Thoracic endovascular repair of chronic type B aortic dissection: a systematic review
Systematic Review

Thoracic endovascular repair of chronic type B aortic dissection: a systematic review

Michael L. Williams1,2,3, Madeleine de Boer4, Bridget Hwang2, Bruce Wilson2, John Brookes2,5, Nicholas McNamara6, David H. Tian7, Timothy Shiraev4, Ourania Preventza8,9

1Department of Cardiothoracic Surgery, John Hunter Hospital, Newcastle, Australia; 2The Collaborative Research (CORE) Group, Macquarie University, Sydney, Australia; 3School of Medicine and Public Health, University of Newcastle, Newcastle, Australia; 4Department of Vascular Surgery, Royal Prince Alfred Hospital, Sydney, Australia; 5Department of Cardiothoracic Surgery, University Hospital Geelong, Geelong, Australia; 6Department of Cardiothoracic Surgery, Royal Prince Alfred Hospital, Sydney, Australia; 7Department of Anaesthesia and Perioperative Medicine, Westmead Hospital, Sydney, Australia; 8Division of Cardiothoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas, USA; 9Department of Cardiovascular Surgery, Texas Heart Institute, Houston, Texas, USA

Correspondence to: Dr. Michael L. Williams. Department of Cardiothoracic Surgery, John Hunter Hospital, Newcastle, NSW 2305, Australia. Email:

Background: At present, the optimal management strategy for chronic type B aortic dissection (CTBAD) remains unknown, as equipoise remains regarding medical management versus endovascular treatment versus open surgery. However, the results over recent years of thoracic endovascular aortic repair (TEVAR) in CTBAD appear promising. The aim of this systematic review was to provide a comprehensive analysis of the available data reporting outcomes and survival rates for TEVAR in CTBAD.

Methods: Electronic searches of six databases were performed from inception to April 2021. All studies reporting outcomes, specifically 30-day mortality rates, for endovascular repair of CTBAD were identified. Relevant data were extracted, and a random-effects meta-analysis of proportions or means was performed to aggregate the data. Survival data were pooled using data derived from original Kaplan-Meier curves, which allows reconstruction of individual patient data.

Results: Forty-eight studies with 2,641 patients were identified. Early (<30 days) all-cause and aortic-related mortality rates were low at 1.6% and 0.5%, respectively. Incidence of retrograde type A dissection in the post-operative period was only 1.4%. There were also low rates of cerebrovascular accidents and spinal cord injury (1.1% and 0.9%, respectively). Late follow-up all-cause mortality was 8.0%, however, late aortic-related mortality was only 2.4%. Reintervention rates were 10.1% for endovascular and 6.7% for surgical reintervention. Pooled rates of overall survival at 1-, 3-, 5- and 10-year were 91.5%, 84.7%, 77.7% and 56.3%, respectively.

Conclusions: The significant heterogeneity in the available evidence and absence of consensus reporting standards are important considerations and concern when interpreting the data. Evaluation of the evidence suggests that TEVAR for CTBAD is a safe procedure with low rates of complications. However, the optimal treatment strategy for CTBAD remains debatable and requires further research. Evidence from high-quality registries and clinical trials are required to address these challenges.

Keywords: Chronic type B aortic dissection (CTBAD); thoracic endovascular aortic repair (TEVAR); descending thoracic aorta

Submitted Sep 07, 2021. Accepted for publication Oct 04, 2021.

doi: 10.21037/acs-2021-taes-25


Aortic disease, and more specifically aortic dissection, comprises a significant disease burden, occurring twice as often in males compared with females and frequently occurring in patients aged between 50–70 years (1,2). With an incidence estimated at 5–30 per million per year, 20% of patients with aortic dissection die before reaching hospital, with a further 30% of those who do reach tertiary centres dying during their hospital admission (1,3,4). In light of this, there has been increased interest in the management of aortic dissections, particularly with the shift towards endovascular management as endovascular graft technology continues to evolve.

Disease processes, such as atherosclerosis, chronic hypertension, or the presence of genetic conditions (such as vascular Ehlers-Danlos or Marfan syndromes) that alter the integrity of the elastic or muscular components of the aortic wall, predispose patients to the development of aortic dissection (4). Whilst this pathology can be classified using multiple systems, one of the most common classifications is the Stanford classification, which describes dissections as either Type A, with the entry tear proximal to the ostium of the left subclavian artery, or Type B, with the entry tear distal to the ostium of the left subclavian artery (4). Whilst most Type A aortic dissections are surgical emergencies and require open replacement of the ascending aorta with or without aortic root or arch replacement (5), uncomplicated Type B aortic dissections have classically been managed medically with strict blood pressure and heart rate control to reduce pulse pressure, statins and lifestyle modification (6,7). Surgical management has classically been reserved for complicated Type B dissections (those associated with rupture or malperfusion syndromes), via open surgical repair or thoracic endovascular aortic repair (TEVAR) (8-10). However, it is estimated that 25–50% of patients with acute Type B aortic dissections who are managed medically will undergo aneurysmal degeneration of the dissected segment and require surgical repair, either via open or endovascular methods, during the chronic phase of their disease process (3,10).

There is ongoing debate within the literature surrounding the management of chronic type B aortic dissection (CTBAD) and whether optimal medical therapy or the use of TEVAR is most effective in the management of this pathology (9-11). Historically, the definition of chronicity in type B aortic dissection has been after 14 days have elapsed from symptom onset. This classification is based on the high rate of mortality (up to 70%) in aortic dissection within the first 2 weeks of onset (12). In recent years, a third “sub-acute” category (between 2 weeks and 3 months) has been proposed in the classification system, as the risk of death remains high in the first 3 months (13). CTBADs are associated with a risk of rupture, with recent guidelines suggesting that this risk increases with aneurysmal dilatation (2,8,10). Rates of aortic rupture have been quoted as high as 28.6% in aortic diameters of up to 6.4 cm (8). As such, aneurysmal dilatation and rapid growth of aneurysms are one of the most frequent indications for the treatment of CTBAD (2,3). Open surgical repair has several significant disadvantages compared to endografting, including the necessity for a posterolateral thoracotomy or thoracoabdominal incision depending on the extent of the required repair, single lung ventilation, full or partial cardiopulmonary bypass, and possible circulatory arrest and hypothermia (4). Subsequently, the use of TEVAR in CTBAD has had an increased focus over the past decade.

This systematic review sought to provide a comprehensive analysis of the currently available literature to determine early outcomes, reintervention rates and mid- or long-term survival rates for endovascular repair of CTBAD.


Literature search strategy

Six electronic databases were used to perform the literature search including Ovid MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews (CDSR), SCOPUS, and Database of Abstracts of Review of Effectiveness (DARE). These databases were searched from date of inception to 26th April 2021. The search strategy included a combination of keywords and Medical Subject Headings (MeSH) including “Aorta” AND “Dissection” AND “Chronic” AND “Endovascular Procedures” OR “Endovascular repair” OR “TEVAR”. Predefined selection criteria were used to assess all relevant articles that were identified. Our methods adhered to the guidelines set forth in the Preferred Reporting Items for Systematic Reviews and Meta-Analyses: The PRISMA Statement (14). Two reviewers (MLW and MDB) independently screened the title and abstract of all identified records in the search. Where the title/abstract provided insufficient detail to determine study relevance, a full-text copy of the article was retrieved for review. The reference lists of selected studies were reviewed manually to identify any extra relevant studies not identified in the electronic search.

Selection criteria

Studies were eligible for inclusion in this systematic review if they included a patient population who underwent TEVAR for Chronic Stanford type B/DeBakey type III aortic dissection. Chronicity of dissection for this systematic review was defined as greater than 2 weeks following symptomatic presentation or documentation of an intimal entry tear. Studies that described mixed populations of acute and chronic dissections without separate patient or outcome data were deemed ineligible for inclusion. Studies had to report the primary outcome of interest (see below) and have a minimum CTBAD cohort greater than ten patients to be eligible for inclusion. Residual CTBAD post previous Type A and open ascending aorta surgical repair were included due to a number of studies reporting mixed populations with no separate data/outcomes for these cohorts. Cases that involved the abdominal aorta only were excluded. Hybrid (open and endovascular) procedures or branched and/or fenestrated endovascular repair for CTBAD were excluded. When trials/registries/institutions published duplicate studies with extended length of follow-up or larger study populations, the most updated and complete study was included. Included studies were limited to those in English and only involving human subjects. Abstracts, case reports, conference presentations, editorials and reviews were excluded.

Outcomes of interest

The primary outcome of interest was in-hospital/30-day mortality. Secondary outcomes of interest included mid- to long-term survival rates and other post-operative outcomes, including aortic related mortality, rupture, retrograde type A dissection, cerebrovascular accident (CVA) and spinal cord injury (SCI).

Data extraction and critical appraisal

Two independent reviewers (BH and BW) extracted data directly from publication texts, tables and figures. A third reviewer (MLW) independently reviewed and confirmed all extracted data. Differences of opinions between the two main reviewers (BH and BW) were resolved through means of discussion and consensus, including primary investigator (MLW) where necessary. Attempts were made to clarify insufficient or indistinct data from corresponding authors of included studies where required. Outcome data was extracted in a manner in which each study was effectively treated as a case series regardless of actual study design, and therefore a critical appraisal of the quality of each individual included study was not performed.

Statistical analysis

A meta-analysis of proportions or means were performed for categorical and continuous variables, as appropriate. A random effects model was used to account for differing center/surgeon experience, different endoprostheses used, and different operative and management protocols across the included studies. To facilitate this statistical pooling, means and standard deviations were calculated from the median (with range or interquartile range), where reported, using the methods described by Wan and colleagues (15). Pooled data are presented as n (%) with 95% confidence intervals (CI). For outcome data, heterogeneity amongst studies was assessed using the I2 statistic. Thresholds for I2 values were considered as low, moderate and high heterogeneity as 0–49%, 50–74% and ≥75%, respectively (16). Meta-analysis of proportions or means were performed using Stata (version 17.0, StataCorp, Texas, USA).

Survival data was calculated from aggregation of Kaplan-Meier survival data from included studies, where reported, using the methods described by Guyot and colleagues (17). Aggregation of this data was performed by reconstructing individual patient data from digitized Kaplan-Meier survival curves and patient number-at-risk data. The reconstructed individual patient data were then pooled and used to generate an aggregated survival curve. Digitization of source Kaplan Meier curves was performed using DigitizeIt (version 2.5.9, Braunschweig, Germany) and survival analysis was performed using R (version 3.5.2, R Foundation for Statistical Computing, Vienna, Austria).


The literature search identified a total 915 studies (Figure 1). An additional nine articles were identified on manual searches of reference lists. After exclusion of duplicates or irrelevant studies, 97 articles were deemed appropriate to undergo full-text review. Forty-eight studies with a total of 2,641 patients undergoing TEVAR for CTBAD were deemed suitable to be included for quantitative analysis. The remaining 49 articles were deemed unsuitable, predominantly for lacking adequate reporting of outcomes of interest. Two articles were excluded for reporting outcomes for branched/fenestrated endovascular repair for CTBAD.

Figure 1 PRISMA flow-chart summarizing the search strategy for relevant publications.

Of the 48 included studies, nine were prospective and the remaining 39 were retrospective cohort studies (Table 1). Included studies had varying cohort sizes from 10 to 208 patients. Definition of chronicity varied between the included studies, however, the majority using greater than 2 weeks after the onset of symptoms or diagnosis to define a CTBAD. The majority of included studies reported outcomes for CTBAD DeBakey type III (type IIIa, IIIb or both), while 13 studies reported outcomes for mixed cohorts of residual type I and III CTBAD patients. The indication for intervention for CTBAD varied amongst the included studies (Table S1). The majority of the included studies included mixed cohorts of both complicated and uncomplicated CTBAD. The weighted mean follow-up period of all included studies was 33.8 months.

Table 1

Study characteristics

Primary author Year Institution(s) Study period Type of study Definition of chronic n Mean follow up time (months) Extent of aortic pathology (DeBakey) Complicated/
Kato (18) 2002 Mie University Hospital, Mie, Japan 1997–2002 RC >1 month after symptoms 14 27.0±12.0 Residual type I and type III Both
Greenberg (19) 2005 The Cleveland Clinic Foundation, Ohio, USA 2001–2004 PC NR 15 14.0 NR NR
Baumgart (20) 2006 West German Heart Center, University Duisburg-Essen, Essen, Germany 1999–2004 PC >2 weeks after symptoms 35 21.0±18.0 NR NR
Böckler (21) 2006 German Cancer Research Center, Heidelberg, Germany 1997–2004 PC >2 weeks after symptoms 15 24.0±14* Type III Both
Song (22) 2006 Harbor-UCLA Medical Center, Harbor, California, USA 1999–2005 RC >2 weeks after symptoms 17 11.0±16.4* NR Complicated
Thompson (23) 2007 7 European Centers 2005–2006 RC NR 52 5.3±3.5 Type III Both
Jing (24) 2008 Shenyang Northern Hospital, Liaoning, China 2002–2007 RC >2 weeks after symptoms 35 17±14 Type III Both
Marcheix (25) 2008 7 European Centers 1996–2004 RC NR 15 25.2±16.8 Residual type I and type III Both
Sayer (26) 2008 St George’s Vascular Institute, London, UK 2000–2007 RC >2 weeks after symptoms 40 30.0 NR NR
Alves (27) 2009 Federal University of Sao Paulo and Hospital do Coracao Da Associacao, Sao Paulo, Brazil 1997–2004 RC >2 weeks after symptoms 61 35.9±28.5 Type III Both
Guangqi (28) 2009 The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China 2001–2006 RC >2 weeks after symptoms 49 22.1±20.8 Type III Both
Kim (29) 2009 Yonsei University College of Medicine, Seoul, Republic of Korea 1994–2007 RC >2 weeks after symptoms 72 64.4±38.8 Type III Uncomplicated
Manning (30) 2009 Malmo University Hospital, Malmo, Sweden 2000–2006 RC >2 weeks after symptoms 10 56.0 Type IIIb Uncomplicated
Czerny (31) 2010 3 European Centers (Switzerland and Austria) 2004–2009 RC NR 14 34.5±14.5* Residual type I and type III Uncomplicated
Xu (32) 2010 Capital Medical University, Beijing Anzhen Hospital, Beijing, China 2001–2007 RC >1 month after symptoms 84 33.2±19.2 Type III Uncomplicated
Kang (33) 2011 Cleveland Clinic Foundation, Cleveland, Ohio, USA 2000–2007 RC >2 weeks after symptoms 76 33.5±29.4 Type III Complicated
Oberhuber (34) 2011 University of Ulm, Ulm, Germany 1990–2011 RC >2 weeks after symptoms 19 37.8±92.9* Type III Uncomplicated
Parsa (35) 2011 Duke University Medical Center, Durham, North Carolina, USA 2005–2009 RC >2 weeks after symptoms 51 27.0±16.5 Residual type I and type III Uncomplicated
Andacheh (36) 2012 Harbor-UCLA Medical Center, Torrance, California, USA 2002–2010 PC >2 weeks after symptoms 73 18.0 Type III Complicated
Mani (37) 2012 Guy’s and St Thomas NHS Foundation Trust, London, UK 2000–2010 RC >2 weeks after symptoms 58 38.0±28.0 Residual type I and type III Both
Nathan (38) 2012 Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA 2005–2010 RC >6 weeks after symptoms 27 27.3±22.1 Residual type I and type III Both
Qing (39) 2012 The University of Hong Kong, Queen Mary Hospital, Hong Kong NR PC >4 weeks after dissection 32 31.7±17 Type III Uncomplicated
Yang (40) 2012 Taipei City Hospital, Taipei, Taiwan 2006–2011 RC >2 weeks after symptoms 28 24.1±15.6 Type III Both
Chen (41) 2013 Nanjing First Hospital, Nanjing, China 2000–2011 PC >2 weeks after symptoms 56 37.6±28.4 Type III Complicated
Jia (42) 2013 Chinese PLA General Hospital, Beijing, China 2007–2010 PC >2 weeks after symptoms 208 16.3±9.5* Type III Uncomplicated
Lee (43) 2013 Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea 1997–2010 RC >2 weeks after symptoms 71 53.2±52.9 Type III Complicated
Leshnower (44) 2013 Emory University School of Medicine, Atlanta, Georgia, USA 2005–2011 RC >8 weeks after acute event 31 21.0±20.0 Residual type I and type III Uncomplicated
Nozdrzykowski (45) 2013 Heart Center Leipzig, University of Leipzig, Leipzig, Germany 2000–2010 RC >2 weeks after symptoms 32 52.2±31.2 Residual type I and type III Both
Patterson (46) 2013 MOTHER Database (Combined data from 5 prospective trials) 2004–2012 PC >2 weeks after symptoms 195 28.8 NR NR
Scali (47) 2013 University of Florida College of Medicine, Gainesville 2004–2011 RC NR 80 31.8±12.2* Residual type I and type III Uncomplicated
Andersen (48) 2014 Duke University Medical Center, Durham, North Carolina, USA 2005–2013 RC >2 weeks after symptoms 44 44.3±14.3* Residual type I and type III NR
Kitamura (49) 2014 Kitasato University School of Medicine, Kanagawa, Japan 1998–2012 RC >2 weeks after symptoms 45 90.0±36.8 Type III Uncomplicated
Lombardi (50) 2014 STABLE Trial Investigators (multicenter) 2007–2012 PC >2 weeks after symptoms 31 24.0 Type IIIb Complicated
Song (51) 2014 Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea 2012–2013 RC >3 months after diagnosis 20 10.3±4.9 Type IIIb Complicated
Nathan (52) 2015 University of Washington, Seattle, Washington, USA 2006–2013 RC >2 weeks after symptoms 47 35.1±20.9 Residual type I and type III Both
van Bogerijen (53) 2015 University of Michigan Hospitals, Ann Arbor, Michigan, USA 1993–2013 RC >8 weeks after diagnosis 32 41.5±54.4* Type IIIb Uncomplicated
Zhang (54) 2017 General Hospital of People’s Liberation Army, Beijing, China 2011–2013 RC >2 weeks after symptoms 25 26.4±15.6 Type III Complicated
Chou (55) 2018 National Taiwan University Hospital, Taipei, Taiwan 2008–2014 RC >2 weeks after symptoms 23 27.5±19.1 Type III Complicated
Huang (56) 2018 Taipei Veterans General Hospital, Taipei, Taiwan 2006–2013 RC >2 weeks after symptoms 65 36.0 Type IIIb Uncomplicated
Tjaden (57) 2018 Gore Global Registry (worldwide multicenter registry) 2010–2016 RC >3 months after symptoms 94 26.0 Residual type I and type III Both
Kim (58) 2019 Yonsei University College of Medicine, Seoul, Republic of Korea 2012–2017 RC >3 months after symptoms 75 37.2±17.7* Type IIIb NR
Wang (59) 2019 VQI TEVAR Registry 2013–2016 RC >30 days after symptoms 193 30.0 NR Both
Zha (60) 2019 The First Affiliated Hospital of Anhui Medical University, Anhui, Chine 2012–2016 RC >2 weeks after symptoms 23 39.5±10.5* Type III Both
Conway (61) 2020 Lenox Hill Hospital, Northwell Health, New York, USA 2010–2016 RC >30 days after symptoms 208 49.2 Type III Both
Li (62) 2020 First Affiliated Hospital, Zhejiang University, Zhejiang, China 2009–2013 RC >3 months after symptoms 34 68.1±22.9 Type III Both
Oishi (63) 2020 Kyushu University Hospital, Higashi, Fukuoka, Japan 2009–2019 RC >3 months after symptoms 40 39.2±27.1 Residual type I and type III Uncomplicated
Puech-Leao (64) 2020 Hospital das Clinicas, University of Sao Paulo, Faculty of Medicine, Sao Paulo, Brazil 2004–2017 RC >2 weeks after symptoms 42 57.2 NR Uncomplicated
Ueki (65) 2021 Shizuoka General Hospital, Kita-Ando Aoi-ku, Shizuoka, Japan 2014–2019 RC >3 months after diagnosis 35 27.3±14.2* Type IIIb Uncomplicated

*, calculated from median and range/IQR using methods of Wan et al. NR, not reported; RC, retrospective cohort study; PC, prospective cohort study.

Baseline characteristics

Overall, the weighted pooled age of all patients was 60.5 years. The entire patient population was comprised of 76.7% males. The majority of patients had a history of hypertension (89.4%). Only a fraction of the included patients had a history of diabetes (10.4%), prior cerebrovascular accident (CVA) (5.6%) or renal insufficiency (11.3%). Pooled interval between diagnosis and endovascular repair of CTBAD was 20.6 months (95% CI, 14.5–25.8). Approximately one third of the patient population had undergone prior cardiac or open aortic surgery (29.2%). Other patient baseline characteristics are seen in Table S2. History of peripheral vascular disease, congestive heart failure and other comorbidities were poorly reported across the included studies.

A number of different endoprostheses were used across the included studies (Table S3). These included the Zenith TX1 and TX2 (Cook Medical Incorporated, Bloomington, Indiana, USA), Talent and Valiant Captiva (Medtronic Incorporated, Santa Rosa, California, USA), TAG and cTAG (W.L Gore & Associates, Newark, Delaware, USA) and Relay endoprostheses (Terumo Aortic, Tokyo, Japan). Operative details were poorly reported across the included studies, which limited the statistical analysis. Left subclavian artery coverage was performed in 38.6% of patients (95% CI, 28.9–48.7). Revascularization of the left subclavian artery in these instances of left subclavian coverage was poorly reported. The pooled weighted technical success was high at 99.0% (95% CI, 97.7–99.8) and the need for open surgical conversion was low at 0.4% (95% CI, 0.01–1.3). The usage of spinal drainage peri- or intra-operatively was poorly reported. Other operative details including number of stents used per patient and stent dimensions are summarized in Table S3.

Early post-operative outcomes

All 48 included papers reported early (<30 days) mortality rates. The weighted pooled estimate of early all-cause mortality was 1.6% (95% CI, 0.8–2.6; I2=44%) (Table 2). Pooled rates for early aortic-related mortality were low (0.5%; 95% CI, 0.1–1.3; I2=35%). Twenty-five studies reported rates for retrograde type A dissection and the pooled estimate for this outcome was 1.4% (95% CI, 0.6–2.5; I2=15%). The weighted pooled rates for CVA and SCI were 1.1% (95% CI, 0.5–1.7; I2=2%) and 0.9% (95% CI, 0.3–1.6; I2=16%), respectively. The rate of renal insufficiency was 3.2% (95% CI, 1.3–5.7; I2=68%). Other early post-operative outcomes were inconsistently reported, such as length of intensive care unit stay/length of hospital stay, pneumonia, infection and access site complications. Rates of endoleaks were inconsistently reported and therefore a meta-analysis for this outcome was not performed. Data regarding reported rates of endoleaks are summarized in Table S4. Other early post-operative outcomes are summarized in Table 2.

Table 2

Early post-operative outcomes (<30 days)

Parameter Events/total Number of studies Weighted pooled estimate (%) (95% CI) Heterogeneity I2 (%)
All-cause mortality 75/2,641 48 1.6 (0.8–2.6) 44
Aortic-related mortality 32/2,000 39 0.5 (0.1–1.3) 35
Retrograde TAAD 32/1,299 25 1.4 (0.6–2.5) 15
Cerebrovascular accident 43/2,051 42 1.1 (0.5–1.7) 2
Spinal cord injury 42/2,017 40 0.9 (0.3–1.6) 16
Rupture 11/880 20 0.5 (0.1–1.3) 0
Renal insufficiency 42/1,125 23 3.2 (1.3–5.7) 68

CI, confidence interval; TAAD, type A aortic dissection.

Late outcomes

Late follow-up all-cause mortality was reported in almost all of the included studies (46/48). Weighted pooled estimate for late all-cause and aortic-related mortality were 8.0% (95% CI, 5.8–10.5; I2=72%) and 2.4% (95% CI, 1.3–3.6; I2=29%), respectively (Table 3). Reintervention mortality rate was low at 0.1% (95% CI, 0.0–0.6; I2=0%). Rates of retrograde type A aortic dissection and aortic rupture were also low at 0.8% (95% CI, 0.2–1.6.; I2=0%) and 1.2% (95% CI, 0.3–2.4; I2=31%), respectively. Rates for CVA and SCI were inconsistently reported for late follow-up, however, when reported these rates were low (between 0 and 3.2%). Rates of endovascular reintervention were 10.1% (95% CI, 6.8–13.9; I2=71%) and open surgical reintervention surgical reintervention were 6.7% (95% CI, 4.0–10.0; I2=74%). Pooled estimate of complete false lumen thrombosis for 823 patients across 23 studies was 54.0% (95% CI, 42.0–65.7; I2=92%). The reported rates of complete false lumen thrombosis varied significantly across studies shown by the high heterogeneity result. Complete false-lumen thrombosis was also inconsistently defined in the included studies as either complete thrombosis along the length of the stent graft or the entire length of the thoracic/thoracoabdominal aortic dissection. Again, reported rates of endoleaks were inconsistently reported for late follow-up (Table S4). Other late outcomes of interest, such as rates of stent graft induced new entry tears, were inconsistently reported among the included studies.

Table 3

Late outcomes (>30 days)

Parameter Events/total Number of studies Weighted pooled estimate (%) (95% CI) Heterogeneity I2 (%)
All-cause mortality 219/2,322 46 8.0 (5.8–10.5) 72
Aortic-related mortality 51/1,494 32 2.4 (1.3–3.6) 29
Reintervention-related mortality 8/949 20 0.1 (0.0–0.6) 0
Retrograde TAAD 18/1,141 21 0.8 (0.2–1.6) 0
Rupture 26/1,179 21 1.2 (0.3–2.4) 31
Endovascular reintervention 136/1,280 29 10.1 (6.8–13.9) 71
Surgical reintervention 132/1,433 29 6.7 (4.0–10.0) 74
Complete false lumen thrombosis 478/873 23 54.0 (42.0–65.7) 92

CI, confidence interval; TAAD, type A aortic dissection.


Aggregation of overall survival was performed from 23 of the included studies (20,26-28,32,33,35,37,38,40,42,45-49,52-54,56,62-64). Overall survival rates at 1-, 2-, 3-, 4- and 5-year were 91.5%, 88.5%, 84.7%, 82.2% and 77.7%, respectively (Figure 2). At 10-year post TEVAR for CTBAD the overall survival rate was 56.3%. Aorta-related survival was aggregated from six included studies (29,35,42,46,54,62). Aorta-related survival rates were 97.2%, 95.8%, 94.9%, 94.4%, 94.4% and 90.9% at 1-, 2-, 3-, 4-, 5- and 10-year, respectively (Figure 3).

Figure 2 Aggregated overall survival after TEVAR in CTBAD (shaded region represents 95% CI). TEVAR, thoracic endovascular aortic repair; CTBAD, chronic type B aortic dissection.
Figure 3 Aggregated aorta-related survival after TEVAR in CTBAD (shaded region represents 95% CI). TEVAR, thoracic endovascular aortic repair; CTBAD, chronic type B aortic dissection.

Freedom from re-intervention

Kaplan-Meier curves reporting rates of freedom from re-intervention were available in 10 of the included studies for aggregation (29,33-35,46-49,63,64). Rates of freedom from re-intervention at 1-, 2-, 3-, 4- and 5-year were 85.2%, 80.6%, 79.2%, 77.6%, and 73.3%, respectively (Figure 4). At 10-year post TEVAR for CTBAD freedom from re-intervention was 55.1%.

Figure 4 Aggregated freedom from re-intervention after TEVAR in CTBAD (shaded region represents 95% CI). TEVAR, thoracic endovascular aortic repair; CTBAD, chronic type B aortic dissection.


CTBAD remains a challenging pathology with regards to the optimal management strategy. TEVAR has undergone considerable evolution and expansion over the past two decades and provides a less invasive procedure compared to open surgery with promising results. However, the role of TEVAR in CTBAD remains controversial with most institutions favoring optimal medical therapy as the primary management strategy for uncomplicated cases. The aim of this systematic review was to provide an updated and comprehensive review of the available evidence regarding the safety and efficacy of TEVAR in patients with CTBAD.

The pooled in-hospital all-cause and aortic-related mortality rates in this present study were low at 1.6% and 0.5%, respectively. On the contrary, some of the included studies reported higher mortality rates, such as the study by Puech-Leao et al., which reported an in-hospital mortality rate of 12.0% (64). However, this was a small cohort of patients (37), and the majority of the deaths were related to retrograde type A dissections. The mortality rates in this present study also highlight the difference between outcomes for acute and chronic aortic dissections undergoing TEVAR, especially in the early post-operative period. A recent meta-analysis assessing TEVAR in type B aortic dissections reported in-hospital all-cause and aortic-related mortality rates of 9.4% and 5.6%, respectively, during the acute phase of the disease (66). Interestingly, in that same study during late follow-up the all-cause mortality rate for TEVAR in acute phase dissection were similar to this present study, reported at 10.0%.

Important causes of early mortality after TEVAR are aortic rupture and retrograde type A dissection. It has been hypothesized that proximal bare springs or barbs for fixation of the stent in some models of endoprosthesis can increase the risk of retrograde dissection, along with guidewire manipulation and device delivery sheaths (67). The incidence of both rupture and retrograde dissection were low in the present review, at 0.5% and 1.4%, respectively. This rate of 1.4% for retrograde type A dissection compares similarly to the 1.33% in the European Registry on Endovascular Aortic Repair complications and favorable to the 3.17% reported in a recent single center study of over 850 patients (68). The rates of CVA and SCI in the present study were 1.1% and 0.9% respectively. This is lower than the rates reported by Boufi et al., who when comparing TEVAR to open surgery for CTBAD reported CVA and SCI rates of 2.7% and 2.2%, respectively, for TEVAR and 4.5% and 5.0%, respectively, for open surgery (69).

One main concern regarding TEVAR for CTBAD is its durability and the requirement for subsequent reintervention. In the present study, the rate of secondary endovascular intervention was 10.1% and 6.7% for open surgical reintervention. These are comparable to a recent review of over 5,000 patients (both acute and chronic cases) that reported rates of 12.5% and 6.1% for endovascular and surgical reintervention, respectively (66). However, another systematic review reported varying rates of endovascular reintervention from 4.3 to 47.4% after TEVAR for CTBAD (70).

It has previously been reported in the literature that TEVAR has higher rates of 1-year survival when compared to open surgery (90–93% vs. 79–81%, respectively), however, at 3-year follow-up this survival benefit was lost (TEVAR 67% vs. open surgery 71%) (71). However, a recent meta-analysis reported that there was no benefit of one technique over the other regarding 1- and 3-year survival (69). In comparison, the results of the current study report a similar 1-year survival rate for TEVAR at 91.5%, however, the 3-year survival rate is considerably higher at 84.7%. When compared to medical therapy alone, the INSTEAD trial reported improved 5-year aorta-specific survival and delayed disease progression for TEVAR with optimal medical treatment for patients with uncomplicated CTBAD (72). This is the only randomized control trial to date comparing TEVAR to optimal medical therapy for uncomplicated CTBAD [the TEVAR cohort of which is included in this present study in the larger MOTHER database (46)].

It is known that aortic remodeling and complete thrombosis of the false lumen are important factors for positive long-term results for TEVAR in type B dissection (26,37,43). In CTBAD, there is thickening of the dissection septum which progresses over time, and consequently, there is usually less aortic remodeling seen in chronic compared to acute dissections. Recently, the VIRTUE study confirmed this, reporting that when compared to acute or sub-acute patients, patients who underwent TEVAR with CTBAD had lesser degrees of aortic remodeling (73). Unfortunately, in the present study, aortic remodeling was either poorly or inconsistently reported across studies, limiting its analysis. Rates of complete false lumen thrombosis were the most consistent outcome reported across approximately half of the included studies. Even though the pooled estimate for this outcome was 54.0%, the specific anatomic location where the false lumen thrombosis was complete (i.e., length of the stent graft versus entire length of dissected aorta) was poorly reported. This is lower than the 71.7% rate of complete false lumen thrombosis reported by Boufi and colleagues for TEVAR patients in CTBAD (69). To improve the future analysis of this important outcome of aortic remodeling and its link to long-term patient outcomes, guidelines and consensus reporting standards should be implemented to improve the degree of heterogeneity in reporting of this outcome in the literature.

Another important consideration when reviewing the available literature is the recent change in definition of chronicity for type B aortic dissections. Some studies divide type B dissection patients into three distinct different groups, acute (<2 weeks), sub-acute (2 weeks to 3 months) and chronic (>3 months), including a separate “sub-acute phase” (74). A large number of the more recent studies included in this review defined CTBAD to be greater than 3 months from diagnosis or symptom onset (51,57,58,62,63,65), whereas the overall majority of studies, especially those published before 2014, used a definition of greater than 2 weeks to define chronicity. It is unclear exactly how this change in classification will affect long-term results or ideal timing for intervention, however, some studies have reported that patients treated in the sub-acute phase exhibit better early, mid- and long-term outcomes when compared to acute or chronic patients who do not need emergent intervention (62). This hypothesis however requires prospective randomized controlled trials to confirm this reported evidence in observational studies.

There are a number of important limitations to consider when interpreting the results described in this present study. As mentioned above, there were different definitions of chronicity and indications for TEVAR in CTBAD used across the included studies. There was also significant heterogeneity for some of the reported outcomes, including late all-cause mortality, endovascular and surgical reintervention rates and false lumen thrombosis rates. This could represent a number of different factors, such as different patient population or selection, differing centers with varying operator experience or the different endoprostheses used across the included studies. Studies also inconsistently reported loss to follow-up and some studies reported outcomes with high complication rates in small patient populations. The observational nature of all included studies also presents an inherent source of bias in the present study. There were also varying definitions of technical success across the included studies.


In summary, TEVAR provides a safe and effective treatment modality for patients with CTBAD. It can be performed with low complication rates in high volume, experienced centers. Due to the limited evidence, based mainly on retrospective cohort studies, and the heterogeneity of the reported outcomes, the optimal treatment strategy for CTBAD remains debatable. Further high quality prospective multicenter registry data and randomized control trials are required to evaluate the different treatment strategies. Consensus reporting standards with a focus on aortic remodeling are required to improve our understanding of the long-term outcomes of TEVAR in CTBAD.


Funding: None.


Conflicts of Interest: Dr. OP provides consultation for and participates in clinical trials with Medtronic and W.L. Gore & Associates. The other authors have no conflicts of interest to declare.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See:


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Cite this article as: Williams ML, de Boer M, Hwang B, Wilson B, Brookes J, McNamara N, Tian DH, Shiraev T, Preventza O. Thoracic endovascular repair of chronic type B aortic dissection: a systematic review. Ann Cardiothorac Surg 2022;11(1):1-15. doi: 10.21037/acs-2021-taes-25

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