Commentary: Conquering the great barrier: Coral reef aorta.

Michael Troncone, MD, and François Dagenais, MD

Endovascular management of proximal symptomatic aortic coral reef lesion may be possible in patients at prohibitive open surgical risk.

See Article page 17.

In this edition of JTCVS Techniques, Le Bars and colleagues report an endovascular management of a symptomatic coral reef aorta (CRA) case affecting the aortic arch, a first in the English literature. The term “coral reef aorta” describes an atypical extensive exophytic atherosclerotic lesion that protrudes into the lumen of the affected vessel, rather than typical atherosclerotic plaques, which follow the curvature of the vessel wall. Unlike typical atherosclerotic processes, which primarily affect the distal aortoiliac and infrainguinal vessels, CRA is most often found in women in the paravisceral aorta, with an incidence of 0.6% to 1.8%. Although the pathophysiology of CRA is not well understood, the main theories include the thrombotic rupture of a previous aortic plaque with subsequent calcification of the thrombus, calcified previous dissections, as well as defects in regulatory molecules leading to extreme ectopic calcification.

CRA is typically asymptomatic. When present, symptoms are related to end-organ malperfusion due to obstruction or distal embolization. Proximal CRA in the thoracic aorta, as in the present case, is rare and can present as an acute aortic syndrome or aortic coarctation, which can mimic supravalvular aortic stenosis.

Literature on the management of proximal CRA is extremely sparse and is classically treated with open surgical techniques such as aortic thromboendarterectomy or extra-anatomic bypass. Unique technical challenges regarding the endovascular management of aortic arch CRA include safely navigating devices across the lesion, with an increased risk of stroke, distal embolization, and aortic rupture/dissection during stent deployment. The choice of device is crucial. In their report, Le Bars and colleagues used a balloon-expandable covered stent graft. Advantages of this platform include the ability to postdilate the stent after initial placement, superior radial force, and precise deployment, all of which are important device characteristics for treating aortic arch occlusive pathology. Although there are reports of using uncovered stents in the visceral aorta to preserve collateral flow, this is not as important a consideration in the thoracic aorta and arch, especially given that rupture in the more proximal aorta is much more catastrophic. In the present case, the decision to revascularize the left subclavian artery concomitantly in a sandwich graft fashion may be debated. While it is always prudent to maintain patency of as many aortic branches as possible, performing an extra-anatomic bypass to the left subclavian or simply “overstenting” the left subclavian artery may have allowed a single larger stent diameter in the aorta without a competing sandwich graft, hence possibly restoring more aortic luminal diameter. Furthermore, the risk of gutter leaks with the use of a sandwich technique may yield a greater risk of complication in the event of aortic rupture during stent deployment. Long-term data are obviously lacking on the endovascular management of CRA in the aortic arch. Late complications such as stent compression/collapse, migration, and re-stenosis must be kept in mind. While the CRA may “anchor” the stent graft and minimize risk of migration, graft erosion may supervene, possibly leading to re-stenosis.

We congratulate Le Bars and colleagues on continuing to advance the field of endovascular interventions on the proximal thoracic aorta and aortic arch. Their report opens a therapeutic door for a patient population often deemed at prohibitive risk for conventional open surgery.