Coarctation of the Aorta

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CHAPTER 38 Coarctation of the Aorta

Coarctation of the aorta is a narrowing of the proximal descending thoracic aorta. It can occur as an isolated lesion or in the presence of other congenital lesions, most commonly a bicuspid valve, patent ductus arteriosus, ventricular septal defects, or hypoplastic left heart. The severity of the coarctation and associated lesions determines the pathophysiology and clinical presentation. The clinical presentation varies from congestive heart failure in the newborn to asymptomatic hypertension or a murmur in older patients. Treatment options are surgical or interventional.

Prevalence and Epidemiology

Coarctation of the aorta occurs in 3.2 of 10,000 births and accounts for 5% to 10% of all cases of congenital heart disease.14 Coarctation is more common in white males than in white females, with a male-to-female ratio of 1.3 to 2.0 : 1.3 Most cases are sporadic, but there may be a genetic inheritance.

Etiology and Pathophysiology

Coarctation is thought to be the result of a malformation of the aortic media, leading to a posterior infolding or shelf.1,5,6 Most often, the shelf is discrete and opposite the ductus arteriosus. However, the malformation may be a long segment and circumferentially surround the aorta. In the latter form, there is typically diffuse tubular hypoplasia of the transverse arch and isthmus.1,7,8

Histologic examination shows thickened intima and media that protrude posteriorly and laterally into the aortic lumen. The ductus arteriosus or ligamentum arteriosus inserts anteromedially at the same level.1

The physiologic changes in cardiovascular function vary with the severity of the coarctation (severe or mild) and the presence of associated anomalies. In critical or severe coarctation, impedance to left ventricular outflow increases. The resultant hemodynamic changes include diminished stroke volume, increased left ventricular end-diastolic pressures, and elevated left atrial pressures. If there is associated aortic stenosis or a large ventricular septal defect, left ventricular systolic pressure and end-diastolic volume will further increase. The end result is heart failure and pulmonary edema. In addition to cardiac abnormalities, there are changes in vascular physiology. The diminished perfusion of the distal aorta and lower body leads to renal failure and bowel ischemia.

In milder forms of coarctation, the left ventricular myocardium hypertrophies to normalize myocardial wall stress and maintain normal systolic ventricular function. Left ventricular ejection fraction is often normal to increased. Collateral vessels also develop, which act as a source of lower body perfusion and help maintain normal flow to abdominal viscera.1


Imaging Studies

Techniques and Findings

Computed Tomography

CT can show anatomy of the coarctation, including the site, extent (i.e., size of the aortic arch) and severity, a bicuspid valve, collateral vessel formation, and left ventricular hypertrophy.

CT angiography is performed with a pulmonary embolism protocol using thin collimation (<1 mm), pitch lower than 1.5,9,10 fast scan time, and a single breath-hold, when possible. In adolescents and adults, contrast medium is injected via a power injector at a high flow rate of 3 to 4 mL/sec using a contrast volume of 100 to 150 mL (280 to 320 mg I/mL). Scan delay time can be determined with an automatic bolus tracking system with the cursor over the aortic isthmus or empiric timing. Empiric timing, using a delay of 20 to 25 seconds after the start of the injection, is a default method if the bolus tracking fails to trigger. Electrocardiographic (ECG) gating is not needed for the evaluation of coarctation.

The volumetric data are reconstructed at 3- to 5-mm slice thickness for routine viewing and at 1- to 2-mm slice thickness for multiplanar reformatting and three-dimensional reconstructions. A standard reconstruction algorithm is used for reconstruction.

Special Considerations for Pediatric Patients

The contrast volume is 2 mL/kg (not to exceed 125 mL). Intravenous contrast medium can be administered with a power injector or manual (hand) injection. A power injector is used when a 22-gauge or larger cannula can be placed in an antecubital vein. For a 22-gauge catheter, flow rates are 1.5 to 2.5 mL/sec.10,11 Flow rates for larger gauge catheters are similar to those described above. With a manual injection, the contrast is pushed as quickly as possible. Determination of the scan initiation time can be made by an empiric or bolus tracking method. In pediatric patients weighing less than 10 kg, an empiric scan delay of 12 to 15 seconds after the start of the intravenous contrast injection suffices.10 In larger patients, the delay time is 15 to 25 seconds.

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