van der Veen ◽  
T. Delhaas ◽  
...  

Aortic valve stenosis impairs subendocardial perfusion with a risk of irreversible subendocardial tissue damage. A likely precursor of damage is subendocardial contractile dysfunction, expressed by the parameter TransDif, which is defined as epicardial minus endocardial myofiber shortening, normalized to the mean value. With the use of magnetic resonance tagging in two short-axis slices of the left ventricle (LV), TransDif was derived from LV torsion and contraction during ejection. TransDif was determined in healthy volunteers (control, n = 9) and in patients with aortic valve stenosis before (AVSten, n = 9) and 3 mo after valve replacement (AVRepl, n = 7). In the control group, TransDif was 0.00 ± 0.14 (mean ± SD). In the AVSten group, TransDif increased to 0.96 ± 0.62, suggesting impairment of subendocardial myofiber shortening. In the AVRepl group, TransDif decreased to 0.37 ± 0.20 but was still elevated. In eight of nine AVSten patients, the TransDif value was elevated individually ( P < 0.001), suggesting that the noninvasively determined parameter TransDif may provide important information in planning of treatment of aortic valve stenosis.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C Quast ◽  
S Zimmer ◽  
F Boenner ◽  
C Jacoby ◽  
I Gyamfi-Poku ◽  
...  

Abstract Background Recently, we established an experimental model of moderate aortic valve stenosis (AS) aiming to mimic human disease progression closely. Functional and structural MRI of a mouse model in experimental aortic valve stenosis has not been accomplished so far. Purpose Here, we aimed at developing comprehensive MRI approach for simultaneous assessment of changes in valvular, left ventricular and aortic morphology and function. Methods Male 12-week-old wildtype mice (C57Bl/6) were subjected to wire injury of the aortic valve to induce aortic valve stenosis. High resolution MRI at 9.4T was used to monitor subsequent functional and structural changes in the aortic valve, the ascending aorta, the left ventricle and aortic flow patterns. Results MRI permits accurate planimetry of the orifice and the thickness of the aortic valve, allows a reliable three-dimensional mapping of transvalvular aortic flow, simultaneously depicts aortic regurgitation in 3D fashion and permits assessment of left ventricular changes due to AS. In our model we observed a reduced valve orifice and an increase in valve thickness. Homogenous flow pattern under control converted to heterogenous and turbulent flow with progression of AS associated with increased aortic strain, aortic wall and left ventricular wall thickness. Conclusions In a murine model of aortic valve stenosis MRI is capable to reliably display a three-dimensional transvalvular aortic flow profile with concomitant quantification of structural and functional changes in aortic valve, left ventricle, and ascending aorta. This comprehensive functional imaging at high resolution and distinct reproducibility offers for the first time serial assessment of disease progression in an experimental model of aortic valve stenosis.


Author(s):  
Thomas Kohl ◽  
Ibrahim Akin ◽  
Juliane Frommberger ◽  
Nadja Riehle ◽  
Dietmar Schranz

Abstract Background Some fetuses scheduled for balloon valvuloplasty present with unfavorable lies that render a successful procedure unlikely or impossible. In these situations, Foetal posturing previously has been achieved by maternal laparotomy. As a less invasive means, we demonstrate the feasibility of a minimally-invasive fetoscopic approach. Case Percutaneous ultrasound-guided Foetal balloon valvuloplasty for severe aortic valve stenosis was attempted in a human fetus at 29 + 4 weeks of gestation under general maternofetal anesthesia. Unfortunately, prior to the procedure, the fetus had been observed on several occasions remaining in a dorso-anterior cephalic position. Therefore, the left ventricle could not be accessed by the conventional percutaneous ultrasound-guided approach. In order to achieve the desired Foetal lie, fetoscopic assistance was employed: using a standardized fetoscopic setup, a fetoscope and two graspers, the fetus was rotated in dorsoposterior position. After this maneuver, successful balloon valvuloplasty was achieved. Mother and fetus tolerated the procedure well and complications were not observed. Discussion Fetoscopy-assisted Foetal posturing offers itself as an alternative to maternal laparotomy in fetuses presenting with a persisting disadvantageous position at the time of ballon valvuloplasty. Due to the increased risks of preterm rupture of membranes and earlier delivery posed by the fetoscopic approach, this technique may preferably be used in more mature fetuses when Foetal posturing cannot be achieved by other means.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S T Niepmann ◽  
E Steffen ◽  
A Zietzer ◽  
M Adam ◽  
J Nordsiek ◽  
...  

Abstract Background Aortic valve stenosis (AS) is the most common valve disease requiring therapeutic intervention. Even though the incidence of AS has been continuously rising and AS is associated with significant morbidity and mortality, to date, no medical treatments have been identified that can modify disease progression. In fact, only invasive interventional or surgical replacement of severely diseased valves is recommended. This unmet medical need is likely attributed to the lack of a clear understanding of the molecular mechanism driving disease development. To investigate the pathophysiology leading to AS, reliable and reproducible animal models that mimic human pathophysiology are needed. Hypothesis Induction of a graded wire-induced aortic valve stenosis model in mice is feasible to reflect and study pathophysiological mechanisms underlying the progression of aortic valve stenosis. Methods We have tested and expanded the protocols of a novel wire-injury induced aortic valve stenosis mouse model. A spring coronary guide wire or a bare metal wire was used to apply shear stress to the aortic valve cusps with increasing intensity with ultrasound-guided monitoring in male 10 to 12-week-old C57Bl/6j mice. These protocols allowed the induction of distinct models with soft, moderate and intense wire injury. Functional analysis including maximum flow velocity (Vmax), ejection fraction, fractional shortening, left ventricular volumes, diameters and wall thickness were assessed by echocardiography before, one and four weeks after induction of aortic valve stenosis. Immunohistological analysis were performed after eight weeks (hematoxylin and eosin, von-Kossa staining, anti-CD68-staining). Results Upon moderate or severe injury, AS developed with a significant increase in aortic valve peak blood flow velocity. While moderate injury promoted solitary AS, severe-injury induced mixed aortic valve disease with concomitant mild to moderate aortic regurgitation. Only 5% of the mice who received a moderate injury displayed a mild aortic regurgitation. In the group of mice with intense injury 50% of the mice had a mild and 18,75% had a moderate aortic insufficiency. The changes in aortic valve function were reflected by dilation and hypertrophy of the left ventricle, as well as a decreased left ventricular ejection fraction after intense injury, while moderate injury did not show significant dilation of the left ventricle. Histological analysis revealed the three classic hallmarks of human disease with aortic valve thickening, increased macrophage infiltration and calcification eight weeks after injury. Conclusion Hereby, we demonstrate that the induction of a graded wire induced aortic valve stenosis model in mice mimicking relevant pathophysiological mechanisms is feasible to study disease progression. We extended existing protocols to induce moderate stenosis allowing to solely study aortic valve stenosis without relevant aortic valve regurgitation. Acknowledgement/Funding S.N. was funded by Else-Kröner-Fresenius-Foundation of the Medical Faculty of the University of Bonn


Author(s):  
I.I. Ryabov

The case of prenatal ultrasound diagnosis of aortic valve stenosis and fibroelastosis of the left ventricle of the heart is presented. The child was successfully operated after birth.


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