Coronary chronic total occlusions (CTOs) are commonly identified in between 18.4% and 52% of patients with coronary artery disease (CAD).1-3 Observational studies have suggested that when successfully performed, percutaneous coronary intervention (PCI) of CTO can reap significant clinical benefits including symptom relief, improved left ventricular function, reduced arrhythmia risk, and better tolerance of an acute coronary syndrome.4 Advanced techniques including the retrograde approach, antegrade dissection/reentry (ADR) techniques, and a systematic algorithmic “hybrid” approach encouraging operators to nimbly move between techniques have developed. And using these strategies, technical and procedural success rates have climbed consistently to above 80%.5-7 However, the major adverse cardiovascular event (MACE) rates of CTO-PCI exceed that of standard PCI.2 Therefore, there is substantial value to be gained from understanding the mechanisms underlying adverse events during CTO-PCI in order to develop strategies to reduce MACE rates.
In this issue of the Journal of Invasive Cardiology, Nguyen-Truong et al improve our understanding of how loss or occlusion of a coronary side branch (SB) during a CTO-PCI associates with clinical outcomes following PCI.8 The authors retrospectively reviewed 109 consecutive CTO-PCI cases performed at their institution between 2012 and 2013. SBs were identified if they were ≥1.0 mm diameter and present at any time during the CTO-PCI procedure. CTO-PCI was complicated by loss of a coronary SB in 28 of these cases (25.7%). Figure 2 of their study provides a distribution of the location of the side-branch losses, occurring in the right coronary artery 69% of the time. The preprocedure clinical characteristics were similar between the SB loss and the SB retained patient groups, except for a decreased prevalence of diabetes in the SB loss patients. SB rescue was attempted in only 28% of cases and rescue was successful approximately 50% of the time. Comparison of procedural characteristics revealed that there was a higher utilization of ADR and retrograde techniques in the SB loss group. The SB loss group also experienced 31% and 26% longer total procedure and fluoroscopy times, respectively.
The authors reported that patients with SB loss experienced poorer clinical outcomes, including a statistically significant increase in CK-MB levels (approximately 4x increase) and, perhaps surprisingly, a lower 12-month survival rate (83% vs 97%). Logistic regression was performed to identify predictors of SB occlusion. The authors found that the most significant predictors of SB loss were: a dissection/reentry strategy (odds ratio [OR], 3.8); an SB present within 5 mm of the distal CTO cap (OR, 2.6); and the number of coronary stents utilized for the procedure (OR, 1.8).
These findings, albeit derived from a retrospective study, remind us that additional technical efforts to preserve SBs, even small ones, might improve outcomes during CTO-PCI. Indeed the fundamental techniques of antegrade wire escalation (AWE), ADR, and the retrograde approach all include inherent strategies aimed at true lumen canalization with minimal compromise of SB territories. In CTO terminology, the “base of operations” corresponds to the CTO segment where most of the procedural effort is expended to cross the occlusion and connect to the true lumen. Often this base of operations is targeted to a location that (among other characteristics) also poses the lowest possible threat of SB occlusion.9 Despite this a priori technical goal of SB preservation and increasing CTO-PCI rates, there have been scant data evaluating the clinical importance of SB preservation in CTO-PCI.2 Our paucity of knowledge on SB loss contrasts starkly with the large body of knowledge on non-CTO SB loss, as reviewed by the European Bifurcation Club in the last decade.10
This work was developed from a small cohort of patients (n = 109 CTO-PCI cases) performed at a single institution. We thus of course must remain cautious of its findings and its broader applicability. The work observed a mortality increase following SB loss that is somewhat difficult to explain. Of note, only 2 of the 4 deaths in patients in the SB loss group and 0 of 2 patients in the non-SB loss group experienced death from cardiac causes. Linking the non-cardiac deaths to SB loss is difficult. Yet the authors describe a higher 12-month incidence of all-cause death (17.3% vs 2.8%; P=.02) and cardiovascular death (7.4% vs 0.0%; P=.02) in the SB loss group. They also found a statistically better rate of freedom from cardiovascular death (log-rank P=.02) in the non-SB loss group. In contradistinction, however, MACE rates (death, acute coronary syndrome, and repeat revascularization with PCI or coronary artery bypass graft surgery) were similar between the SB loss and non-SB loss groups.
Furthermore, we would expect that the occlusion of a non-CTO SB would be more prone to cause negative clinical consequences than the occlusion of a CTO-SB. This would be expected due to the lack of ischemic preconditioning of the non-CTO SB territory as well as due to the presumed increased frequency of viable myocardium perfused by a non-CTO SB. And yet though this paper reports a worsened mortality associated with CTO-SB occlusion, no such worsened mortality has been demonstrated in non-CTO SB occlusions of similar size (≥1 mm).11 Caution interpreting this study is therefore appropriate. Overall, the results of this study are hypothesis generating and should motivate more investigation into the importance of SB loss during CTO-PCI. Should additional studies find conclusively worse outcomes following SB loss, intensified strategies to prevent SB loss would become important to evaluate. For example, this might increase efforts to wire lesions true-to-true, when possible, before committing to intentional dissection approaches. Or it may accelerate conversion to a retrograde approach before ADR reentry attempts progress downstream and clip SBs. We congratulate the authors and look forward to additional light shed on the importance of SB loss during CTO-PCI.
1. Fefer P, Knudtson ML, Cheema AN, et al. Current perspectives on coronary chronic total occlusions: the Canadian multicenter chronic total occlusions registry. J Am Coll Cardiol. 2012;59:991-997.
2. Brilakis ES, Banerjee S, Karmpaliotis D, et al. Procedural outcomes of chronic total occlusion percutaneous coronary intervention: a report from the NCDR (National Cardiovascular Data Registry). JACC Cardiovasc Interv. 2015;8:245-253.
3. Jeroudi OM, Alomar ME, Michael TT, et al. Prevalence and management of coronary chronic total occlusions in a tertiary veterans affairs hospital. Catheter Cardiovasc Interv. 2014;84:637-643.
4. Garcia S, Abdullah S, Banerjee S, Brilakis ES. Chronic total occlusions: patient selection and overview of advanced techniques. Curr Cardiol Rep. 2013;15:334.
5. Karmpaliotis D, Michael TT, Brilakis ES, et al. Retrograde coronary chronic total occlusion revascularization: procedural and in-hospital outcomes from a multicenter registry in the united states. JACC Cardiovasc Interv. 2012;5:1273-1279.
6. Galassi AR, Tomasello SD, Reifart N, et al. In-hospital outcomes of percutaneous coronary intervention in patients with chronic total occlusion: insights from the ERCTO (European Registry of Chronic Total Occlusion) registry. EuroIntervention. 2011;7:472-479.
7. Michael TT, Karmpaliotis D, Brilakis ES, et al. Procedural outcomes of revascularization of chronic total occlusion of native coronary arteries (from a multicenter United States registry). Am J Cardiol. 2013;112:488-492.
8. Nguyen-Trong PJ, Rangan BV, Karatasakis A, et al. Predictors and outcomes of side-branch occlusion in coronary chronic total occlusion interventions. J Invasive Cardiol. 2016;28:168-173. Epub 2016 Jan 15.
9. Spratt JC, Strange JW. Retrograde procedural planning, skills development, and how to set up a base of operations. Interv Cardiol Clin. 2012;1:325-338.
10. Lassen JF, Holm NR, Stankovic G, et al. Percutaneous coronary intervention for coronary bifurcation disease: consensus from the first 10 years of the European Bifurcation Club Meetings. EuroIntervention. 2014;10:545-560.
11. Aliabadi D, Tilli FV, Bowers TR, et al. Incidence and angiographic predictors of side branch occlusion following high-pressure intracoronary stenting. Am J Cardiol. 1997;80:994-997.
From the Cardiac Catheterization Laboratory, Division of Cardiology, Massachusetts General Hospital, Boston, Massachusetts.
Disclosures: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Jaffer has a consulting agreement with Abbott Vascular and Boston Scientific. Dr Monteleone reports no conflicts of interest regarding the content herein.
Address for correspondence: Farouc A. Jaffer, MD, PhD, Division of Cardiology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114. Email: email@example.com