Comprehensive transthoracic cardiac imaging in mice using ultrasound biomicroscopy with anatomical confirmation by magnetic resonance imaging

2004 ◽  
Vol 18 (2) ◽  
pp. 232-244 ◽  
Author(s):  
Yu-Qing Zhou ◽  
F. Stuart Foster ◽  
Brian J. Nieman ◽  
Lorinda Davidson ◽  
X. Josette Chen ◽  
...  

High-frequency ultrasound biomicroscopy (UBM) has recently emerged as a high-resolution means of phenotyping genetically altered mice and has great potential to evaluate the cardiac morphology and hemodynamics of mouse mutants. However, there is no standard procedure of in vivo transthoracic cardiac imaging using UBM to comprehensively phenotype the adult mice. In this paper, the characteristic mouse thoracic anatomy is elucidated using magnetic resonance (MR) imaging on fixed mice. Besides the left parasternal and apical windows commonly used for transthoracic ultrasound cardiac imaging, a very useful right parasternal window is found. We present strategies for optimal visualization using UBM of key cardiac structures including: 1) the right atrial inflow channels such as the right superior vena cava; 2) the right ventricular inflow tract via the tricuspid orifice; 3) the right ventricular outflow tract to the main pulmonary artery; 4) the left atrial inflow channel, e.g., pulmonary vein; 5) the left ventricular inflow tract via the mitral orifice; 6) the left ventricular outflow tract to the ascending aorta; 7) the left coronary artery; and 8) the aortic arch and associated branches. Two-dimensional ultrasound images of these cardiac regions are correlated to similar sections in the three-dimensional MR data set to verify anatomical details of the in vivo UBM imaging. Dimensions of the left ventricle and ascending aorta are measured by M-mode. Flow velocities are recorded using Doppler at six representative intracardiac locations: right superior vena cava, tricuspid orifice, main pulmonary artery, pulmonary vein, mitral orifice, and ascending aorta. The methodologies and baseline measurements of inbred mice provide a useful guide for investigators applying the high-frequency ultrasound imaging to mouse cardiac phenotyping.

Author(s):  
Reza H. Khiabani ◽  
Maria Restrepo ◽  
Elaine Tang ◽  
Diane De Zélicourt ◽  
Mark Fogel ◽  
...  

Single Ventricle Heart Defects (SVHD) are present in 2 per 1000 live births in the US. SVHD are characterized by cyanotic mixing between the de-oxygenated blood from the systemic circulation return and the oxygenated blood from the pulmonary arteries. Palliative surgical repairs (Fontan procedure) are performed to bypass the right ventricle in these patients. In current practice, the surgical interventions commonly result in the total cavopulmonary connection (TCPC). In this configuration the systemic venous returns (inferior vena cava, IVC, and superior vena cava, SVC) are directly routed to the right and left pulmonary arteries (RPA and LPA), bypassing the right heart. The resulting anatomy has complex and unsteady hemodynamics characterized by flow mixing and flow separation. Pulsation of the inlet venous flow during a cardiac cycle results in complex and unsteady flow patterns in the TCPC. Although various degrees of pulsatility have been observed in vivo, non-pulsatile (time-averaged) flow boundary conditions have traditionally been assumed in modeling TCPC hemodynamics, and only recently have pulsatile conditions been incorporated without completely characterizing their effect or importance. In this study, 3D numerical simulations were performed to predict TCPC hemodynamics with both pulsatile and non-pulsatile boundary conditions and to investigate the accuracy of applying non-pulsatile boundary conditions. Flow structures, energy dissipation rate and pressure drop were compared under rest and estimated exercise conditions. The results show that TCPC hemodynamics can be strongly influenced by the presence of pulsatile flow. However, there exists a minimum pulsatility threshold, identified by defining a weighted pulsatility index (wPI), above which the influence is significant.


2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
S Naganur

Abstract Funding Acknowledgements Not applicable OnBehalf Not applicable 11 years boy with shortness of breath/easy fatigability. On examination obese, comfortable at rest, pulse : 80bpm, regular, normal JVP. Blood pressure : 170/100 in upper limb, 120/80 in lower limb. Mild cardiomegaly, normal S2, no S3/S4/click, harsh 4/6 ESM in left 3rd intercostal space, faint continuous murmur at the back. CXR : mild cardiomegaly, adequate pulmonary blood flow. ECG : sinus rhythm, normal QRS axis/intervals, biventricular hypertrophy. Echo : severe pulmonary stenosis (predominantly subvalvular, gradient 100mmHg) coarctation (gradient 50mmHg) preserved biventricular function. Cardiac CT : confirmed echo" findings, additional ? DCRV, anomalous RCA from left sinus. Cardiac MRI couldn"t yield more information. Hence, catheterization was performed. Pressure data : severe infundibular and mild valvular RVOT obstruction, normal PA pressure, severe coarctation. Oximetry : small L–>R shunt. RV angiogram : obstruction at sub-valvular/valvular levels, doming/reverse doming of pulmonary valve. LV angiogram : small subaortic VSD, L–>R. Aortic root angiogram : bicuspid aortic valve, no AR, anomalous RCA from left sinus, severe coarctation, no PDA. Plan : Single antihypertensive, surgical resection of infundibular RVOTO, pulmonary valvotomy, VSD closure, coarctation repair. Cath data Pressure in mm of Hg Right atrium (mean) 8 Right ventricle (apex) systolic 100 end diastolic 12 Right ventricle (outflow) systolic 60 end diastolic 12 Main pulmonary artery 25/10 (15) Left ventricle systolic 158 end diastolic 14 Ascending aorta 165/75 (140) Descending aorta 116/80 (100) Right Femoral artery 117/76 (98) Oximetry Superior vena cava 68% Inferior vena cava 74% Pulmonary artery 82% Aorta 99% Pulmonary vein 100% Qp/ Qs 1.6:1 Abstract P1485 Figure. CT/MRI/Cath


PEDIATRICS ◽  
1963 ◽  
Vol 32 (5) ◽  
pp. 841-854
Author(s):  
Brian Kiely ◽  
Francisco Morales ◽  
David Rosenblum

When the pulmonary valve is atretic and the ventricular septum intact, the right ventricle usually consists of a small chamber with a very thick wall capable of developing high pressure. This pathologic picture is associated with clinical findings similar to those in tricuspid atresia—cyanosis, decreased pulmonary flow, left ventricular preponderance on the electrocardiogram, and early death. The diagnosis may be confirmed by heart catheterization and selective angiocardiography with injection into the right ventricle, but the risk is great. Surgery has never been successful in the past; but because of the equally hopeless prognosis on medical treatment, attempts should continue to be made. Anastomosis of the superior vena cava to the right pulmonary artery appears to offer hope of success in the future.


1983 ◽  
Vol 244 (4) ◽  
pp. H607-H613 ◽  
Author(s):  
W. C. Randall ◽  
J. X. Thomas ◽  
M. J. Barber ◽  
L. E. Rinkema

Total denervation of the canine heart consisted of intrapericardial neural dissection of the left atrium, left superior pulmonary vein, and main pulmonary artery and cutting of the ventrolateral cardiac nerve (stage I). The fat pad and all nerves were removed from between the pulmonary artery and aorta (stage II). Dissection proceeded from the pericardial reflection along the superior vena cava to the azygos vein, which was cleared, double tied, and cut. The right pulmonary artery was cleaned, and the superior right atrium was dissected to its intersection with the left atrium (stage III). Denervation was tested by electrical stimulation of both vagi and stellate ganglia, while recording inotropic, chronotropic, and dromotropic events, before and after each stage. Stage I deleted most left autonomic input to the heart without interrupting right sympathetics. Stage II completed left autonomic denervation but preserved much of the right sympathetic input. Large nerves along the dorsal surface of the pulmonary artery carried inputs from both left and right sympathetics. Stage III completed the denervation of atrioventricular and sinoatrial nodal structures and removed all remaining ventricular inotropic influences. Selective denervation of atrioventricular and sinoatrial nodal regions appears feasible for preparation of chronic canine models.


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