EVAS How does this Impact EVAR Therapy John S. Lane III, MD, FACS Professor and Acting Chief of Vascular Surgery University of California, San Diego PNEC, 2017 Endologix products and associated components are not available in all countries or regions. Please contact your Endologix representative for details regarding product availability. Prior to use, refer to the Instructions for Use for complete and specific indications, contraindications, all warnings and precautions. Rx only.
DISCLOSURES John Lane, MD Consultant/Advisory Board: Endologix Speakers Bureau: Endologix Endologix products and associated components are not available in all countries or regions. Please contact your Endologix representative for details regarding product availability. Prior to use, refer to the Instructions for Use for complete and specific indications, contraindications, all warnings and precautions. Rx only.
EVAR has an early survival benefit but an inferior late survival compared with open repair, which needs to be addressed by lifelong surveillance of EVAR and prompt reintervention if necessary.
EndoVascular Aneurysm Sealing (EVAS) IS NOT EVAR New therapy, potentially disruptive Conceptually different to EVAR Fundamental evolution in concept to using polymer to treat entire aneurysm Active management of aneurysm sac, reduce type II endoleaks Fundamentally different procedure requires adherence to SPS (Selection, Placement, Sealing)
Nellix IDE 1 Year Outcomes 2 Year Outcomes Primary safety and effectiveness endpoints have been achieved 100% technical success obtained Lowest overall endoleak (3.1%) and secondary intervention (3.3%) rates reported at 1-year as compared to FDAapproved EVAR devices Successful at treating a broad range of infrarenal AAA and common iliac artery aneurysms Preliminary results showed unexpected outcomes in a limited number of patients Reports of migration and aneurysm enlargement were observed Comprehensive engineering evaluation, statistical analysis, and clinical assessment were completed
NELLIX STENT MIGRATION Thrombus plays primary role Small blood volumes Asymmetric or inadequate endobag filling Mechanism is lateral displacement and bending Resistance to Migration Seal zone engagement Thrombus volume and stability Polymer thickness and distribution
NELLIX AND SAC EXPANSION Iliac artery morphology implicated OR for sac expansion 23/cm iliac diameter Lack of bag attachment 3SQ Incomplete treatment iliac aneurysm Sac expansion 2o migration
Indication Refinements
IFU Refinement And Clinical Outcomes (Expansion, Migration, Type 1 Endoleak) IFU REFINEMENT AND MIGRATION (10mm) 100.0% 99.4% 97.5% 92.5% 1.0 0.9 Freedom From Migration >10 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 LEGEND OFF IFU 0 0 2 4 6 8 10 12 14 16 18 20 22 24 Month SURVIVAL ESTIMATES: At Risk 131 129 125 122 118 108 101 97 95 95 88 73 61 202 202 201 195 187 179 171 161 157 145 133 117 94 OFF IFU
IFU Refinement And Clinical Outcomes (Expansion, Migration, Type 1 Endoleak) IFU REFINEMENT AND SAC GROWTH 99.2% 99.5% 98.1% 93.8% 1.0 0.9 Freedom From Sac Enlargement 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 LEGEND OFF IFU 0 0 2 4 6 8 10 12 14 16 18 20 22 24 Month SURVIVAL ESTIMATES: At Risk 131 129 125 122 118 107 101 98 96 96 87 73 62 202 202 200 195 187 179 172 163 159 148 135 119 96 OFF IFU
IFU Refinement And Clinical Outcomes (Expansion, Migration, Type 1 Endoleak) IFU REFINEMENT AND TYPE1A ENDOLEAK 100.0% 97.4% 98.9% 96.5% 1.0 0.9 Freedom From Type IA Endoleaks 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 LEGEND OFF IFU 0 0 2 4 6 8 10 12 14 16 18 20 22 24 Month SURVIVAL ESTIMATES: At Risk 131 129 125 122 118 108 101 98 96 96 87 73 62 202 199 198 193 185 177 169 162 159 148 135 120 101 OFF IFU
IFU Refinement And Clinical Outcomes (Expansion, Migration, Type 1 Endoleak) TREATMENT FAILURE IN COHORT 99.2% 97.4% 95.6% 84.7% Freedom From Type IA Endoleaks, Sac Enlargement, or Migration >10 1.0 0.9 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 LEGEND OFF IFU 96% Freedom from Migration, Type Ia Endoleak, or Sac Expansion Freedom from Core Lab-Reported Migration >5mm Type Ia Endoleak Sac Enlargement >5mm 0 0 2 4 6 8 10 12 14 16 18 20 22 24 Month SURVIVAL ESTIMATES: At Risk 131 129 125 122 118 107 101 97 95 95 87 73 61 ON 202 199 198 193 185 177 169 157 153 141 129 114 87 OFF
IFU Refinement And Clinical Outcomes (Expansion, Migration, Type 1 Endoleak) MORTALITY - ARM / ACM 98.5% 99.5% 98.5% 98.7% 92.9% 97.9% 92.0% 94.7% 1.0 0.9 1.0 0.9 Freedom From AAA-Related Mortality 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 LEGEND OFF IFU Freedom From Overall Mortality* 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 LEGEND OFF IFU 0 0 2 4 6 8 10 12 14 16 18 20 22 24 Month 0 0 2 4 6 8 10 12 14 16 18 20 22 24 Month SURVIVAL ESTIMATES: At Risk SURVIVAL ESTIMATES: At Risk 131 129 125 122 118 108 101 98 96 96 88 73 62 131 129 125 122 118 108 101 98 96 96 88 73 62 202 202 201 195 188 179 172 165 161 150 137 121 102 OFF IFU 202 202 201 195 188 179 172 165 161 150 137 121 102 OFF IFU * 10 deaths total in each group.
ACTIVE MANAGEMENT ANEURYSM SAC ENDOLEAK RATE 99.2% Persistence Incidence 97.0% Type II Endoleak Global Registry < 1% of Persistent Type II Endoleaks at 2 years
EVAS AND PERSONALIZED MEDICINE EVAS is particularly suited for AAA with low thrombus burden EVAS reduces Type 2 Endoleak EVAS low rate sac expansion SAC EXPANSION TYPE 2 ENDOLEAKS EVAR ++ +++ EVAS + --- CLINICAL RESULTS +/- +++
ACTIVE ANEURYSM SAC MANAGEMENT PIS and CVM 99% Freedom from Cardiovascular Mortality through 2 Years 98.5% 97.4% 89.1% CVM ARM ACM 99% Freedom from Cardiovascular Mortality through 2 Years
Why would EVAS carry a lower ACM and CVM than EVAR? EVAR is associated with acute sac thrombosis EVAS minimal acute thrombosis Acute thrombosis may trigger a systemic inflammatory response (Post-Implantation Syndrome) and influence post-operative outcomes
IFU Refinement And Clinical Outcomes (Expansion, Migration, Type 1 Endoleak) AAA METABOLISM AND ALL CAUSE MORTALITY AAA sac remains biologically active after EVAR Cytokine levels after EVAR are highest in aneurysms that remain static or expand MACE associated with systemic inflammation Lowering markers of systemic inflammation prevent MACE Role of EVAS in long term cardiovascular mortality? Otterhag et al Cytokine 2014; 70: 151 Ridker et al NEJM 2008; 20: 359
Why would EVAS carry a lower ACM and CVM than EVAR? Potential reduction in post-implantation syndrome and inflammatory response following endovascular aneurysm sealing EVAS (n=69) or EVAR (n=42); Lower MAEs in EVAS (10%) vs. EVAR (40%); Lower rate of cardiac AE after EVAS (2.4%) vs. EVAR (11.6%) EVAR) No endoleaks in the EVAS group; 8 (11.6%, p<0.5) in EVAR group Metabolic activity: Metabolic activity: Berg et al., Pending Publication CRP mg/dl WBC Leucocytes x 10^3/µl Platelets Thrombocytes x 10^3/µl Temp C N EVAS 69 7.0 10.69 253 37.2 EVAR 42 15.7 14.21 276 37.6 p<0.05 p<0.05 NS p<0.05
Conclusions - EVAS Low endoleak, rupture, and mortality rates through 2 years Migration signal at 2 years in AAA with large thrombus burden IFU Refinements demonstrated high freedom from Type Ia endoleak, migration, and sac growth Nellix well suited with patients with low AAA thrombus burden, and with patient lumbars, IMA Relationship between EVAS, reduction in post implant syndrome and CV mortality warrants further investigation