Saphenous Vein Graft Occlusion Following Native Vessel Chronic Total Occlusion Percutaneous Coronary Intervention

Abstract

Background. Whether saphenous vein grafts (SVGs) should be occluded after successful chronic total occlusion (CTO) percutaneous coronary intervention (PCI) of the corresponding native vessel remains controversial. Methods. We analyzed the clinical and angiographic characteristics and procedural outcomes of 51 patients who underwent SVG occlusion following successful CTO-PCI of the corresponding native vessel between 2015 and 2022 at 14 centers. Results. Mean patient age was 71 ± 8 years and 80% were men. The most common CTO target vessel was the right coronary artery (41%), followed by the left circumflex (37%). Retrograde crossing through the SVG was the successful crossing strategy in 40 cases (78%). SVG occlusion was achieved with coils (1.9 ± 1.0) in 35 of 51 patients (69%) and vascular plugs in the other 16 cases (31%). All procedures were technically successful and the SVG was occluded completely (TIMI 0 flow) in 38 of the cases (75%), with the remaining cases having TIMI 1 flow. Follow-up was available for 37 patients (73%); during a mean follow-up of 312 days from CTO-PCI, the incidence of target-lesion failure due to restenosis was 5.4% (n = 2) with no other major events reported. Conclusion. Following native vessel CTO-PCI, SVG occlusion is often performed and is associated with favorable mid-term outcomes.

J INVASIVE CARDIOL 2022;34(12):E836-E840. Epub 2022 November 23.

Key words: chronic total occlusion, percutaneous coronary intervention, saphenous vein graft

Percutaneous coronary intervention (PCI) of the native coronary vessels is the preferred treatment strategy for most patients with previous coronary artery bypass graft (CABG) surgery because PCI of the saphenous vein graft (SVG) lesions or surgical reoperation is associated with higher incidence of short- and long-term major adverse events.^1-3 Native coronary artery PCI in patients with patent SVGs could be complicated by stent thrombosis or restenosis due to unfavorable flow from the SVG.^4,5 Occluding the SVG stops competitive flow, but this may lead to complications if flow through the native coronary artery becomes compromised. The practice of occluding patent SVGs after successful PCI of the corresponding native coronary artery remains controversial and was the focus of the present study.

Methods

Patient population. We analyzed the baseline clinical and angiographic characteristics and procedural outcomes of 51 patients who underwent SVG occlusion after successful recanalization of the corresponding native coronary artery chronic total occlusion (CTO) between 2015 and 2022 at 14 centers. Data collection was recorded in a dedicated online database (PROGRESS CTO: Prospective Global Registry for the Study of Chronic Total Occlusion Intervention; Clinicaltrials.gov identifier: NCT02061436). Study data were collected and managed using REDCap (Research Electronic Data Capture) electronic data-capture tools hosted at Minneapolis Heart Institute Foundation.^6,7 The study was approved by the institutional review board of each center.

Definitions. Coronary CTOs were defined as coronary lesions with Thrombolysis in Myocardial Infarction (TIMI) grade 0 flow of at least 3-month duration. Estimation of the duration of occlusion was clinical, based on the first onset of angina, prior history of myocardial infarction (MI) in the target-vessel territory, or comparison with a prior angiogram. Technical success was defined as successful CTO revascularization with achievement of <30% residual diameter stenosis within the treated segment and restoration of TIMI grade 3 antegrade flow. Procedural success was defined as the achievement of technical success without any in-hospital major adverse cardiac event (MACE). In-hospital MACE included any of the following adverse events prior to hospital discharge: death, MI, recurrent symptoms requiring urgent repeat target-vessel revascularization with PCI or CABG surgery, tamponade requiring either pericardiocentesis or surgery, and stroke. MI was defined using the Third Universal Definition of Myocardial Infarction (type 4a MI).⁸ The Japanese CTO (J-CTO) score was calculated as described by Morino et al,⁹ the PROGRESS-CTO score as described by Christopoulos et al,¹⁰ and the PROGRESS-CTO MACE score as described by Simsek et al.¹¹

Statistical analysis. Categorical variables were expressed as percentages and compared using Pearson’s Chi-square test. ­Continuous variables are presented as mean ± standard deviation or as median (interquartile range [IQR]) unless otherwise specified and were compared using the Student’s t test for normally distributed variables and the Wilcoxon rank-sum test for non-parametric variables, as appropriate. All statistical analyses were performed using JMP, version 16.0 (SAS Institute). A P-value of <.05 was considered to indicate statistical significance.

Results

During the study period, 51 patients underwent SVG occlusion after successful PCI of the corresponding native coronary artery CTO. The baseline clinical characteristics of the study patients are summarized in Table 1. Mean patient age was 71 ± 8 years and 80.4% of the patients were men. The grafted native vessel was the right coronary artery in 41.2%, the left circumflex artery in 37.3%, and the left anterior descending artery in 13.7%.

Mean J-CTO and PROGRESS-CTO scores were 3.1 ± 0.9 and 1.7 ± 0.9, respectively, reflecting the high complexity of the CTO target vessels that were treated. The initial crossing strategy was antegrade wiring in 47.1% (n = 24), retrograde wiring in 47.1% (n = 24) and antegrade dissection and re-entry in 5.8% (n = 3). Retrograde crossing was the successful crossing strategy in 78.4% (n = 40) and the SVG was the collateral used for all retrograde cases. The angiographic and procedural characteristics of the study patients are summarized in Table 1.

Recurrent SVG failure (64.7%) was the most common reason for treating the native vessel instead of the SVG supplying the same vessel. In 5 cases (9.8%), the SVG was aneurysmal. In 11 cases (21.6%), PCI of the SVG was feasible but the operator chose to treat the corresponding native CTO lesion instead (Table 2).

The SVG closure characteristics are shown in Table 2. Coils were used to occlude the SVG in 68.6% (n=35) (mean number of coils, 1.9 ± 1.0). Amplatzer vascular plugs (AVP II, III, or IV; Abbott Vascular) were used in 31.4% (n = 16), with only a single plug required for closure in each patient. All procedures in the native CTO lesions were technically successful (100%) and the SVG was occluded completely (TIMI 0 flow) in 74.5% of the cases (n = 38). In the remaining 13 cases, the SVGs had TIMI 1 flow and were expected to completely occlude over time.

A perforation occurred in 4 cases (7.8%), all in the CTO target vessel (3 large vessel and 1 one distal vessel perforation) and was successfully treated with covered stent implantation in all 4 cases without the need for pericardiocentesis. Two patients had major bleeding, 1 at the vascular access site that was managed conservatively and 1 retroperitoneal bleeding that required surgery.

Follow-up was available for 37 patients (72.5%). During a mean follow up of 312 ± 331 days from the date of SVG closure, the incidence of target-lesion failure (TLF) was 5.4% (n = 2). One patient presented with unstable angina and angiography showed in-stent restenosis at the site of the SVG anastomosis. The other patient developed recurrent angina, was found to have in-stent restenosis, and revascularization was performed. In both cases, the SVG was occluded. No other follow-up events were reported.

Discussion

To the best of our knowledge, our study is the largest to date reporting the outcomes of SVG occlusion following PCI of the corresponding native vessel CTO. The main findings are as follows: (1) recurrent SVG failure was the most common reason for treating the native vessel instead of the failing SVG; (2) retrograde crossing via the SVG was the most common successful crossing strategy in these cases; (3) coils were used more frequently than vascular plugs to intentionally occlude the SVGs; and (4) the incidence of TLF was 5.4% during a mean follow-up of almost 1 year.

Previous studies have reported that SVG-PCI is associated with poor short- and long-term outcomes and higher event rates, due to high rates of periprocedural MI and in-stent restenosis.^2,3,12,13 This has motivated native vessel PCI (if feasible) over SVG-PCI, and is a class 2a indication in the most recent American College of Cardiology/American Heart Association/Society for Cardiovascular Angiography and Interventions guidelines for coronary artery revascularization.¹⁴ The DIVA (Drug-Eluting Stent Versus Bare-Metal Stent in Saphenous Vein Angioplasty) trial,¹⁵ showed no significant difference in subsequent clinical outcomes between drug-eluting stents and bare-metal stents in patients undergoing stenting of de novo SVG lesions. In our study, recurrent SVG failure (54.9%) was the most common reason for treating the native vessel instead of the SVG.

In the present study, retrograde crossing through the SVG was the successful crossing strategy in most cases (78.4%). Previous studies have reported that the use of SVGs as retrograde conduits is associated with favorable outcomes,^4,16,17 although the risk of perforation is significant (7.8% in our study).^18,19

If CTO-PCI of the native vessel is performed instead of SVG-PCI, competitive flow from the SVG might predispose to stent thrombosis or restenosis in the native artery.^4,5 Occluding patent SVGs after successful CTO-PCI of the corresponding native vessel may decrease those risks. In a study by Dautov et al,⁴ coiling of the SVG was performed in 15 of 34 post-CABG retrograde CTO cases performed via SVGs after successful recanalization of the corresponding native coronary artery without periprocedural or in-hospital complications.

Wilson et al⁵ reported SVG occlusion following PCI of the native vessel in 33 patients with a high (97%) success rate (defined as TIMI 0 flow or TIMI ≤1 flow with complete resolution of competitive flow). In contrast to our study, in which coils were used more frequently than vascular plugs to intentionally occlude SVGs, vascular plugs (1 plug in 72.7% and 2 plugs in 24.2%) were used in all patients, with an additional neurovascular coil implanted in 1 patient.

In the present study, mid-term outcomes were favorable, with a 5.4% incidence of TLF after 312 ± 331 days from CTO-PCI without any stent thrombosis of the native coronary artery stents. Wilson et al⁵ reported a TLF rate of 9.1% during a mean follow-up of almost 2 years. Although our study supports the safety and effectiveness of SVG closure after successful CTO-PCI of the native vessel to terminate the effects of residual competitive flow, further clinical studies are needed.

Study limitations. First, PROGRESS-CTO is an observational study with no core laboratory assessment of the study angiograms or clinical event adjudication. Second, the procedures were performed at dedicated, high-volume CTO centers by experienced operators, limiting the generalizability of our findings to centers with limited CTO-PCI experience. Third, there were no predefined criteria for when to perform SVG closure, which was done at the discretion of the operator.

Conclusion

SVG occlusion after successful recanalization of the corresponding native vessel CTO can be performed with high success rates and favorable mid-term outcomes. Before routine adoption of this approach, data from randomized controlled trials are required to establish the risk/benefit ratio.

Affiliations and Disclosures

From ¹Minneapolis Heart Institute and Minneapolis Heart Institute Foundation, Abbott Northwestern Hospital, Minneapolis, Minnesota; ²Henry Ford Cardiovascular Division, Detroit, Michigan; ³Massachusetts General Hospital, Boston, Massachusetts; ⁴Cleveland Clinic, Cleveland, Ohio; ⁵University Hospitals, Case Western Reserve University, Cleveland, Ohio; ⁶Wellspan York Hospital, York, Pennsylvania; ⁷Emory University Hospital Midtown, Atlanta, Georgia; ⁸St. Boniface General Hospital, Winnipeg, Manitoba, Canada; ⁹London Health Sciences Centre, Division of Cardiology, Department of Medicine, Schulich School of Medicine & Dentistry, Western University, London, Ontario, Canada; ¹⁰Wellstar Health System, Marietta, Georgia; ¹¹University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania; ¹²Oklahoma Heart Institute, Tulsa, Oklahoma; ¹³North Oaks Health System, Hammond, Louisiana; ¹⁴Memorial Bahcelievler Hospital, Istanbul, Turkey; and ¹⁵Aswan Heart Center, Magdi Yacoub Foundation, Cairo, Egypt.

Funding: The authors are grateful for the philanthropic support of our generous anonymous donors, and the philanthropic support of Drs Mary Ann and Donald A. Sens, Mrs Diane and Dr Cline Hickok, Mrs Wilma and Mr Dale Johnson, Mrs Charlotte and Mr Jerry Golinvaux Family Fund, the Roehl Family Foundation, and the Joseph Durda Foundation. The generous gifts of these donors to the Minneapolis Heart Institute Foundation’s Science Center for Coronary Artery Disease (CCAD) helped support this research project.

Study data were collected and managed using Research Electronic Data Capture (REDCap) electronic data capture tools hosted at the Minneapolis Heart Institute Foundation (MHIF), Minneapolis, Minnesota.^6,7 REDCap is a secure, web-based application designed to support data capture for research studies, providing: (1) an intuitive interface for validated data entry; (2) audit trails for tracking data manipulation and export procedures; (3) automated export procedures for seamless data downloads to common statistical packages; and (4) procedures for importing data from external sources.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Alaswad reports consultant and speaker income from Boston Scientific, Abbott Cardiovascular, Teleflex, and CSI. Dr Jaffer reports sponsored research from Canon, Siemens, Shockwave, Teleflex, Mercator, Boston Scientific, HeartFlow, Amarin; consultant income from Boston Scientific, Siemens, Magenta Medical, IMDS, Asahi Intecc, Biotronik, Philips, Intravascular Imaging, and DurVena; equity interest in Intravascular Imaging Inc, and DurVena; licensing arrangements to Massachusetts General Hospital with Terumo, Canon, Spectrawave, for which he has the right to receive royalties. Dr Khatri reports personal honoria for proctoring and speaking from Abbott Vascular, Asahi Intecc, Terumo, and Boston Scientific. Dr Davies reports speaking honoraria from Boston Scientific, Medtronic, Siemens Healthineers, and Shockwave Medical. Dr Rinfret reports consultant income from Abbott Vascular, Abiomed, Boston Scientific Corporation, SoundBite Medical, and Teleflex. Dr Ybarra is a speaker for Bayer, Inc. Dr Abi-Rafeh reports proctor and speaker honoraria from Boston Scientific and Abbott Vascular. Dr El Guindy reports consulting honoraria from Medtronic, Boston Scientific, Asahi Intecc, and Abbott; proctorship fees from Medtronic, Boston Scientific, Asahi Intecc, and Terumo; educational grants from Medtronic. Dr Sandoval previously served on the advisory boards for Roche Diagnostics and Abbott Diagnostics without personal compensation; and has also been a speaker without personal financial compensation for Abbott Diagnostics. Dr Burke reports consulting and speaker honoraria from Abbott Vascular and Boston Scientific. Dr Brilakis reports consulting/speaker honoraria from Abbott Vascular, American Heart Association (associate editor, Circulation), Amgen, Asahi Intecc, Biotronik, Boston Scientific, Cardiovascular Innovations Foundation (Board of Directors), ControlRad, CSI, Elsevier, GE Healthcare, IMDS, InfraRedx, Medicure, Medtronic, Opsens, Siemens, and Teleflex; research support from Boston Scientific, GE Healthcare; owner of Hippocrates, LLC; shareholder in MHI Ventures, Cleerly Health, and Stallion Medical. The remaining authors report no conflicts of interest regarding the content herein.

Manuscript accepted September 16, 2022.

Address for correspondence: Emmanouil S. Brilakis, MD, PhD, Director of the Center for Complex Coronary Interventions, Minneapolis Heart Institute, Chairman of the Center for Coronary Artery Disease at the Minneapolis Heart Institute Foundation, 920 E 28th Street #300, Minneapolis, MN 55407. Email: esbrilakis@gmail.com

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