What is the pathophysiology of coarctation of the aorta (CoA)?

Updated: Nov 20, 2018
  • Author: Syamasundar Rao Patnana, MD; Chief Editor: Stuart Berger, MD  more...
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Coarctation of the aorta imposes significant afterload on the left ventricle (LV), which results in increased wall stress and compensatory ventricular hypertrophy.

The afterload may be imposed acutely, as occurs following closure of the ductus arteriosus in neonates with severe coarctation. These infants may rapidly develop CHF and shock. Rapid constriction of the ductus arteriosus, producing sudden severe aortic obstruction, seems to be the most likely explanation. As the ductus (aortic end) constricts, the left ventricular afterload rapidly increases, with a resultant increase in left ventricular pressures (systolic and diastolic). This causes elevation of the left atrial pressure, which may open the foramen ovale, causing left-to-right shunt and dilatation of the right atrium and right ventricle. If the foramen ovale does not open, pulmonary venous pressures and pulmonary artery pressures increase, and right ventricular dilatation develops.

Cardiomegaly revealed by chest roentgenography and right ventricular hypertrophy seen on ECG and echocardiography are related to the indirect effects of rapid development of severe aortic obstruction.

LV afterload may also gradually increase, allowing children with less severe coarctation to develop arterial collateral vessels that partially bypass the aortic obstruction. These children may be asymptomatic until hypertension is detected or another complication develops.

The mechanism for development of hypertension is not clearly understood; mechanical obstruction and renin-angiotensin–mediated humoral mechanisms have been postulated.

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