Evolving Technologies for the Treatment of Type B Aortic Dissections—A Case Report and Review of the Literature

Article Citation:

Meghana R. K. Helder and J. Michael Bacharach (2018) Evolving Technologies for the Treatment of Type B Aortic Dissections—A Case Report and Review of the Literature. Journal of the Minneapolis Heart Institute Foundation: Spring/Summer 2018, Vol. 2, No. 1, pp. 38-43.

Case Report

Meghana R. K. Helder, MD

J. Michael Bacharach, MD

Department of Cardiovascular Surgery, Mayo Clinic, Rochester, MN; North Central Heart Institute, Sioux Falls, SD

Disclosures: None

Address for correspondence:
J. Michael Bacharach, MD
North Central Heart Institute
4520 W 69th St.
Sioux Falls, SD 57108
Tel: 605-977-5000

E-mail: mbacharach@ncheart.com

ABSTRACT

Uncomplicated type B aortic dissections have been traditionally treated with anti-impulse therapy. We present an interesting case of a 63-year-old male who presented with an uncomplicated type B aortic dissection, who within a week represented with a rupture and was successfully treated with endovascular therapy. Given enlightening data on the use of endovascular therapy of type B aortic dissection, we also give a brief review of new and emerging technologies.

Keywords: type B aortic dissection, endovascular repair

INTRODUCTION

Stanford Type B aortic dissections, with the intimal tear in the descending aorta, account for 25% to 40% of all dissections. These include the Debakey type IIIa (dissection in the descending thoracic aorta distal to the left subclavian artery and proximal to the celiac artery) and IIIb dissections (involving the thoracic and abdominal aorta distal to the left subclavian artery; Figure 1). They carry an 11.7% mortality rate with most deaths occurring in the first 24 hours. Type B aortic dissections can be either complicated or uncomplicated. By complicated, we mean the presence of acute life-threatening side effects of the dissection such as aortic rupture, impending rupture, or peripheral malperfusion. Or in a more subacute fashion, complication could also mean that hypertension or pain cannot be controlled. A total of 75% of type B dissections are uncomplicated1 and the standard of care, thus far, has been medical management to lower blood pressure and heart rate with anti-impulse therapy, most commonly beta-blockade or calcium channel blockade.

FIGURE 1
Debakey and Stanford classifications of aortic dissections.

In patients treated only with medical management, aneurysmal degeneration can occur in up to 28.5% of patients in an average follow up of 18.1 months.2 The 3-year survival is 77%3 and at 10 years, the survival drops to 56%.4 Even with this dismal survival rate, perhaps medical management is chosen as operative mortality rates were reported as 13% for those with acute type B dissections5 with limited survival rates of 11% at 15 years when including all complicated and noncomplicated patients with type B aortic dissections.6 Given less-than-stellar outcomes for either medical management or open surgical therapy for type B aortic dissections, endovascular therapy was introduced.

Patients with chronic type B dissections were randomized to optimal medical therapy (OMT) versus optimal medical therapy and thoracic endovascular repair (TEVAR) in the investigation of stent grafts in aortic dissection (INSTEAD) trial. In the long-term follow up of this study of 140 patients, 5-year aorta specific mortality was lower (6.9%) in TEVAR patients compared to patients receiving OMT alone (19.3%, P = 0.04). There was also less progression of the disease with TEVAR and increased expansion of the true lumen7 (Figure 2).

FIGURE 2
Data adapted for this figure from the investigation of stent grafts in aortic dissection trial, 5-year follow-up.7 Maximum aortic root diameter and false lumen diameter was smaller with thoracic endovascular repair (TEVAR) (P < .0001) than with optimal medical therapy (OMT).

Acute complicated type B dissections treated with endovascular therapy also show a benefit over open surgical repair in survival as shown by a meta-analysis of 29 studies. In these studies, the indications for intervention were aortic rupture, impending rupture, peripheral malperfusion, uncontrolled hypertension, or refractory pain. Early outcomes included a 9% 30-day mortality, 1.9% risk of paraplegia, and a 2% rate of type A dissection development.8 This is compared to a 30-day mortality of 33% undergoing open surgical repair, although this is likely a biased surgical population.9

The only randomized controlled trial looking at acute uncomplicated type B dissections is the ADSORB trial. A total of 61 patients will be randomized to endovascular therapy plus OMT versus OMT alone at 17 centers. The 1-year results of this study are promising in reduction of false lumen size reduction with stenting.10

However, even with this trial, the disseminated care for acute, uncomplicated type B dissections seems to be anti-impulse therapy alone. The reason for this stagnation in practice is unclear. However, this may be perhaps that the trials are not reaching the referring physicians or that, still, only select groups of surgeons and interventionalists are comfortable with endovascular therapy of the aorta. We present the case of 63-year-old gentleman who presented initially with an uncomplicated acute type B dissection but went on to rupture 7 days later. A review of the literature is presented as well, to highlight some emerging technologies to treat type B aortic dissections.

CASE REPORT

A 63 year-old white male was admitted to the hospital with a 1- to 2-day history of increasing abdominal and left-sided chest discomfort. The patient had previously been well but was known to have had a previous Type 1 aortic dissection repair in 1995. At that time, he underwent an emergent composite resection with reconstruction of the ascending aorta and aortic valve replacement with a 29-mm composite graft prosthesis with reimplantation of the coronaries.

The patient had originally presented to a health care institution other than ours with some abdominal discomfort. At that time, a computed tomography (CT) evaluation was done that demonstrated a complete dissection of the abdominal aorta. Dissection flaps were noted to extend to the brachiocephalic artery as well as the origin of the left carotid and left subclavian artery. The dissection flaps descended into the thoracic aorta and appeared extensive with the descending thoracic aorta measuring 6.7 cm. The dissection extended into the abdominal aorta to the level of the renal arteries. There was no evidence of rupture or extravasation of contrast outside the true or false lumens. He was discharged from the hospital with abdominal discomfort improved.

Over the subsequent 7 days, he again developed increasing abdominal and chest discomfort. Upon presentation to our institution, repeat CT at that time demonstrated a thoracoabdominal aortic dissection with what appeared to be a contained rupture of the descending thoracic aorta false lumen. The true lumen of the aorta at this point was 4.7 cm and the false lumen was 3.3 cm for a total diameter of 8 cm. The rupture was very localized. The entry tear again appeared to be just distal to the left subclavian and the dissection extends as to a level just below the renal arteries in which the aorta now again appears to be normal and measures 2.5 cm. (Figure 3).

FIGURE 3
Computed tomography scan on patient re-presentation showing complete dissection of the abdominal aorta from the (A) origins of cerebral vessels including (B) the thoracic aorta to the abdominal aorta at the (C) level of the renal arteries.

At the time of his clinical presentation, he was complaining of severe discomfort rated as 10 out of 10 severity. His vital signs demonstrated a systolic blood pressure of 110/63 with a heart rate of 70.Laboratory Assessment

At the time of presentation his hemoglobin was 12.2, which was a 2-gm decrease from 14.1 at the time of his emergency room evaluation 4 hours prior. Creatinine was 1.0 mg/dL and the INR was 3.3.Procedure

The patient was taken emergently to a hybrid operating room where he was prepped and draped from neck to knees in the usual sterile fashion. The patient was placed under general anesthesia. Access was obtained in the right common femoral artery and digital subtraction angiography was performed. The digital subtraction angiography revealed the proximal portion of the ascending aorta to be intact. There was a dissection plane with a large false lumen extending from approximately the left subclavian artery down through the descending thoracic aortic segment. Intravascular ultrasound (Volcano, 9 mhz, Phillips) was used. The proximal and distal landing zones were evaluated. There appeared to be a rupture with extravasation of contrast in the descending thoracic aorta. Based on the intravascular ultrasound measurements, a 45 × 150 mm thoracic stent graft (Gore TAG; WL Gore and Associates, Flagstaff, Arizona) was used. This was placed across the origin of the left subclavian artery just proximal to the origin of the left carotid. The device was then deployed. An additional 45 × 150 mm device was placed in an overlapping fashion. Balloon dilatation was then performed of the proximal and distal landing zones.

Subsequent contrast injection revealed near total occlusion of the false lumen. There was no evidence of extravasation of contrast outside the lumen. Further angiographic assessment demonstrated the celiac artery, superior mesenteric artery, and both renal arteries to be filling (Figure 4). The hospital course was uneventful. The patient’s abdominal and chest discomfort resolved and postoperative CT scan demonstrated no flow in the false lumen proximally. However, there was a residual dissection with fenestration at the level of the diaphragm. There was no evidence of endoleak (Figure 5). He was subsequently discharged on postoperative day 7 in stable condition.

FIGURE 4
Digital subtraction angiography images intraoperatively showing A. a large false lumen extending from approximately left subclavian artery down through the descending thoracic aortic segment. B.Poststenting, the false lumen is excluded.

FIGURE 5
A. Comparison of preoperative computed tomography (CT) scan to B. postoperative CT scan.

DISCUSSION

Our patient’s clinical presentation and subsequent emergent repair of his descending thoracic aortic rupture highlight the advantages of endovascular technology in treating these acute vascular emergencies. The case also highlights the importance of doing serial follow-up in patients who suffered previous type B aortic dissections for the development of false lumen enlargement.

The management of the left subclavian artery during TEVAR has varied widely with preoperative revascularization rates ranging from 0% to 60%. Symptoms in patients who did not undergo revascularization also ranged from 0% to 63%.11 The 2009 Society of Vascular Surgeons guidelines recommends individualization of subclavian artery revascularization during urgent intervention.12 We covered the left subclavian artery to get a good proximal seal in our patient and in the urgent state did not do a preoperative revascularization. Postoperatively the patient did not have symptoms and as such, revascularization was unnecessary.

Additionally, endovascular stenting for acute, uncomplicated type B dissections likely would have prevented the rupture in our patient. Several authors have looked at certain high-risk features that should prompt repair of an acute, uncomplicated type B dissection.13 These high-risk factors are initial aortic diameter >4 cm with a patent false lumen,14–16 initial false lumen diameter ≥22 mm in the proximal descending thoracic aorta,17 intramural hematoma with penetrating aortic ulcer in the proximal descending thoracic aorta,14,15 and recurrent or refractory pain or hypertension not controlled with optimal medical therapy18 (Table 1). Our patient’s initial aortic diameter was 6.7 cm, which was a high-risk anatomic factor; repair should have been considered at that time.

TABLE 1
Indications for repair of type B dissections.

Endovascular stenting of dissections has better clinical outcomes than medical management alone. This is likely due to the remodeling and volumetric changes that happen after a stent is deployed. Schoder et al.19 looked at 28 patients with acute type B dissection who were treated with endovascular stent repair and measured their false-lumen diameter at 1 year. Complete thrombosis of the false lumen was seen in 90% of patients who had stenting to the L1 vertebral level.19 Conrad et al.20 examined the postoperative remodeling of the false lumen in 33 patients with acute type B dissection and noted that 88% of patients had complete thrombosis within 1 year. Complete false-lumen thrombosis as a surrogate for a positive outcomes is secondary to prevention of flow in the false lumen. However a longer term study by the same authors showed that the diameter of the non-stented aorta increased in size,21 prompting promotion of more aorta being covered.

Because of the inconsistent thrombosis of the false lumen past the stented portion of the aorta, bare metal stenting distally to conventional covered thoracic stent grafts have been proposed. Melissano et al.22 utilized the PETTICOAT (Provisional Extension to Induce Complete Attachment) technique in 25 patients for the treatment of complicated type B dissections where bare metal stents were positioned over the origin of the renal and splanchnic arteries. The volumetric analysis for these patients showed decreased false lumen volumes in both thoracic and abdominal segments of the aorta.22 The utility of a covered stent plus distal bare metal stents was tested in a prospective multicenter trial by Lombardi and colleagues.23 In these 40 patients, an increase in true lumen size was seen along with a concomitant decrease in false lumen. Renal failure was seen in 12.5% of patients who required transient dialysis and 2.5% of patients experienced paraplegia.23 Potential downsides of bare metal stenting could be compromise of visceral arteries. Randomized controlled trials are required to see if distal bare metal stenting would truly result in better aortic remodeling and lower paraplegia rates without any untoward consequences.

Other strategies to induce favorable aortic remodeling have been to concentrate on achieving false-lumen thrombosis. Professor Kolbel and colleagues24 introduced the Knickerbocker technique where the true lumen is lined with a covered stent and the dissection membrane in the midsection of this coverage is ruptured in a controlled manner with a large compliant balloon in order to occlude the false lumen distally. This has only been reported in three patients thus far with technical success.24 The same group has described utilization of a vascular plug to occlude a large distal false lumen after traditional thoracic endovascular repair. A 3-month follow in one patient showed complete false-lumen thrombosis.25 A group from South Korea published a series of 25 patients undergoing similar false lumen occlusion procedures and reported a decrease in false lumen diameter, but more importantly, 0% spinal cord injury or renal failure rate in these patients.26 These techniques of occluding the false lumen may have benefits of aortic remodeling without the added risk of stenting across visceral arteries. However, these types of procedures could risk propagating the dissection.

Given the expanding indications for endovascular treatment of type B aortic dissections, newer therapies, and ways of treating the pathology have been introduced. Failure of current endovascular stenting for type B dissections is usually secondary to aortic aneurysmal growth because of complex hemodynamics through the false lumen. Multilayer flow modulators focus on altering hemodynamics. They are self-expanding mesh constructs of cobalt alloy wires interconnected in 5 layers and serve as channels of blood flow to native branches and laminate the blood flow in the aorta.27Computational fluid dynamics of the effects of potential flow modulators on 12 complex type B dissections were evaluated and the flow modulators were found to decrease the false lumen index from 0.29 ± 0.13 preoperatively to 0.21 ± 0.15 postoperatively. The 1-year outcomes of patients actually treated with flow modulators were recently presented and seemed promising in terms of reducing false lumen index with 0% rates of renal failure, paraplegia, or neurologic events.28 This manuscript is yet to be published. Because this is a newer technology that relies on hemodynamic changes instead of mechanical obstruction, the risk of failure is theoretically higher.

Endovascular therapy for type B dissections should strive to achieve more than coverage of the entry tear and in fact aim for aortic remodeling with ideally, complete thrombosis of the false lumen. Several new technologies and strategies have been developed and are being trialed to achieve this aim all in an attempt to improve the survival and decrease the reintervention rate in this difficult and high-risk group of patients. With these new technologies, lifelong follow-up of these patients is crucial with time intervals dictated by individual patient scenarios and success of therapy.

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