Radiologic Findings in the Developmental Complex of Parachute Mitral Valve, Supravalvular Ring of Left Atrium, Subaortic Stenosis, and Coarctation of Aorta

Radiology ◽  
1964 ◽  
Vol 82 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Lewis S. Carey ◽  
Robert D. Sellers ◽  
John D. Shone
1963 ◽  
Vol 11 (6) ◽  
pp. 714-725 ◽  
Author(s):  
John D. Shone ◽  
Robert D. Sellers ◽  
Ray C. Anderson ◽  
Paul Adams ◽  
C.Walton Lillehei ◽  
...  

1979 ◽  
Vol 130 (1) ◽  
pp. 59-64 ◽  
Author(s):  
Shizen Ishikawa ◽  
Enid F. Gilbert ◽  
Lorraine F. Meisner ◽  
Gary Gutcher ◽  
J�rgen Herrmann

Author(s):  
Liuyang Feng ◽  
Hao Gao ◽  
Nan Qi ◽  
Mark Danton ◽  
Nicholas A. Hill ◽  
...  

AbstractThis paper aims to investigate detailed mechanical interactions between the pulmonary haemodynamics and left heart function in pathophysiological situations (e.g. atrial fibrillation and acute mitral regurgitation). This is achieved by developing a complex computational framework for a coupled pulmonary circulation, left atrium and mitral valve model. The left atrium and mitral valve are modelled with physiologically realistic three-dimensional geometries, fibre-reinforced hyperelastic materials and fluid–structure interaction, and the pulmonary vessels are modelled as one-dimensional network ended with structured trees, with specified vessel geometries and wall material properties. This new coupled model reveals some interesting results which could be of diagnostic values. For example, the wave propagation through the pulmonary vasculature can lead to different arrival times for the second systolic flow wave (S2 wave) among the pulmonary veins, forming vortex rings inside the left atrium. In the case of acute mitral regurgitation, the left atrium experiences an increased energy dissipation and pressure elevation. The pulmonary veins can experience increased wave intensities, reversal flow during systole and increased early-diastolic flow wave (D wave), which in turn causes an additional flow wave across the mitral valve (L wave), as well as a reversal flow at the left atrial appendage orifice. In the case of atrial fibrillation, we show that the loss of active contraction is associated with a slower flow inside the left atrial appendage and disappearances of the late-diastole atrial reversal wave (AR wave) and the first systolic wave (S1 wave) in pulmonary veins. The haemodynamic changes along the pulmonary vessel trees on different scales from microscopic vessels to the main pulmonary artery can all be captured in this model. The work promises a potential in quantifying disease progression and medical treatments of various pulmonary diseases such as the pulmonary hypertension due to a left heart dysfunction.


Author(s):  
A. Thomas Pezzella ◽  
Joe R. Utley ◽  
Thomas J. Vander Salm
Keyword(s):  

1969 ◽  
Vol 77 (6) ◽  
pp. 809-813 ◽  
Author(s):  
Allan L. Simon ◽  
William F. Friedman ◽  
William C. Roberts

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
uzoma obiaka ◽  
Anna Chow ◽  
Jen Lie Yau ◽  
Valeria Matto Morina ◽  
Shubhika Srivastava

Background: The incidence of congenital mitral valve disease is 0.4%; Double Orifice Mitral Valve (DOMV) and Parachute Mitral Valve (PMV) are two morphologic pathologies that may result in mitral valve dysfunction. The objectives of this study are 1) To describe valve function and progression and 2) To define factors contributing to disease progression. Methods: Retrospective database review. Fyler codes for DOMV, PMV and text search was performed. Echocardiographic images, echo reports, and chart review were used to identify mitral regurgitation (MR), mitral stenosis (MS), morphology, and associated lesions. Results: 39 patients with DOMV and 76 patients with PMV were identified. In the DOMV cohort, 51% were male, median age at diagnosis was 0.17 years (IQR 0.01, 3.88); median follow-up of 5.92 years (IQR 0.46, 10.22). In the PMV cohort, 44% were male, median age at diagnosis at was 0.01 years (IQR 0, 0.34); median follow-up of 2.56 years (IQR 0.25, 9.55). 41% of DOMV and 23% of patients with PMV had normal valve function at initial visit. DOMV was associated with MR (p=0.04), and PMV with MS (p<0.0001). 23% of patients in the PMV cohort had progressive MS compared to 5% of patients in the DOMV cohort (p<0.0001). There was no significant difference in MR progression between both groups (p=0.02). Papillary muscle (PM) morphology was evaluated in 37 (excluding canals) of 76 patients in the PMV cohort. 5 had true PMV (single PM), 32 had variant PMV with two PM groups of which 62.5% had dominant posterior medial PM. 67% of those with posterior medial PM dominance had progressive MS irrespective of association with Shone’s complex. The anterolateral PM muscle group dominant PMV were not associated with Shone’s complex and progressive MS. Conclusion: DOMV are more likely to have MR while PMV are more likely to have MS. DOMV has non progressive MR and MS. Posterior medial PM dominance in PMV is more likely to have progressive MS.


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