Case of the Month Header 2011  

April 2013  

Dear SCCT Member:

 

As you know, the SCCT is the only professional medical membership organization dedicated to ensuring patient access to the appropriate use of cardiovascular CT. The SCCT Board of Directors thought that it would be beneficial to our members to create a Case of the Month series showcasing cardiac CTA in various clinical scenarios. Please provide feedback or forward any questions to info@scct.org 

 

Sincerely,

 

John R Lesser, MD, FSCCT

Suhny Abbara, MD, FSCCT  

J. Jeffrey Carr, MD, FSCCT

Dan Entrikin, MD, FSCCT  

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Coronary Aneurysm Resulting in Serial Infarcts: Assessment with Invasive and CT Coronary Angiography

Lesser JR, Han BK, Longe TL, Knickelbine T, Flygenring BJ, Newell M, Schwartz RS
Minneapolis Heart Institute and Children's Hospital of Minnesota

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History
A 39 year old man presented in 2005 with the abrupt onset of persistent chest pain and no ECG changes. He had mild hypertension with no other risk factors, no illicit drug use, and no known significant childhood infections. His troponin was mildly elevated and an invasive coronary angiogram showed an aneurysmal LAD with a subtotal small thrombotic second septal branch lesion (fig. 1, short arrow). 

Figure 1
Figure 1

Findings
A coronary CT angiogram was performed to better define the aneurysm. The LAD at its maximal dimensions was 8.5 x 7.5 mm (fig. 2a, long arrow) and prominent non-calcified plaque or thrombus (fig. 2a and 2b, short arrows).  The proximal RCA was 6.5 x 5.3 mm with no plaque seen and all other arterial segments appeared normal. He initially was treated with Warfarin, ASA, and atorvastatin but then substituted clopidogrel for Warfarin.

Figure 2
Figure 2

Eight years later, he abruptly developed a small infarction without ECG changes. Coronary angiography showed a linear decreased density in the LAD (fig 3, arrows) with no other changes except the total septal occlusion.

Figure 3
Figure 3

Intracoronary ultrasound documented this was not a dissection but could not distinguish thrombus from plaque. Dabigatran replaced clopidogrel and a coronary CT angiogram was performed 1 month later.  The CT coronary angiogram showed the LAD was slightly larger at 9.2 x 8.5 mm with a similar extent of non-calcified plaque (fig. 4a). The plaque and/or thrombus now had a small degree of lower attenuation material (fig. 4b, short arrow). Our patient remains on dabigatran, ASA, and atorvastatin and is asymptomatic.

Figure 4
Figure 4
Discussion
The etiology of the coronary aneurysms in our patient remains unclear, but it seems most consistent with previously unrecognized and untreated Kawasaki disease. One to two years after exposure, over 50% of aneurysms resolve by angiography.  Rupture of a coronary aneurysm is extremely rare after the first few months after disease onset (1).  Progression to a coronary stenosis occurs most in those with giant aneurysms (> 8 mm).  Thrombotic coronary occlusion is the most common cause of death and combined warfarin and anti-platelet therapy is recommended for giant aneurysms (2). Endothelial dysfunction likely persists in those with regressed coronary aneurysms and empiric preventative measures are recommended (3).

The new linear low density on invasive coronary angiography and low attenuation plaque components on CT without a coronary dissection all point to new thrombus formation as the cause of a small embolic infarction. Our serial imaging findings strongly support the recommendation for warfarin or anti-thrombin therapy in this patient group.
References
1. Newberger JW, Takahashi M, Gerber MA, Gewitz MH, et al. AHA scientific statement: Diagnosis, treatment, and long-term management of Kawasaki disease. Circulation 2004;110:2747-2771.

2. Sugahara Y, Ishii M, Lemura M, Matsuishi T, Kato H. Warfarin therapy for giant aneurysm prevents myocardial infarction in Kawasaki disease. Pediatr Cardiol 2008;29:398-401.

3. Lemura M, Ishii M, Akagi T, et al. Long term consequences of regressed coronary aneurysms after Kawasaki disease: vascular wall morphology and function. Heart 2000;83:307-311.

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