Introduction of New Advances In Chronic Total Occlusions

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Summary

Coronary chronic total occlusions (CTOs) are identified in up to one third of patients with coronary artery disease referred for nonurgent coronary angiography,^1,2 with an incidence increasing with age.³ Conceptually, you may argue that the motivation to reopen a totally blocked artery is not as strong as for subocclusive lesions, that have the potential to progress and cause acute events. The evidence for coronary chronic occlusions goes into the opposite direction, suggesting that when viability and ischaemia are present reopening a coronary CTO yields a greater benefit than reopening subocclusive lesions. Data from mainly retrospective and observational series relate successful CTO recanalisation with improved survival, improvement in anginal status and left ventricular function, increased exercise tolerance and decreased need for coronary artery bypass grafting (CABG).^4–8

CTOs still represent the most complex lesion subset that interventional cardiologists face. Lesions with severe tortuosities, calcifications or large bifurcations present technical challenges, but the success rate in expert hands remains far above 95 %.⁹With the exception of dedicated centres applying new strategies, the success rate of CTO PCI was over long period of time in the range of 60-70 %,⁵ considerably lower than the success rate in non-occlusive coronary artery disease. Restenosis and reocclusion were also high before the introduction of Drug eluting stents (DES).¹⁰ The perception that CTOs are challenging lesions with a low success rate, limited scope for revascularisation and questionable impact on patient outcome led to underutilisation of percutaneous recanalisation, with the majority of lesions left to medical therapy or referred for surgical revascularisation. No more than 10 % of all CTOs have been treated with percutaneous techniques over a long period of time.^1,3,11–14 The following review reexamines the evidence leading to this conservative attitude and reports the advances in the treatment of CTOs, promoting a more balanced and proactive approach in patients suffering of this often highly disabling condition.

Definition
A chronic total occlusion is defined as a complete interruption of antegrade coronary flow (thrombolysis in myocardial infarction [TIMI-0] flow) of greater than three months standing.¹⁵ The long persistence of the occlusion implies the development of collateral circulation and this leads to opacification of the occluded distal vessel during injection in most cases. The pattern of distal filling – anterograde or with flow coming retrograde from the distal vessel – clarifies whether we are dealing with a real occlusion or a functional subocclusive lesion. Occasionally, non-intralesional bridging collaterals may give antegrade flow to the vessel beyond the occlusion. The careful examination of the occlusion in multiple views delineates the extraluminal course of these collaterals. Intraluminal channels are demonstrated pathologically in the majority of cases and may play a role in facilitating wire crossing^16,17; yet they mostly remain below the resolution of angiography (100 μm) and, by definition, have no continuity throughout the occluded segment or they violate the TIMI-0 criterion.¹⁸

The second criterion of CTO definition, occlusion duration, is more difficult to assess. Three levels of certainty are commonly used; occlusion duration angiographically confirmed, clinically confirmed and undetermined.¹⁵ A previous angiographic study confirming the presence of the CTO for more than three months is available in less than 30 % of cases, if you exclude high volume CTO centres receiving patients after previous attempts. A history of an acute coronary event or of a sudden change in symptoms can be used as a clinical surrogate in the absence of angiographic confirmation. A greater than three months duration is also assumed when there is a clear angiographic pattern compatible with total occlusion in the absence of recent symptom deterioration or with new symptoms clearly caused by an acute lesion in a different culprit artery.