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Page 2 of 8 Tumscitz et al. Vessel Plus 2019;3:20 I http://dx.doi.org/10.20517/2574-1209.2018.71

INTRODUCTION
Coronary chronic total occlusion (CTO) is characterized by heavy atherosclerotic plaque burden within
the artery, resulting in complete occlusion of the vessel. Although the duration of the occlusion is difficult
to determine, a coronary occlusion is defined as true CTO when the duration is at least 3 months or
[1]
undetermined . Patients with CTO usually develop collaterals, which can be visualized through coronary
angiography, from ipsilateral or contralateral vessel. However, these collaterals often do not provide sufficient
[2]
blood flow to prevent myocardial ischemia during exercise and therefore anginal symptoms may appear .
The incidence of CTO among patients who have a clinical indication for coronary angiography has been
reported to be as high as 15% to 30% .
[3,4]
The first important step made in CTO revascularization was to recanalize the occluded vessel using
coronary collaterals. The septal channel has historically been the first described solution.The progressive
improvement in the the technology of guidewires and microcatheters expanded the ability to cross different
collateral channels even in very complex cases. Nowadays, examples of collaterals which can be used in CTO
procedures, also include epicardial collaterals, even ipsilateral, and occluded saphenous grafts. Experienced
operators are able to successfully treat very difficult CTO lesions using a combination of different pathways
and techniques.

The results of older data registry (early CTO era) showed low success rate and higher MACE compared
with non-CTO PCI, whereas CTO revascularization performed in experienced centers has now proven
success rate up to 80%-90%. On the other hand, due to the higher lesion and technical complexity, CTO
complications rate has shown to be higher than non-CTO PCI (1.6% vs. 0.8%; P < 0.0001) .
[5]
Perforation is one of the most troublesome complications of CTO PCI. Despite the fact that coronary
perforations are infrequent (0.33% of all cases) they are associated with poorer short‐ and long‐term
outcomes. In the British Cardiovascular Intervention Society Database CTO PCI was one of independent
predictors of risk of perforation .
[6]

Coronary artery perforations (CAP) are categorized according to Ellis classification as: Type I, extraluminal
crater without extravasation; Type II, epicardial fat or myocardial blush without contrast jet extravasation;
Type IIIa, extravasation through frank (> 1 mm) perforation; Type IIIb "cavity spilling" (CS), which refers
to perforations with contrast spilling directly into either the left ventricle, coronary sinus or other anatomic
circulatory chamber [Table 1] . Grade I or II perforation are usually managed conservatively since they
[7]
have a more benign clinical course. On the other hand, type III CAP was associated with a worse outcome.
In earlier registers CAP Type III was associated with a very high in-hospital mortality rate (44%), with the
[8]
majority of patients requiring emergency surgery (60%) , while more recent data shows lower mortality rate
(15.2%) and lower rate of emergency surgery (16%) .
[9]
Among interventional collaterals suitable for CTO procedures, epicardial channels are considered the
trickiest ones and appear more prone to perforation or rupture. This is caused by the relative high frequency
of tortuosity and their small size (CC1 in Werner classification) . Perforation of epicardial channels carries
[10]
a higher risk of cardiac tamponade and death when the treatment is delayed. This is due to the spillage of
blood directly into the pericardial space.
The current endovascular treatment for perforated coronary arteries involves the use of prolonged balloon
inflation and/or the use of covered stents (CS). The use of CS is feasible only when CAP is located in a large
[11]
vessel due to the availability of CS starting just from a diameter of 2.25-2.5 mm . Moreover, when collateral
vessels emerge at a short distance from the CAP, the use of CS could lead to the occlusion of the collaterals
and to the subsequent myocardial infarction. When CAP occurs in smaller vessels or collaterals (< 2 mm),