Risks for Retrograde Type-A Dissection After TEVAR Frank R. Arko, III, MD Chief, Vascular and Endovascular Surgery Professor, Cardiovascular Surgery Co-Director, Aortic Institute Sanger Heart and Vascular Institute Charlotte, NC
Retrograde Type-A Dissection After TEVAR TEVAR has shown to be an effective and durable repair option in the treatment of thoracic aortic pathology Retrograde Type A dissection (RTAD) following TEVAR remains a highly lethal complication Nearly two-thirds of the RTAD cases present within the first month RTAD risk factors as described in literature are: Device Oversizing (>20%) Large Stent Graft Diameter Proximal Landing Zone Ascending Aortic Diameter (> 40mm) Gender Ballooning/Iatrogenic injury Smoking Arch Angulation and STJ Dilation 1. Hogendoorn W, Hunink MG, Schlosser FJ, Moll FL, Sumpio BE, Muhs BE. Endovascular vs: open repair of complicated acute type B aortic dissections. J Endovasc Ther 2014;21:503 14 2. Makaroun MS, Dillavou ED, Wheatley GH, Cambria RP, Gore TAGI. Five-year results of endovascular treatment with the Gore TAG device compared with open repair of thoracic aortic aneurysms. Journal of Vascular Surgery 2008;47:912 8 3. Canaud L, Ozdemir BA, Patterson BO, et al: Retrograde aortic dissection after thoracic endovascular aortic repair. Ann Surg 2014;260(2):389 395
Retrograde Type-A Timing Intra op 20.9% <30d 50.0% >30d 29.1% Over 70% occur within the first 30-days Delayed onset suggests disease progression 37% overall mortality Canaud et al. Ann Surg 2014;00:1-7 Range: 0 1825 days
Hata M, Shiono M, Inoue T, Sezai A, Niino T, Negishi N, Sezai Y. Optimal treatment of type B acute aortic dissection: long-term medical follow-up results. Ann Thorac Surg. 2003;75:1781 1784 Pathology Treated Patients treated for Aortic Dissection have the highest pooled rates of RTAD 4 Acute TBAD had the highest associated rate for RTAD at 8.4% Chronic TBAD associated rate for RTAD at 3% The influence of acute dissection and aortic fragility on RTAD has been illustrated in other reports 5 Retrograde Type A Aortic Dissection After Thoracic Endovascular Aortic Repair: A Systematic Review and Meta-Analysis Yanqing Chen, MD;* Simeng Zhang, MD;* Lei Liu, MD;* Qingsheng Lu, MD; Tianyi Zhang, MD; Zaiping Jing, MD
Landing Zone and RTAD Landing Zone RTAD (%) OR (relative to zones 3/4) RTAD rates vary significantly based on zone 6 Significantly higher in Zones 0-2 0 6.8 5.7 1 2.4 1.9 7.5% during zone 0 total debranching 7 Significant correlation between pathology, zone and repair complexity 2 4.1 3.3 3/4 1.3 1 Canaud et al. Ann Surg 2014;00:1-7 Czerny M, Weigang E, Sodeck G, et al. Targeting landing zone 0 by total arch rerouting and TEVAR: midterm results of a transcontinental registry. Ann Thorac Surg. 2012;94:84 89
Device Oversizing Patients with RTAD had significantly greater device oversizing 8 22.0% vs. 10.3% (p<0.0001) Each 1% oversizing above 9% Increase in OR of RTAD - 14% (p<0.0001) Device Oversizing in TBAD resulted in a higher RTAD rate - 24.4% vs 14.1% Canaud et al. Ann Surg 2014;00:1-7
Ascending Arch Condition Several arch characteristics for RTAD Enlarged aortic diameter >40mm (4.8% vs 0.9%; P =.047) 9 Bicuspid valve Presence of angulated (>60 ) Gothic arch type Abnormal aortic root morphology 10 o Valsalva diameter >40mm (33% vs 15%, P ¼.31) o Loss of STJ (> diameter of aortic root) Williams JB, Andersen ND, Bhattacharya SD, et al. Retrograde ascending aortic dissection as an early complication of thoracic endovascular aortic repair. J Vasc Surg. 2012;55:1255-1262 Factors favoring retrograde aortic dissection after endovascular aortic arch repair Thomas Gandet, MD, Ludovic Canaud, MD, PhD, Baris Ata Ozdemir, MBBS, Vincent Ziza, MD, Roland Demaria, MD, PhD, Bernard Albat, MD, PhD, and Pierre Alric, MD, PhD; (J Thorac Cardiovasc Surg 2015;150:136-42)
Proximal Configuration No significant differences between the proximal configuration of devices 2.8% Proximal Bare Stent (48/1724) VS 2.4% NBS, p=0.5895 (28/1159) Zone placement and dynamic arch motion may also play a role
RTAD Experience at Carolinas Medical Center Retrospective review of TBAD treated with TEVAR (2012 2017) 186 patients; Mean follow-up 569 days Overall incidence of RTAD 8.0% (15/186) Number Presentation (Days) Percentage 1 Intra-Op 0.5% 5 1 30 2.6% 6 31-365 3.2% 3 366-569 1.6%
Demographics and Comorbidities Variable; n (%)/ Mean (SD) RTAD (n-15) Non-RTAD (n-171) P-value Male Sex 8 (46.7) 0.6 Age 61.5 (14.4) 0.9 Race 0.5 African-American 8 (53.3) 72 (42.1) White 7 (46.7) 94 (55.0) CAD 1 (6.7) 45 (26.3) 0.1 CKD/CRI 3 (20.0) 44 (25.7) 0.8 COPD 1 (6.7) 36 (21.1) 0.3 Diabetes 1 (6.7) 30 (17.5) 0.5 HLD 6 (40.0) 71 (41.5) 0.9 HTN 13 (86.7) 160 (93.6) 0.3 Smoking < 1yr 7 (46.7) 85 (49.7) 0.8 Marfans 1 (6.7) 5 (2.9) 0.4 Other Genetic/Connective Tissue 0 (0) 2 (1.2) 1.0 Previous Ascending/Arch Repair 2 (13.3) 11 (6.4) 0.3
Indication for Intervention Procedural Indication RTAD (n - 15) Non-RTAD (n 171) Acute Complicated 8 (53.3) 50 (29.2) Acute High Risk 3 (20.0) 69 (40.8) Acute Uncomplicated 2 (13.3) 17 (9.9) Chronic 2 (13.3) 35 (20.5) Variable n(%) or Mean (SD) RTAD (n = 15) Non-RTAD (n = 171) P-value Mesenteric Ischemia 2 (13.3) 8 (4.7) 0.2 Renal Ischemia 6 (40.0) 29 (17.0) 0.04 Lower Limb Ischemia 1 (6.7) 11 (6.4) 1.0 Spinal Ischemia 1 (6.7) 3 (1.8) 0.3 Aneurysm (> 6cm) 0 (0.0) 4 (2.3) 1.0 Rupture 1 (6.7) 6 (3.5) 0.5 High Risk: Refractory HTN 0 (0.0) 11 (6.4) 0.6 High Risk: Continued Pain 2 (13.3) 32 (18.7) 1.0 High Risk: Pain and HTN 1 (6.7) 23 (13.5) 0.7
Intervention Timing Variable; n(%) or mean(sd) RTAD (n=15) No RTAD (n=171) p-value Acute (less than two weeks) Presentation 10 (66.7) 94 (55.6) 0.4 Time to Intervention 0.4 Acute Early (<48 hours) 1 (6.7) 30 (17.5) Acute Delayed (48 hrs-2 weeks) 9 (60) 64 (37.4) Subacute (2-6 weeks) 1 (6.67) 19 (11.1) Chronic 4 (26.7) 56 (32.8) Unknown 0 (0) 2 (1.2)
Aorta Characteristics Mean (SD); Frequency (%) RTAD (n=15) No-RTAD (n=171) P-value Ascending Diameter 37.1 (4.9) 36.4 (4.3) 0.5 Ascending > 4cm 7 (46.7) 35 (21.5) 0.05 Arch Type 0.6 Type I 6 (40.00) 49 (28.99) Type II 3 (20.00) 53 (31.36) Type III 6 (40.00) 67 (39.64) Bovine 5 (33.33) 49 (28.65) 0.8 Dissection proximal to LSA 5 (33.3) 26 (15.3) 0.1 Presence of IMH 10 (66.67) 65 (38.01) 0.03 IMH in Arch 3 (20.00) 12 (7.02) 0.1
Procedural Details Variable; n(%) or mean(sd) RTAD (n=15) No RTAD (n=171) p-value Proximal Landing Zone 0-2 14 (93.3) 109 (63.7) 0.02 Zone 0 1 (6.7) 2 (1.17) Zone 1 4 (26.7) 8 (4.68) Zone 2 9 (60.0) 99 (57.9) Zone 3 1 (6.7) 44 (25.7) Zone 4-5 0 (0.0) 18 (10.6) Struts at most proximal attachment 11 (73.3) 124 (77.5) 0.7 Graft oversizing (based on CTA) 4.6 (6.1) 5.4 (6.9) 0.2 Diameter of most proximal graft 33.3 (3.3) 31.8 (4.1) 0.1 Length of most proximal graft 173.3 (25.8) 159.3 (35.1) 0.2 Number of stent grafts in thoracic aorta 1.8 (0.4) 1.7 (0.7) 0.2 Number of stents in visceral arteries 0.7 (1.0) 0.3 (0.8) 0.05 Had stents placed in visceral arteries 5 (33.3) 26 (15.2%) 0.1
Case Review Patient Presentation Snorkel repair of LSA and LCA with TEVAR in 2011 Routine follow-up (2 year) with a Type A dissection and occlusion of LSA stent Non-operative candidate for standard repair of ascending arch Additional snorkel of innominate artery and placement of graft decided as treatment plan
Initial Angiogram Type A Dissection
Device Placement
Final Angiogram
Minimizing Risks for RTAD Careful patient presentation BEFORE determining treatment approach Establish a systematic protocol to minimize threat of RTAD Iatrogenic injury is REAL - minimize manipulation and wire/catheter movement Size appropriately based on pathology and treatment zone Use IVUS for all aortic procedures
Conclusions The occurrence of RTAD after TEVAR remains relatively infrequent but devastating Several risk factors influence risks for RTAD: Pathology Anatomy, Procedural techniques Device selection Continued Cocaine Use Oversizing Treatment timing Acute Complicated TBAD Ischemia of Visceral/Renal Arteries At risk patients for RTAD may require enhanced surveillance Additional R & D and investigation must continue to further reduce the risk of RTAD
Thank You Frank R. Arko, III, MD Chief, Vascular and Endovascular Surgery Professor, Cardiovascular Surgery Co-Director, Aortic Institute Sanger Heart and Vascular Institute Charlotte, NC