Fig. 6.1
(a) Single frontal view of the chest of a 13-year-old patient with shortness of breath shows biapical hazy opacities and perihilar pulmonary edema in a patient with known Kawasaki disease. Notice the round calcification projecting over the left upper heart border. (b) Multiple right coronary aneurysms shown in a maximum intensity projection (MIP) image from a 3D color-coded CT angiogram (CTA)
Ultrasound : Echocardiography may show proximal coronary artery aneurysms. Evaluation of the entire course of the coronaries is often difficult. Wall motion abnormalities may be detected in patients suffering from ischemia or infarct.
CT scans : Gated coronary CT angiography (CTA) offers a robust assessment of the coronary arteries with the ability to assess size of aneurysms, thrombosis, stenosis, and calcifications (Figs. 6.1b and 6.2). Functional assessment of the left ventricle may be obtained with retrospective cardiac gating to evaluate wall motion abnormalities and ventricular function. Myocardial infarction may be seen on delayed imaging as enhancement of the myocardium.
Fig. 6.2
MIP image on the left and posterior view from a 3D color-coded CTA on the right, in a 13-year-old patient with history of Kawasaki disease. These images show calcified (B) and non-calcified (C) coronary aneurysms. Notice that there is a complete occlusion of the left coronary artery (A)
MRI: Cardiac MRI may show edema within the myocardium on T2-weighted images. Perfusion imaging may show decreased perfusion on immediate imaging and delayed enhancement in areas of infarction. MR angiography (MRA) may be an effective tool for evaluating the size of coronary aneurysms but may overestimate the degree of stenosis. Calcifications can cause artifact on MR imaging; when present, it may limit the evaluation of luminal diameters. Steady state free precession cine imaging is the most effective way to evaluate wall motion abnormalities and offers the most accurate assessment of ventricular function (ventricular volumes and ejection fraction) (Fig. 6.3).
Fig. 6.3
Short-axis gradient echo (GRE) cine image at end systole from a cardiac MRI exam (left image) shows normal thickening of myocardium of the left ventricle except for the anterior wall (arrow), which did not thicken normally and demonstrated poor wall motion. A single short-axis cardiac perfusion image (right image) shows decreased perfusion on immediate images in the anterior and anteroseptal wall of the left ventricle (arrows) in a patient with known Kawasaki disease with complete obstruction of the left main coronary artery. No delayed enhancement was seen to suggest infarction
Nuclear medicine : Thallium or technetium (Tc-99m) myocardial imaging can evaluate perfusion of the myocardium and reliably evaluate viability of the myocardium.
Conventional angiography : This is an excellent method for evaluating the luminal diameters of coronary arteries with aneurysms (Fig. 6.4).
Fig. 6.4
Conventional angiogram in a 6-year-old boy showing a 1-cm left coronary aneurysm (white arrow). Notice the aneurysms of the subclavian arteries bilaterally (black arrows)
Imaging recommendations: Current recommendations for patients with small aneurysms are an echocardiogram at 30 days after the acute illness, with an echocardiogram and ECG every 3 months until the dilatation has disappeared. Patients with medium-sized aneurysms should be evaluated every 1–3 months with echocardiography and chest x-ray until dilatation is no longer observed. These patients should undergo coronary CTA or coronary MRA every 5 years.
6.2 Takayasu Arteritis
6.2.1 General
Takayasu arteritis is an inflammatory large-vessel vasculitis of unknown etiology. It is more common in females and people of Asian descent. The onset of symptoms typically occurs between 15 and 30 years of age.
Vascular injury is mediated by the actions of macrophages, cytotoxic T cells, and natural killer cells, which are the main cellular components of inflammatory infiltrates. The inflammatory process leads to myointimal proliferation, with subsequent vessel wall thickening and luminal stenosis. Lesions that predominantly cause destruction of the muscularis and the elastic lamina can result in vascular dilatation or aneurysms.
The initial inflammatory phase is characterized by systemic illness with fever, night sweats, fatigue, and fainting. Fainting may be due to a subclavian steal syndrome with obstruction of the subclavian artery, which then steals flow from the vertebral artery. The “pulseless phase” is due to proximal narrowing of arteries resulting in blunted arterial waveforms and decreased peripheral pulses. Similar pathology in abdominal vessels may result in hypoperfusion of abdominal organs with the development of renal and hepatic failure as well as bowel ischemia. Lightheadedness, poor vision, and fainting are also seen in this phase.
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