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Old 06-17-2012
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Heart Aortic Coarctation and Aortic Atresia!


I have two quick questions I was hoping you might be able to help me out with; one is about aortic coarctation and the other aortic atresia.

1. Why is adult (post-ductal) coarctation clinically less severe than infantile (pre-ductal) coarctation despite there always being a PDA present in the latter? I would have thought the PDA would be beneficial as it will provide more systemic blood flow.

I can only imagine this is to do with worse collateral formation & increased chance of R-sided heart failure in the infantile form?

2. How is the blood circuit completed in cases of severe congenital aortic stenosis/atresia? I appreciate a PDA is required to provide blood flow from the pulmonary artery to the aorta & hence coronary arteries, but how does oxygenated blood get back from the lungs to the body? I suppose with severe stenosis there is still an opening for blood from the lungs to enter the L heart & then proceed to the body, but what about in atresia (which I understand to be COMPLETE occlusion)?

I hope I have worded these questions well enough for you to understand what I mean! Any help would be great.

Thank you,

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Old 06-17-2012
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1 infentile PDA is more severe then the adult because usually it can impaire the blood flow to the carodits - hence brain as it is preductal.

2 in those conditions you described yes PDA is essential to allow circulation during intrauterine period, but after birth only deoxygeneted blood will be transfered from the PDA and if there is complete absence of the aortic valve the baby will be cynotic and without prompt repair he will die from 2 reasons 1 unability to pump of the left ventricle will cause back failure with pilmonary edema and acute right decompansation and 2 because of the cynosis in case there is aortic stenosis then it may still allow some.circulation and might even go as subclinical, it all depands on the amount of oxygenation.

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Old 08-06-2012
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Search infantile coarctation

Clinical Presentation:
Infantile type presents in the neonate or young infant with congestive heart failure and bounding upper extremity pulses and diminished lower extremity pulses. This infantile type is also known as preductal coarcation. The infantile type is the most frequent cause of pulmonary venous hypertension and congestive heart failure that presents in the second and third week of life. Etiology/Pathophysiology:
Usually caused by a congenital indentation in the posterior wall of the aorta that usually is distal to the origin of the left subclavian artery at the level of the ductus arteriosus. Infantile type coarctation causes a diffuse narrowing while adult type coarctation causes a focal narrowing.
Seventy-five percent of patients have a bicuspid aortic valve, and ASD / VSD / PDA / mitral valve deformities can also be seen.
Since the ductus arteriosus is still often open, a pressure gradient is not present across the coarctation, and collateral circulation does not develop. Right ventricular volume overload and dilation develops because almost all blood reaching the descending aorta must come through the ductus arteriosus from the right ventricle. As the ductus begins to close, a pressure gradient develps across the coarctation and the relatively underdeveloped left ventricle begins to fail. Increased left atrial pressure is then transmitted to the pulmonary veins with progressive venous engorgement and pulmonary edema. Post stenotic dilation of the aorta is not seen due to prenatal lack of flow across the coarctation.
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Cardiovascular-, Pathology-

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