Indication, Timing and Results of Endovascular Treatment of Type B Dissection

Indication for Stent-graft Repair in Type B Aortic Dissection 

The natural course of aortic dissection is determined by two elements: early complications and chronic events. Early complications comprise any kind of malperfusion syndrome or rupture, while late events are usually a continued false lumen expansion with the risk for late rupture. Once a patient survives the first 2 weeks after the impact of dissection, the process is defined as chronic. Acute and chronic dissections differ considerably with respect to medical treatment, taking into consideration that even acute dissections can be complicated or uncomplicated.

The feasibility of stent grafting of the descending thoracic aorta has already been established as an alternative to surgical treatment of type B aortic dissection. However, due to the lack of both randomised controlled trials with long-term follow-up data and randomised comparisons with medical and surgical techniques, the indications for endovascular strategies remain to be fully defined for dissection (Table 1). There is clear observational evidence that depressurisation and shrinkage of the false lumen are beneficial in acute dissection, ideally followed by complete thrombosis of the false lumen and remodelling of the entire dissected aorta. Similar to previously accepted indications for surgical intervention, scenarios such as intractable pain, rapidly expanding false lumen, diameter >55mm and signs of imminent rupture or distal malperfusion are increasingly being accepted as indications for stent-graft placement in type B dissection.8, 9 Even in some cases of retrogradely extended type A dissections, stent-graft treatment of the descending thoracic aorta can also be performed as a single step or as two steps after initial surgical repair of the proximal part of the aorta or the arch. Open surgery may include an elephant trunk or transposition of arch vessels to allow optimal landing zones for endovascular completion in a hybrid approach. In case of retrograde type A dissection, an isolated distal-entry tear can sometimes be sealed by a stent graft, hence enabling thrombosis and remodelling even of the proximal false lumen in type A dissection. With endografting, paraplegia generally appears to be a rare phenomenon (0.8%), but is known to be associated with extensive coverage of the aorta exceeding 20cm and with the use of multiple stent grafts, or in case of previously operated aortas.10

Table 1. Distribution of differential therapeutic strategies in aortic dissection

	Surgery
	Type A aortic dissection
	Acute type B dissection complicated by
	Retrograde extension into the ascending aorta
	Dissection in fibrillinopathies (e.g., Marfan's syndrome, Ehlers–Danlos syndrome)
	Medical
	Uncomplicated, acute type B dissection
	Stable, isolated aortic arch dissection
	Chronic type B dissection
	Interventional
	Unstable, acute type B dissection
	Malperfusion
	Rapid expansion (>1cm per year)
	Critical diameter (≥5.5cm)
	Refractory pain
	Stable type B dissection (under evaluation)
	Type B dissection with retrograde extension into the ascending aorta
	Hybrid procedure for extended type A aortic dissection

Stable, Acute, Type B Aortic Dissection 

Patients with suspected acute aortic dissection should be admitted to the intensive care unit for prompt diagnostical evaluation under clinical and haemodynamic monitoring. Reduction of systolic blood pressure to 100–120mmHg, with an eye on the renal function and pain relief, is the initial priority and is achieved by morphine sulphate and intravenous beta-blocking agents (e.g., metoprolol, esmolol or labetolol) or by a combination with vasodilating drugs such as sodium nitropusside, at a dose of 0.3μgkg−1min−1, or angiotensin-converting enzyme inhibitors. Intravenous verapamil or diltiazem may also be used, if beta-blocking agents are contraindicated. A monotherapy with beta-blocking agents may be adequate to control mild hypertension (Table 2). In addition, heart rate should be kept low – a heart rate below 60bpm significantly decreases secondary adverse events (aortic expansion, recurrent aortic dissection, aortic rupture and/or need for aortic surgery) in type B aortic dissection compared to a conventional rate of more than 60bpm.11 Once both stable blood pressure and symptom relief are achieved, the patient with an acute, uncomplicated, type B aortic dissection can be discharged (usually within 14 days), and clinical and imaging follow-up should be offered and advised at 3 and 6 months and annually thereafter. In a series of 384 patients with type B dissections from the International Registry of Acute Aortic Dissection (IRAD), 73% were managed medically with an in-hospital mortality of 10%.1, 7, 12 The short-term survival rates were 91% at 1 month and 89% at 1 year. The reported long-term survival rate with medical therapy varies between 60% and 80% at 4–5 years and is around 40–45% at 10 years.1, 2, 7, 12 Yet again, the predictors of early mortality were malperfusion, hypotension, lack of chest or abdominal pain and partial thrombosis of the false lumen.7, 13

Table 2. Initial medical treatment in aortic dissection

	Name	Mechanism	Dose	Cautions/contraindications
	Esmolol	Cardioselective beta-1 blocker	Load: 500μgkg−1 IV	Asthma or bronchospasm
			Drip: 50μgkg−1min−1 IV	Bradycardia
			Increase by increments of 50μgmin−1	2nd- or 3rd-degree AV block
				Cocaine or methamphetamine abuse
	Labetalol	Non-selective beta-1,2 blocker	Load: 20mg IV	Asthma or bronchospasm
		Selective alpha-1 blocker	Drip: 2mgmin−1 IV	Bradycardia
				2nd- or 3rd-degree AV block
				Cocaine or methamphetamine abuse
	Enalaprilat	ACE inhibitor	0.625–1.25mg IV q 6h	Angio-oedema
			Max dose: 5mg q 6h	Pregnancy
				Renal artery stenosis
				Severe renal insufficiency
	Nitroprusside	Direct arterial vasodilator	Begin at 0.3μgkg−1min−1 IV.	May cause reflex tachycardia
			Max dose 10μgkg−1min−1	Cyanide/thiocyanate toxicity – especially in renal or hepatic insufficiency
	Nitroglycerin	Vascular smooth muscle relaxation	5–200μgmin−1 IV	Decreases preload – contraindicated in tamponade or other preload-dependent states
				Concomitant use of sildenafil or similar agents

Unstable, Acute, Type B Aortic Dissection 

About 30–42% of the acute type B aortic dissections are complicated, as evidenced by haemodynamic instability or peripheral vascular ischaemia.12 In contrast to the previously described stable, acute dissection, unstable patients have a highly unpredictable outcome. Among other complications, acute lower limb and visceral ischaemia have been reported in 30–50% of patients; malperfusion syndrome occurs frequently in cases of distally extended dissections and may lead to death in 50–85% of patients if not treated properly.5, 14, 15 In a necropsy study of 18 patients with type B dissection, a compression of the true aortic lumen with aortic obstruction was evident in 56% of patients.16 One mechanism of malperfusion may be the result of either static extension of the dissection flap directly into the orifice of a visceral or lower-limb artery, thereby narrowing its lumen, or of a dynamic obstruction of the vessel by means of the flap prolapsing into the vessel origin. Once diagnosed, these complications require emergent therapeutic action. However, despite a wide array of open surgical strategies, operative mortality rate for patients with acute aortic dissection, complicated by renal ischaemia, has been reported as high as 50%, and even 88% when mesenteric perfusion is impaired.17, 18, 19, 20 Fattori et al. compared the impact on survival of different treatment strategies in 571 patients with acute type B aortic dissection.21 Of the 571 patients with acute type B aortic dissection, 390 (68.3%) were treated medically; among the complicated cases, 59 (10.3%) underwent standard open surgery and 66 (11.6%) were subjected to an endovascular approach. The in-hospital mortality was significantly higher after open surgery (33.9%) than after endovascular treatment (10.6%; p=0.002) for those patients with complicated type B aortic dissection (Fig. 1). Thus, stent-graft repair is an attractive alternative to surgical repair for correcting ischaemic complications (Fig. 2)48. Usually, stent-graft occlusion of the entry site in the descending thoracic aorta results in thrombosis of the false lumen and predominant flow in the true lumen, thus normalising distal-vessel perfusion and restoring branch-vessel patency22 (Fig. 3). The PETTICOAT (provisional extension to induce complete attachment) concept takes the idea even further by extending the stent-graft scaffold distally with open-cell bare-metal stents. For instance, if malperfusion persists after coverage of the primary entry tear, additional distal open stents are the devices deployed until distal malperfusion is corrected.23 With this concept, aortic fenestration manoeuvres or branch-vessel re-vascularisation with uncovered stent are usually not needed and almost obsolete.

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Figure 1 Comparison of medical, surgical and endovascular treatment in patients with acute type B aortic dissection.21

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Figure 2 Comparison of elective- and emergency-treated patients with type B aortic dissection. Data from the TTR registry.48

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Figure 3 Malperfusion of distal aorta by occlusive type B dissection. Stent-graft placement in the true lumen of the proximal descending aorta re-established flow to the abdomen and legs.

The EUROSTAR/United Kingdom registry report represents a first large series of patients treated with thoracic aortic stent grafts; in this combined registry, 131 patients with aortic dissection (5% proximal, 81% distal and 14% not classified) were treated with stent grafts, with 57% of patients presenting with symptoms of rupture, aortic expansion or side-branch occlusion. Although meaningful long-term data are still lacking, primary technical success was achieved in 89% of patients, at the expense of a 30-day mortality rate of only 8.4%.24 A series of patients at the Arizona Heart Institute, comprising 40 patients (23 acute and 17 chronic) treated with a thoracic endograft for complicated, distal, aortic dissection, enjoyed a technical success rate of 95%. There was one peri-operative death due to iliac rupture and one case of paraplegia, while 15 patients (38%) experienced transient postoperative complications, mostly renal and pulmonary, the 1-year survival rate was 85%. Of the patients available for follow-up computed tomography (CT), 97% (30 of 31 patients) exhibited a stable or decreasing aortic diameter and no rupture occurred during the observational period, therefore justifying the conclusion that thoracic aortic stent grafting obviously stabilised the aorta and decreased the incidence of late expansion and aortic rupture.25 A meta-analysis of the literature from 2000 to 2004 replicated those results on patients subjected to endovascular stent-graft repair of aortic dissection in 609 patients.10 Procedural success was obtained in 98.2% of patients, with an in-hospital surgical conversion rate of 2.3% and an in-hospital mortality rate of 5.2%. Complications such as retrograde extension of the dissection into the ascending aorta were reported in 1.9% and neurological complications in 2.9% of patients. The 30-day mortality rate and in-hospital complications were documented more often in patients undergoing stent-graft treatment for acute aortic dissection as compared to patients undergoing treatment for chronic aortic dissections (9.8% vs. 3.2% and 21.7% vs. 9.1%, respectively; p<0.05). Schoder et al. reported a 30-day mortality of 10.7% in a series of 28 patients with complicated type B aortic dissection; at 1-year follow-up, the false lumen was thrombosed in 90% of the patients, and the mean difference of diameter reduction was highly significant.26 Similar results were reported by Chen et al. in their series of 62 patients.27 In a series of 16 patients with complicated, acute, type B aortic dissection treated with stent grafts within 48h after presentation, Verhoye et al. reported an early mortality rate of 25%, with no late death and a 5-year survival rate of 73%.28 In a single series in which the indication for stent grafting was strictly applied to those deemed unsuitable candidates for conventional open surgical repair, the 1- and 5-year survivals were 74% and 31%, respectively, after stent grafting compared to 93% and 78% (p<0.001) survival rates, respectively, after stent grafting in patients who were reasonable candidates for conventional open repair.29 Interestingly, a comparison between endovascular treatment of complicated type B aortic dissection with medical therapy of uncomplicated type B dissections in 56 patients and a follow-up of 18.1±16.9 months reported similar outcomes in both groups with better mid-term fate of the descending thoracic aorta in the stent-graft group, no paraplegia and no differences in the 5-year survival rate (86.3% in both groups)30 (Table 3).

Table 3. Results of endovascular stent-graft implantation in different clinical conditions

	Author	Year	n	Technical success (%)	Paraplegia (%)	Mortality (%)	Follow-up (month)
	Acute complicated type B dissection
	Beregi8	2003	46	96	n.a.	17	8
	Bortone45	2004	43	100	0	7	21
	Leurs24	2004	131	89	0.8	8.4	12
	Eggebrecht10	2006	609	98	0.8	11.2	24
	Chen27	2006	62	100	0	4.8	1
	Xu46	2006	63	95	0	10.6	48
	Schoder26	2007	28	86	3.6	10.7	36
	Verhoye28	2008	16	100	0	27	36
	Fattori21	2008	66	100	3.4	10.6	1
	Szeto47	2008	35	97.1	2.8	2.8	18
	Chronic type B dissection
	Nienaber37	1999	12	100	0	0	12
	Kato38	2001	15	100	0	0	24
	Eggebrecht35	2005	28	100	0	13.6	12
	Chen27	2006	19	100	0	11	27

Chronic Type B Aortic Dissection 

The evolution of an acute dissection to a chronic dissection involves progressive thickening of the intimal flap due to fibrosis. In addition, more intimal tears are reported in chronic type B aortic dissection compared to acute dissection. The growth rate of the chronically dissected distal aorta is estimated to range from 0.1 to 0.74cm per year depending on both the initial aortic diameter and the state of hypertension.31, 32 Unfortunately, the long-term outcome of medical therapy alone is suboptimal, with a reported mortality rate of 50% at 5 years and delayed expansion of the false lumen in 20–50% patients at 4 years.1, 33 This expansion of the false lumen, for which an initial diameter of more than 4cm and a persistent perfusion of the false lumen were determined as predictors, predisposes patients to aortic rupture or retrograde migration of the dissection towards the ascending aorta with an increased mortality rate.34, 35 Spontaneous thrombosis of the false lumen has been identified in <4% of patients.36 Endovascular treatment should be considered when the aortic diameter exceeds 55–60mm, when permanent thoracic pain occurs or in case of uncontrolled blood pressure and rapid growth of the dissecting aneurysm (>1cm per year) (Fig. 4). Nienaber et al. prospectively evaluated stent-graft management in 12 patients with chronic type B dissection and compared the results with 12 matched surgical controls. Proximal entry closure and complete thrombosis of the false lumen at 3 months were achieved in all the patients. Stent-graft treatment resulted in no morbidity or mortality, whereas surgical treatment resulted in four deaths (33%; p=0.04) and five adverse events (42%; p=0.04).37 Similar results were obtained by Kato in a series of 15 patients with no mortality during a follow-up of 2 years.38 Eggebrecht et al. compared the clinical outcome of 38 patients with type B aortic dissection (10 acute and 28 chronic) after endovascular stent-graft treatment. They observed significantly lower in-hospital mortality and a trend towards better 4-year survival rate in patients with underlying chronic aortic dissection39 (Table 3). Whether a prophylactic implantation of stent graft in patients with chronic type B aortic dissections is superior to medical treatment alone is actually under long-term follow-up evaluation in the prospective, randomised, controlled INSTEAD trial.34 At 12 months, Kaplan–Meier life-table analysis showed no mortality advantage of prophylactic stent-graft placement. The 2-year results are expected to be published.3, 4

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Figure 4 Type B aortic dissection in a 48-year-old man; note that there is a dynamic obstruction of the true lumen (TL) in the acute phase. In the chronic phase, there is still a partial perfusion of the false lumen with additional partial thrombosis. After stent-graft placement across the proximal thoracic entry, the entire true lumen of the thoracic aorta is reconstructed with time, with complete ‘healing’ of the dissected aortic wall and shrinking of the completely thrombosed false lumen (FL). TH: thrombus.

Timing of Endovascular Repair 

The optimal timing for endovascular intervention in type B dissections remains controversial. In 2002, Bortone et al. defended an immediate intervention within 2 weeks of the initial diagnosis; a stent-graft placement was successful in all the patients referred for intervention within the first 2 weeks.40 Conversely, others have obtained higher mortality rates in patients with acute type B aortic dissection compared to patients with chronic aortic dissections.39 Kato et al. speculated that morphological changes of the initially fragile dissecting membrane to a more fibrotic and seemingly stable membrane in the chronic phase are critical for endovascular repair and recommend a treatment after a minimum period of 4 weeks after the onset of aortic dissection.41 In addition, the more stable clinical status of the patients in the chronic phase of aortic dissection may be an important determinant of better survival following endovascular repair. On the other hand, patients with acute aortic dissection have the greater potential for stent-graft-induced complete remodelling of the entire aorta (Fig. 5). Shimono et al. reported that complete obliteration and resolution of the false lumen following endovascular stent-graft treatment were more frequently achieved in patients with acute aortic dissection compared to patients with chronic aortic dissection (70% vs. 38.5%).42 In fact, due to lack of prospective randomised data comparing immediate and delayed intervention in various clinical and anatomical constellations, no general recommendation has been issued with respect to timing of endovascular treatment so far; observational evidence, however, may favour an early intervention, when justified by complications.

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Figure 5 Impact of treatment timing on event (MAVE) free survival in patients with acute aortic dissection (own results).

Long-Term Follow-Up and Adjunctive Treatment 

The long-term approach to patients with successful initial treatment of aortic dissection begins with an appreciation that such patients have a systemic illness that invariably involves the entire aorta and branches as targets for future complications. Systemic hypertension, advanced age, aortic size and presence of patent false lumen are all factors that identify higher risk.33, 43 Therefore, all patients deserve aggressive medical therapy, follow-up visits and surveillance, including serial imaging. Treatment with effective beta-blocking agents, and potentially sartans, is the cornerstone of medical therapy regardless of whether their in-hospital definitive treatment was surgical, medical or interventional. Pure vasodilators, such as dihydropyridine calcium-channel antagonists or hydralazin, may cause an increase in dP/dt and should therefore be used only in conjunction with adequate beta-blockade. ACE inhibitors are attractive antihypertensive agents for treating aortic dissection and may be of particular benefit in patients with some degree of renal ischaemia as a consequence of the dissection. Late aneurysm rupture after aortic dissection is 10 times more common in patients with poorly controlled hypertension than in those with controlled blood pressure.33 The guidelines recommend progressive up-titration of dosage to achieve a blood pressure <135/80mmHg.1, 2, 44 Serial imaging for the aorta is an essential component of long-term treatment and follow-up of patients with aortic aneurysm (before and after surgery or stent-graft placement) in all cases of chronic dissection. Choice of imaging modality may vary with institutional availability and expertise, and also with the extent of aortic involvement and age of the patient. Previous recommendations suggest follow-up imaging and examination at 1, 3, 6, 9 and 12 months after discharge and annually thereafter.1, 2 This aggressive strategy supports the notion that both hypertension and aortic expansion/dissection are common and not easily predicted in the first months after hospital discharge. Furthermore, imaging is not confined simply to the region of initial involvement because both dissection and aneurysm formation may occur anywhere along the entire length of the aorta. The patients who have been treated by open surgery and/or endovascular stent grafting warrant similar a follow-up than those whose initial strategy was limited to medical treatment alone.

Conflict of Interest/Funding 

None.