Thoracic Endovascular Aortic Repair With Additional Distal Bare Stents in Type B Aortic Dissection Does Not Prevent Long-Term Aneurysmal Degeneration

Abstract

Purpose:

TEVAR (thoracic endovascular aortic repair) + PETTICOAT (Provisional ExTension to Induce COmplete ATtachment) technique has been selectively employed since 2005 at our institution during endovascular treatment of type B aortic dissection (TBD). The aim of this study is to evaluate the long-term (>5 years) clinical results and the evolution of aortic volume.

Materials and Methods:

All the patients receiving an endovascular treatment for TBD with the PETTICOAT technique were collected in a prospectively maintained database and follow-up computed tomography scan were retrospectively analyzed. Study endpoints included short- and long-term clinical success (absence of need for reintervention) and any major adverse event. The volumes of thoracic and abdominal aorta at long-term follow-up were also analyzed.

Results:

Twenty-eight patients received a TEVAR + PETTICOAT and were followed up (median follow-up 85 months). Primary 30-day clinical success rate was 82% with an adverse event rate of 31%; 4 type I endoleak and 1 retrograde dissection were recorded. Secondary mid-term clinical success was 96% while the long-term clinical success rate was 79%. Six cases (21%) received either an open repair or an endovascular repair for a significant distal aortic enlargement at follow-up. With regards to volumetric analysis, an increase of overall (thoracic and abdominal) aortic volume was observed in 8 cases mainly related to an increase (mean: +31%) of the abdominal volume that was observed in 11 cases.

Conclusions:

PETTICOAT technique does not protect from long-term significant aneurysmal degeneration that may require aortic open or endovascular reinterventions. Aortic growth occurs mainly in the bare-stented aorta and thus, life-long surveillance is advisable in these patients.

Keywords

type B aortic dissection endovascular treatment aortic volume TEVAR PETTICOAT

Introduction

Current guidelines for acute/subacute type B aortic dissection (TBD) recommend treatment in case of complicated dissection.¹ The management in case of uncomplicated TBD has been strongly debated: although medical management has been widely considered as first line treatment, TEVAR has also been advocated to prevent long-term aortic dilatation and rupture. IRAD (International Registry of Acute Aortic Dissection) reported reduced mortality at 5 years in acute TBD patients treated by TEVAR, compared with those managed medically.² ADSORB, the only randomized control trial in patients with uncomplicated acute TBD, shows higher rates of false lumen (FL) thrombosis in patients randomized to TEVAR, and FL thrombosis is associated with fewer late complications and increased aortic remodeling following repair of acute TBD.³

Standard thoracic endovascular aortic repair (TEVAR) associated with disease specific bare stents (referred to with the acronym PETTICOAT)⁴ have been proposed to both cover the entry tear and treat malperfusion, however, it is still uncertain whether it also prevent aneurysmal degeneration of the dissected aorta.^5,6

The aim of this study was to evaluate the long-term (>5 years) clinical results of a single-center patient cohort treated selectively with the TEVAR + PETTICOAT technique for TBAD, as well as evaluate the fate of the dissected aorta at follow-up and the rate of late reinterventions required for aneurysmal degeneration.

Our short- and mid-term results of this technique were previously published in 2012.⁷ A significant immediate increase in true lumen could be achieved with resolution of all cases of dynamic malperfusion and true lumen collapse but the efficacy in preventing the aneurysmal degeneration was unclear. In this article, the longer follow-up allowed us to evaluate the role of PETTICOAT technique to prevent secondary aortic reintervention due to aneurysmal degeneration or other complications.

Materials and Methods

Study Design and Patient Population

Between 2005 and 2014, data from consecutive patients treated in our institution for TBD by means of TEVAR + PETTICOAT technique was collected in a prospectively maintained database and retrospectively analyzed. The 2-year results of the first 25 patients were previously published.⁵ The study complies with the Declaration of Helsinki, all patients having signed an informed consent to the procedure itself and to allow the use of de-identified collected data for scientific purposes at the moment of the admission. Preoperative, intraoperative, and postoperative data were reported according to the Society for Vascular Surgery Suggested Reporting Standards and to the Society for Vascular Surgery/American Association for Vascular Surgery (SVS/AAVS).^8,9 The indication to the use of the PETTICOAT technique was the presence of complicated dissection with malperfusion, symptomatic for renal, visceral or limb malperfusion. The timing from the onset of dissection was various, from acute to chronic, within 2 weeks from onset to over 3 months after the initial acute event.

Diagnostic Work-up and Procedure

Routine preoperative assessment, procedure details and technique were described in previous publications.⁵ All procedures were performed in the operating room (Ziehm Vision RFD Hybrid edition; Ziehm Imaging, Nürnberg, Germany) under general anesthesia with transesophageal echography monitoring. Supra-aortic debranching procedures were performed to obtain an adequate proximal landing zone when needed. The origin of the left subclavian artery was occluded, when appropriate, with an Amplatzer Vascular Plug (AVP I or II; AGA Medical, Plymouth, MN). Ballooning of the stent-graft or the bare stents was never performed in this cohort of patients. Primary left subclavian revascularization was indicated for paraplegia prevention in patients requiring more than 25 cm of aortic coverage and in which at least one hypogastric artery was occluded.^10,11 All procedures were performed using the Zenith Dissection Endovascular System (Cook Inc, Bloomington, IN) that is a modular system specifically designed to treat aortic dissection that consists of a proximal component, the Zenith TX2-P TAA (thoracic aortic aneurysm) endovascular graft, and a distal component, the Zenith dissection endovascular stent. The proximal component was a one-piece (cylindrical or tapered) endovascular stent graft that was intended to close the primary entry tear and was available in lengths from 115 to 216 mm with diameters ranging between 22 and 42 mm. Off-the-shelf tapered grafts are 4 mm smaller at the distal end. The endograft diameter was always chosen about 10% more than aortic diameter. The distal component, the Zenith dissection stent (TXD), is a one-piece cylindrical device that was provided in a single diameter size (46 mm) that may be used in transaortic diameter of 24 to 38 mm due to the low radial force and in three different lengths (82, 123, and 164 mm).

Clinical Outcomes and Imaging Follow-up

All patients were followed up with a yearly clinical visit and/or computed tomography (CT) scan at the outpatient clinic. For patients not showing up at the annual visit, phone interviews were performed asking to send CT scans. Patients who did not show up for the visit and did not answer to 2 consecutive phone calls, were considered lost at follow-up. As for the previous analysis,⁵ the evolution of the aorta was studied by volume analysis. Volumes of the entire aorta starting from the origin of the innominate artery up to the aortic bifurcation were measured. The thoracic segment was considered from the origin of the innominate artery to the celiac trunk; the abdominal segment was considered from the celiac trunk to the aortic bifurcation. In the volume change analysis, we assessed the mean percentage volume variation as compared to the preoperative CT scan, used as reference, and the number of cases with a volume increase of more than 10%. Aortic diameter at the thoracic and abdominal level were measured and collected. All the CT scans were stored and analyzed using the OsiriX software vs 3.9 (Pixmeo SARL, Bernex, Switzerland) by the same operators (DM and SS).

Clinical success was considered as the absence of aortic complications needing a reintervention. Any aortic complication needing a reintervention or death due to the aortic procedure is considered as adverse events.

Statistical Analysis

Continuous variables are expressed as median, first quartile and third quartile (IQR = Q1-Q3) and differences were tested with the 2-sided t-test or the Mann-Whitney U test. Categorical variables are expressed as counts and percentage and the chi-square or Fischer exact test were used for analysis. Wizard Statistics (Version 1.9.36, EvanMiller.org) software for MacOS was used for data analysis.

Results

Demographic details and preoperative risk factors of the 28 patients (25 males, 89.2%) are described in Table 1. The pattern of perfusion of the visceral vessel is reported in Table 2. Six patients were treated within 2 weeks from onset, 15 patients between 2 weeks and 3 months, and seven patients at 3 months after the initial acute event. Ishimaru’s zone 1 was chosen as TEVAR landing zone in 2 cases (7%), zone 2 in 18 cases (64%) and zone 3 in 8 cases (29%). Carotid-to-carotid bypass debranching was performed in all Ishimaru’s zone 1 cases while left carotid-subclavian bypass was performed selectively in 8 out of 18 cases (29%) who underwent zone 2 coverage.

Table 1.

Preoperative Risk Factors of the Cohort (Total 28 Cases), According to the Society for Vascular Surgery Reporting Standards.^a

Variable	n (%)
Male	25 (89)
Age, y, mean	60.2
Hypertension (grade ≥1)^b	24 (85)
1	4 (14)
2	4 (14)
3	16 (57)
Smoking (grade ≥1)^c	14 (50)
1	8 (29)
2	2 (7)
3	4 (14)
Diabetes (grade ≥1)^d	3 (11)
1	1 (4)
2	2 (7)
3	0 (0)
Renal status (grade ≥1)^e	7 (25)
1	6 (21)
2	0 (0)
3	1 (4)
Cardiac status (grade ≥1)^f	1 (4)
1	1 (4)
2	0 (0)
3	0 (0)
Pulmonary status (grade ≥1)^g	5 (18)
1	5 (18)
2	0 (0)
3	0 (0)
Connective tissue disorder	1 (4)
Aortic pathology^h	28 (100)
1	27 (96)
2	0 (0)
3	1 (4)

Categorical data are given as the number (percentage).

Hypertension: 1, easily controlled with single drug; 2, controlled with 2 drugs; 3, required more than 2 drugs or uncontrolled.

Smoking: 1, none current, but smoked in past 10 years; 2, current, less than 1 pack/day; 3, current, greater than 1 pack/day.

Diabetes: 1, adult onset and diet controlled; 2, adult onset and oral medication controlled; 3, adult onset and insulin controlled.

Renal status: 1, creatinine 1.5–3.0 mg/dL, clearance 30–50 mL/min; 2, creatinine 3.0–6.0 mg/dL, clearance 15–30 mL/min; 3, creatinine >6.0 mg/dL, clearance <15 mL/min or on dialysis or with transplants.

Cardiac status: 1, asymptomatic, remote myocardial infarction (MI) by history >6 months or occult MI by electrocardiogram; 2, stable angina, controlled ectopy or symptomatic arrhythmia, drug compensated congestive heart failure (CHF); 3, unstable angina, symptomatic or poorly controlled ectopy or arrhythmia or poorly compensated CHF, MI within 6 months.

Pulmonary status: 1, asymptomatic or mild dyspnea on exertion, mild X-ray parenchymal changes, pulmonary function test (PFT) 65% to 80% of predicted; 2, between 1 and 3; 3, vital capacity less than 1.85 L, forced expiratory volume (FEV) less than 35% of predicted, maximal voluntary ventilation less than 28 L/min or less than 50% of predicted, pCO2 greater than 45 mm Hg, supplemental oxygen use necessary or pulmonary hypertension.

Aortic pathology: 1, none; 2, previous abdominal aortic intervention; 3, previous thoracic aortic intervention.

Table 2.

Preoperative Perfusion of Aortic Side Branches.^a

	TL	FL	TL and FL	Obstruction
Celiac trunk	20 (71)	1 (4)	7 (25)	0 (0)
Superior mesenteric artery	25 (89)	0 (0)	3 (11)	0 (0)
Right renal artery	13 (46)	5 (18)	7 (25)	3 (11)
Left renal artery	11 (39)	9 (32)	7 (25)	1 (4)

Abbreviations: FL, false lumen; TL, true lumen.

Categorical data are given as the number (percentage).

The overall 30-day clinical success was 82%. No 30-day mortality was recorded, 1 open conversion was required for intraoperative retrograde dissection and 4 cases of type IA entry flow were observed. One type II entry flow from the left subclavian artery plug was recorded. Spinal cord ischemia was observed in 4 cases (14%), 2 of which with a late onset due to hemodynamic instability. All patients with spinal cord ischemia received cerebrospinal fluid drainage at the onset of symptoms. Symptoms resolved in the 2 cases with delayed onset and remained unchanged in the 2 cases with immediate onset. Five cases (18%) had a transient mild renal failure. No strokes were recorded. Mean follow-up was 85 months (range 5–156 months) with an overall procedure unrelated mortality rate of 7% (2 cases) and 6 cases (21%) were lost at follow-up.

The secondary mid-term (<5 years) clinical success was 96%. Two perioperative type IA entry flow spontaneously solved, 2 were treated with proximal stent-grafting with the need for adjunctive debranching procedure: 1 case of carotid-to-carotid bypass and 1 complete supra-aortic trunks rerouting from the ascending aorta. The type II entry flow was sealed with the deployment of an adjunctive plug to occlude the origin of the left subclavian artery and 1 case of left renal artery stenosis received a primary stenting, 5 months after the procedure.

The secondary long-term (>5 years) clinical success was 75%. Seven cases (25%) of open or endovascular aortic reinterventions due to a significant distal aortic enlargement were performed (Figure 1). Five cases (17%) were treated by means of an open conversion for a thoraco-abdominal aneurysm (3 cases) and an infrarenal aortic aneurysm (2 cases). One patient received a distal stent-grafting to seal a limited thoracic FL dilatation. One patient received a branched stent graft (Zenith t-Branch Thoracoabdominal Endovascular Graft) for endovascular treatment of aneurysmal degeneration and bare stent disconnection. No splanchnic or renal arteries occlusion were recorded during the entire follow-up.

With regard to aortic volumetric analysis the preoperative CT scan was compared with the last available postoperative one (Table 3). Twelve patients were lost at follow-up. On 16 patients we found a mean increase of the thoracic aortic volume of 3% (203.9±73.8 vs 210.7±63.6 cm³) and a mean increase of the abdominal aortic volume of 48% (71.0±24.1 vs 105.3±41.4 cm³) with a total aortic volume increase of +16% (274.9±88.5 cm³ vs 318.9±88.1 cm³). In addition, we recorded an increase of more than 10% of the overall aortic volume (thoracic + abdominal) in 8 of 16 cases (50%) and an increase of the abdominal volume in 11 of 16 cases (69 %) (Figure 2).

Table 3.

Mean Volume (cm³) and Rate of Volumes Change (+10%) of the Different Aortic Segments After PETTICOAT Technique.^a

	Preoperative Volume	Long-Term Volume	Patients (n) With Long-Term Variation (+10%)
	(28 cases)	(16 cases)	(16 cases)
Overall (thoracic + abdominal)	274.9±88.5	318.9±88.1 (+16%)	8 (50)
Thoracic aorta	203.9±73.8	210.7±63.6 (+3%)	3 (18)
Abdominal aorta	71.0±24.1	105.3±41.4 (+48%)	11 (69)

Continuous data are presented as average ± standard deviation. Categorical data are given as the number (percentage).

Furthermore, a diametric analysis on the 16 patients at long-term follow-up was performed: The larger diameter in the thoracic and abdominal segment in the preoperative CT scan was evaluated and compared with the last one available (Figure 3). The preoperative maximum diameter was 42.4±7.1 mm in the thoracic segment and 30.6±5.2 mm in the abdominal segment. At the long-term follow-up we observed an increase of +5.9% and +27.8%, respectively, in thoracic (44.9±12.6 mm) and abdominal segment (39.1±8.2 mm).

Discussion

In the past 2 decades, TEVAR has emerged as the treatment of choice for complicated acute TBD. However, the natural history of the aorta after TEVAR performed for acute TBD is still unclear. Results from the IRAD registry show a 27% 1-year risk of aneurysmal degeneration and 20% risk of reintervention with 73% of aneurysmal degeneration at 5 years in a similar population.² In our experience, we found that late aneurysmal degeneration was present in 7 of 28 patients (25%) needing open conversion in 5 (2 AAAs and 3 TAAAs open repair) and endovascular relining in 2 case.

There are several potential mechanisms that have been advocated in order to explain aneurysmal degeneration of the dissected aorta. Of them, the thinning of the aortic wall may be intuitively considered to be at the basis of subsequent dilatation; however, there is fairly strong clinical and experimental evidence that this is not the case. Chiu et al¹² reviewed 11 articles on endarterectomy as surgical management of atherosclerotic aorto-iliac occlusive disease with at least 10 years of follow-up and they did not find any case of secondary aneurysm at endarterectomy site. Another indication that aortic wall thickness is unrelated to aneurysmal degeneration emerges from data published by Panneton et al¹³ about surgical fenestration and septectomy for complicated TBD in which the authors showed that at 5.1 years of follow-up, there were no false aneurysm formations at the fenestration site.

A pivotal finding to clarify the physiopathology of aortic dissection was that patients with partial thrombosis of the FL had worse outcomes than those with either complete thrombosis or fully patent FL.¹⁴ Also the existence of a large proximal entry tear and small distal entry tears play a major role, as it has been proved that those patients have a significant higher risk of late aortic dilatation mostly because of a persistent high pressure in the false lumen.^15,16 A bench top model constructed on these assumptions has been tested by Berguer et al¹⁷ to determine the relationship between the area of tears and the value of pressure differential among true lumen (TL) and FL. They found that the wider the areas of proximal and distal tears, the lower the pressure differential between TL and FL, concluding that septectomy from distal to proximal entry tears should be the initial treatment for these patients. Clearly there is a strong need for a better understanding of the mechanisms that induce aneurysmal degeneration after TBD even in the presence of simple TEVAR. Several adjunctive procedures have been proposed in order to prevent the tendency to aneurysmal degeneration and their basic mechanism of action is either the induction of thrombosis of the false lumen^18–20 or the creation of unrestricted flow in the two lumina or even better the restitution of a single channeled vessel. Among these procedures, one in particular has been first proposed in 2006 by Nienaber and coworkers² and provides the use of bare self-expandable stents in the distal portion of the dissected aorta for the purpose of solving those issues like persistent dynamic malperfusion, intimal lamella flapping, renal/visceral arteries perfusion, not addressed by simple TEVAR.

It has been referred to by the acronym PETTICOAT (Provisional ExTension To Induce COmplete ATtachment) and demonstrated to be particularly useful when the true lumen is still collapsed after the proximal stent graft placement with persisting dynamic malperfusion. Both single center experiences and an international multicenter trial² have shown significant increase in the true lumen diameters and volume. In our previous article,⁵ we observed a resolution of all cases of dynamic malperfusion after the deployment of the Zenith Dissection Endovascular System; the use of adjunctive endovascular procedure allowed to solve some cases of static malperfusion.

Our previous mid-term volumetric analysis observed that the overall aortic volume remained unchanged and the FL shrinkage was related to the redistribution of the lumina after TL re-expansion related to the PETTICOAT technique.⁵ As a matter of fact we reported that even if shrinkage of the FL was evident over time mainly in the thoracic segment (−35% at 1 year and −38% at 2 years), overall volume of the abdominal segment, after initial TL expansion, failed to progressively remodel and tended to enlarge due to FL expansion. This peculiar behavior has already been shown by other authors, and in a recent review²¹ we analyzed 11 studies using the PETTICOAT technique in 439 cases of type A (n=40; 9.1%) and type B (n=399; 90.9%) dissection. Results of this review showed that FL remained stable with no shrinkage in 4 studies and increased in 2 at 2-year follow-up.

Moreover, our study shows a total aortic volume increase of 16% (274.9±88.5 vs 318.9±88.1 cm³) and this was mainly due to an increase of 48% in the abdominal segment (71.0±24.1 vs 105.3±41.4 cm³). Furthermore, in the thoracic segment volume increased with time of 3% (203.9±73.8 vs 210.7±63.6 cm³). This finding confirms that entry tears coverage is the key for having FL depressurization, aortic remodeling, and healing over time. The diameter analysis confirms the volumetric results: We observed a greater variation in the abdominal segment (+27.8%) while the thoracic portion remained nearly unchanged (+5.9%).

In addition, we found that 69% of our patients experienced an aortic volume increase of more than 10% at long term follow-up. These data suggest once again that the risk of late evolution in these patients is significant and it should be taken into account, by confirming the need of lifelong surveillance. Another reported issue is the long-term patency of visceral branches after PETTICOAT.²² Our late results suggest that prophylactic stenting of renal and splanchnic vessels is not indicated in patients without malperfusion, as only 1 case of short-term stenosis of a renal artery was observed after reintervention.

In this scenario, it is now recognized that as some degree of perfusion of the FL is maintained after PETTICOAT, as the aorta shows a tendency to grow distally to the stent-graft.^23–25 In this scenario, Hofferberth and coworkers²⁶ in 2012 proposed an evolution of the PETTICOAT technique, consisting of ballooning the TL inside the previously deployed covered stent-grafts and uncovered BMS, in order to obtain the rupture of the intimal lamella and allow full expansion of the stent in a “renewed” uni-luminal aorta. This procedure was named the “Stent-Assisted Balloon-Induced Intimal Disruption and Relamination in Aortic Dissection Repair” (STABILISE).²⁶ It produced excellent initial results in the authors’ experience, especially with regard to the relief of malperfusion, and the reduction of reintervention rate. At first, the STABILISE technique did not gain immediate acceptance in the vascular community, this because of concerns regarding the potential risk of rupturing the aorta during ballooning.

We acknowledge that this is a retrospective study that analyses data of patients coming from a prospectively maintained database and followed over a mean period of 7.1 years. The small number of patients may be considered a limitation of this study, preventing us from performing a stratification of results or subgroup analysis. Despite that, long-term follow-up remains an important finding for helping to understand the mechanisms that induce aneurysmal degeneration after TBAD. The need for a treatment that not only fulfills requirements of patients in the acute and subacute phase but also prevents their aorta from undergoing aneurysmal dilatation and the STABILISE technique is emerging as a valuable candidate.^27,28

Conclusion

The long-term results in this small cohort of patients treated with TEVAR and PETTICOAT for TBAD show that while the initial clinical results are satisfactory, this treatment does not protect from aneurysmal degeneration in a significant number of cases. Therefore, long-term follow-up is warranted in these patients and additional procedures may be required.

Footnotes

Declaration of Conflicting Interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

ORCID iDs

Daniele Mascia

Andrea Melloni

Andrea Kahlberg

Luca Bertoglio

Fabrizio Monaco

References

Riambau

Böckler

Brunkwall

, et al. Editor’s Choice. Management of descending thoracic aorta diseases: clinical practice guidelines of the European Society for Vascular Surgery (ESVS). Eur J Vasc Endovasc Surg. 2017;53:4–52.

Fattori

Montgomery

Lovato

, et al. Survival after endovascular therapy in patients with type B aortic dissection: a report from the International Registry of Acute Aortic Dissection (IRAD). JACC Cardiovasc Interv. 2013;6:876–882.

Brunkwall

Kasprzak

Verhoeven

, et al; the ADSORB Trialists. Endovascular repair of acute uncomplicated aortic type B dissection promotes aortic remodelling: 1 year results of the ADSORB trial. Eur J Vasc Endovasc Surg. 2014;48:285–291.

Nienaber

Kische

Zeller

, et al. Provisional extension to induce complete attachment after stent-graft placement in type B aortic dissection: the PETTICOAT concept. J Endovasc Ther. 2006;13:738–746.

Fattori

Cao

De Rango

, et al. Interdisciplinary expert consensus document on management of type B aortic dissection. J Am Coll Cardiol. 2013;61:1661–1678.

Famularo

Meyermann

Lombardi

JV.

Aneurysmal degeneration of type B aortic dissections after thoracic endovascular aortic repair: a systematic review. J Vasc Surg. 2017;66:924–930.

Melissano

Bertoglio

Rinaldi

, et al. Volume changes in aortic true and false lumen after the “PETTICOAT” procedure for type B aortic dissection. J Vasc Surg. 2012;55:641–651.

Johnston

Rutherford

Tilson

, et al. Suggested standards for reporting on arterial aneurysms. J Vasc Surg. 1991;13:452–458.

Chaikof

Fillinger

Matsumura

, et al. Identifying and grading factors that modify the outcome of endovascular aortic aneurysm repair. J Vasc Surg. 2002;35:1061–1066.

10.

Czerny

Eggebrecht

Sodeck

, et al. Mechanisms of symptomatic spinal cord ischemia after TEVAR: insights from the European Registry of Endovascular Aortic Repair Complications (EuREC). J Endovasc Ther. 2012;19:37–43.

11.

Melissano

Bertoglio

Mascia

, et al. Spinal cord ischemia is multifactorial: what is the best protocol? J Cardiovasc Surg. 2016;57:191–201.

12.

Chiu

Davies

Nightingale

, et al. Review of direct anatomical open surgical management of atherosclerotic aorto-iliac occlusive disease. Eur J Vasc Endovasc Surg. 2010;39:460–471.

13.

Panneton

Teh

Cherry

Jr , et al. Aortic fenestration for acute or chronic aortic dissection: an uncommon but effective procedure. J Vasc Surg. 2000;32:711–721.

14.

Tsai

Evangelista

Nienaber

, et al. International Registry of Acute Aortic Dissection. Partial thrombosis of the false lumen in patients with acute type B aortic dissection. N Engl J Med. 2007;357:349–359.

15.

Tsai

Schlicht

Khanafer

, et al. Tear size and location impacts false lumen pressure in an ex vivo model of chronic type B aortic dissection. J Vasc Surg. 2008;47:844–851.

16.

Rudenick

Bijnens

García-Dorado

, et al. An in vitro phantom study on the influence of tear size and configuration on the hemodynamics of the lumina in chronic type B aortic dissections. J Vasc Surg. 2013;57:464–474.

17.

Berguer

Parodi

Schlicht

, et al. Experimental and clinical evidence supporting septectomy in the primary treatment of acute type B thoracic aortic dissection. Ann Vasc Surg. 2015;29:167–173.

18.

Pellenc

Roussel

De Blic

, et al. False lumen embolization in chronic aortic dissection promotes thoracic aortic remodeling at midterm follow-up. J Vasc Surg. 2019;70:710–717.

19.

Kölbel

Lohrenz

Kieback

, et al. Distal false lumen occlusion in aortic dissection with a homemade extra-large vascular plug: the candy-plug technique. J Endovasc Ther. 2013;20:484–489.

20.

Kölbel

Carpenter

Lohrenz

, et al. Addressing persistent false lumen flow in chronic aortic dissection: the knickerbocker technique. J Endovasc Ther. 2014;21:117–122.

21.

Bertoglio

Rinaldi

Melissano

, et al. The PETTICOAT concept for endovascular treatment of type B aortic dissection. J Cardiovasc Surg. 2019;60:91–99.

22.

Canaud

Ozdemir

Alric

The Provisional Extension To Induce Complete Attachment (PETTICOAT) technique to promote distal aortic remodelling in repair of acute DeBakey type I aortic dissection: is the best the enemy of the good?

Eur J Cardiothorac Surg. 2016;50:153–154.

23.

Lombardi

Cambria

Nienaber

, et al; STABLE Investigators. Aortic remodeling after endovascular treatment of complicated type B aortic dissection with the use of a composite device design. J Vasc Surg. 2014;59:1544–1554.

24.

Alsac

Girault

El Batti

, et al. Experience of the Zenith Dissection Endovascular System in the emergency setting of malperfusion in acute type B dissections. J Vasc Surg. 2014;59:645–650.

25.

Sobocinski

Lombardi

Dias

, et al. Volume analysis of true and false lumens in acute complicated type B aortic dissections after thoracic endovascular aortic repair with stent grafts alone or with a composite device design. J Vasc Surg. 2016;63:1216–1224.

26.

Hofferberth

Boston

McLachlan

, et al. Stent-assisted balloon-induced intimal disruption and relamination in aortic dissection repair: the STABILISE concept. J Thorac Cardiovasc Surg. 2014;147:1240–1245.

27.

Melissano

Bertoglio

Rinaldi

, et al. Satisfactory short-term outcomes of the STABILISE technique for type B aortic dissection. J Vasc Surg. 2018;68:966–975.

28.

Dalman

Wanhainen

Mani

, et al. Top 10 candidate aortic disease trials. J Intern Med. 2020;288:23–37.