Case Report

Coral Reef Aorta Successfully Treated With Self-Expanding Nitinol Stent

Kazuki Haraguchi, MD, Yoshiaki Shintani, MD, Tomohiro Kawasaki, MD, Cardiovascular Center, Shin-Koga Hospital, Kurume, Japan

Kazuki Haraguchi, MD, Yoshiaki Shintani, MD, Tomohiro Kawasaki, MD, Cardiovascular Center, Shin-Koga Hospital, Kurume, Japan

This report highlights a coral reef aorta, of special interest because it was successfully treated in Japan with a self-expanding nitinol stent in October 2012 and followed up a year later, in October 2013.

Coral reef aorta is a rare disease resulting in calcifying aortic stenosis. It is normally treated using conventional surgery such as thromboendarterectomy, covered stent graft replacement of the aorta, and thoracoabdominal bypass graft. Although these surgeries are the norm, they often come with serious complications. We report a case of a coral reef aorta treated using a self-expandable nitinol stent, placed successfully and without complications.

Case Report

 A 61-year-old man who had lost his left leg in a childhood car accident was referred to the cardiovascular center of our hospital with lifestyle-limiting claudication of his right leg. He had a medical history of hypertension, dyslipidemia, and hemodialysis, and was a current smoker. The patient was experiencing severe right side calf discomfort as well as suffering overall gluteal pain that left him unable to walk more than 200 meters. Despite this limitation, he had no history of ischemic-rest leg pain or wounds.

When examined, the patient’s right side ankle-brachial index (ABI) was 0.63 and his leg was free of any abnormal echo lesions. Ultrasound demonstrated localized aortic stenosis with severe calcification. Using multi-detector computed tomography (CT), we were able to reveal a severe aortic stenosis with severe circumferential calcification located between the common iliac artery and the renal artery (Figure 1). The patient then received medical therapy; however, there was no improvement in his symptoms. After discussion with a cardiovascular surgeon, it was decided that conventional surgery was not suitable for this patient because of his comorbidities. After informed consent was obtained, the patient was treated with an endovascular procedure and placement of a self-expanding nitinol stent. For an extended period of over three months prior to undergoing treatment, the patient was administered 100 mg of aspirin and 200 mg of cilostazol per day.

Procedure

A 6 French (Fr) 50 cm sheath via the right brachial artery and a 4 Fr 11 cm sheath via the left femoral artery were inserted. Angiography confirmed an abdominal aorta obstructed with severe endophytic calcification, along with collateral circulation from the superior mesenteric artery to the inferior mesenteric artery (Figure 2). Our initial attempts to cross the aortic obstruction via the left femoral artery with a .035-inch guidewire (Terumo) supported by a Glidecath (Terumo) were unsuccessful; however, secondary attempts using a .014-inch Aguru guidewire Boston Scientific) enabled us to achieve our goal. The systolic pressure gradient across the stenosis was 50 mmHg across the aortic stenosis by catheter. We performed intravascular ultrasound and confirmed there was a calcified circumferential stenosis without dissection or a false lumen in the aorta. Because of the calcified circumferential stenosis, poor expansion of the lesion was expected. Balloon dilatation was repeated with the use of an AngioSculpt 4.0 mm x 20 mm (Spectranetics), which provides a scoring effect to complex lesions. After scoring the calcification, a Gekira 10 mm x 40 mm (Boston Scientific) was used. After the balloon dilatation, considering the possibility that recoil could occur in the lesion, a 12 x 100 mm E-Luminexx strong radial force nitinol stent was chosen for its superior strength (Bard PV) and was post dilated using a pre dilated balloon. Angiography showed no severe dissection, rupture, or thrombosis (Figure 3). After the procedure, the pressure gradient disappeared, the ABI increased to 0.9, and there was no intermittent claudication. The patient was discharged with no apparent complications.

In post-procedural follow-up, the patient continued to show no intermittent claudication and ABI increased to 0.99 at the one-year and 1.02 at the two-year mark. A contrast-enhanced CT scan showed the stent had maintained patency, as there was no recurrent stenosis (Figure 4).

Discussion

A coral reef aorta is described as having rock-hard calcification in the visceral part of the aorta. A number of cases have been previously reported. In 1984, a number of female patients with heavily calcified coral reef aorta were reported by Qvafordt.1 More recently, there have been cases reported of lesions that are not restricted to the suprarenal aorta or just to women. In a report by Grotemeyer, 70 patients with coral reef aorta were reported, with a mean age of 59.5 years (women: 66% men: 34.3%).2 Although the pathophysiological basis for those 70 patients is unknown, there were observations of comorbidities such as syphilis, neurofibromatosis, rubella, and amyloidosis in some of the patients.

Patients with coral reef aorta show various symptoms including renovascular arterial hypertension, intermittent claudication, and chronic visceral ischemia.3-5 Diagnosis is through the routine measurement of blood pressure in the upper and the lower extremities in all hypertensive patients, regardless of the presence of intermittent claudication. Traditionally, endarterectomy and angioplasty have been the treatments for localized aortic atherosclerosis. In a study by Inahara looking at operative therapy, 59 patients with aortic atherosclerosis (53 claudication, 3 rest pain, 3 ulcer/gangrene) underwent endarterectomy.6 Two patients (3.7%) died within 30 days after endarterectomy.

The risks of the operation increase for lesions demonstrating severe resistant calcification. In a study by Grotemeyer et al, 59 patients with aortoiliac calcification disease underwent endarterectomy. Mortality was 5.8% and morbidity (acute leg ischemia, pleural effusion, bleeding, brain infarction, myocardial infarction, spleen rupture, terminal renal insufficiency, necrotizing pancreatitis, colon ischemia) was 30.4% within 30 days after endarterectomy.2 In another study by Vries et al, 69 patients with aortic atherosclerosis (61 claudication, 4 resting pain, 4 trophic changes) underwent percutaneous transluminal angioplasty (PTA) (24 lesions needed stent placement).7 The initial endovascular treatment succeeded technically and clinically in 68 patients. No procedure-related deaths occurred. Yet endovascular therapy for coral reef aorta has few reports.

Covered stent grafts are another method for the treatment of coral reef aorta. While relatively non-invasive, this approach is limited due to the low capacity for self-expansion of covered stent grafts and complications such as paraplegia due to occlusion of the side branch.8,9

In our case, the patient was treated with a self-expanding nitinol stent, an E-Luminexx 12 x 100 mm (Bard PV). Before the stent was deployed, balloon dilatation was performed to achieve the full capacity of the stent. In the case of a failed stent expansion, post dilatation can be performed. Treatment with a self-expanding nitinol stent can be done with minimal invasiveness, less so than surgical procedures or covered stent grafts. We hypothesize that there could be fewer complications, including spinal and visceral artery ischemia, when using an uncovered cell stent.

Conclusion

In this patient, endovascular therapy using a self-expanding nitinol stent was appropriate and beneficial for treatment of the coral reef aorta. Endovascular therapy is a potential alternative treatment to surgical therapy and a covered stent graft. 

References

  1. Qvarfordt PG, Reilly LM, Sedwitz MM, Ehrenfeld WK, Stoney RJ. “Coral reef” atherosclerosis of the suprarenal aorta: a unique clinical entity. J Vasc Surg. 1984 Nov; 1(6): 903-909.
  2. Grotemeyer D, Pourhassan S, Rehbein H, Voiculescu A, Reinecke P, Sandmann W. The coral reef aorta – a single centre experience in 70 patients. Int J Angiol. 2007 Fall; 16(3): 98-105.
  3. Bowman BT, Bernhard MR, Ibidapo AA, Okusa MD. Acute kidney injury due to ‘coral reef syndrome’. Kidney Int. 2013 Jan; 83(1): 182. doi: 10.1038/ki.2012.318.
  4. Blay E Jr, Zhou W. Rapid renal function deterioration: an unusual presentation of coral reef plaque. Ann Vasc Surg. 2014 January; 28(1): e13-260e16
  5. Berger L, Coffin O, Saplacan V, Pellissier A, Belin A. Aortic coral reef as an unusual possible cause of heart failure. Int J Cardiol. 2014 December; 177(3): e113-e114
  6. Inahara T. Evaluation of endarterectomy for aortoiliac and aortoiliofemoral occlusive disease. Disease Arch Surg. 1975; 110(12): 1458-1464.
  7. Vries JP, van Den Heuvel DA, Vos JA, van Den Berg JC, Moll FI, et al. Freedom from secondary interventions to treat stenotic disease after percutaneous transluminal angioplasty of infrarenal aorta: long-term results. J Vasc Surg. 2004 Feb; 39(2): 427-431.
  8. Holfeld J, Gottardi R, Zimpfer D, Dorfmeister M, Dumfarth J, Funovics M, et al. Treatment of symptomatic coral reef aorta by endovascular stent-graft placement. Ann Thorac Surg. 2008 May;85(5): 1817-1819.
  9. Chung TL, Mukherjee D. Successful endovascular management of an aortic rupture following stent placement for severe atherosclerotic stenosis: A case report. Int J Angiol. 2007 Summer; 16(2):73-76.

The authors can be contacted via Dr. Kazuki Haraguchi at superiot2000@yahoo.co.jp.

Disclosures: The authors report no conflicts of interest regarding the content herein.

Ethical approval: This treatment was performed in accordance with the Declaration of Helsinki.