CTO pathophysiology: how does this affect management?

Abstract

Chronic total occlusion (CTO) pathophysiology has been described in a few, small studies using post mortem histology, and more recently, in vivo intravascular ultrasound (IVUS) to analyse the constituents of occluded segments. Recent improvements in equipment and techniques have revealed new insights into physical characteristics of occluded coronaries, which in turn enable predictable procedural success. The purpose of this review is to consider the published evidence describing CTO pathophysiology from the perspective of the hybrid algorithm approach to CTO PCI.

Methods: Literature searches using "Chronic Occlusion", "angioplasty", and" pathology" as keywords. Further searches on "coronary" "collateral", "Viability". Bibliographies were scrutinised for further key publications in an iterative process. Papers describing animal models were excluded.

Fig. (1)

Image of coronary angiogram of RCA from late presenting STEMI. Normal LV function. Bulky thrombotic occlusion extending to small calibre marginal branch.

Fig. (2)

Coronary angiogram following aspiration thrombectomy. Culprit lesion 15mm distal to proximal margin of occlusive thrombus.

Fig. (3)

Still from angiogram of CTO of circumflex. Epicardial collaterals from diagonal. Symptoms predated this investigation by 6 months.

Fig. (4)

Still from PCI procedure, 1 year following angiogram in (Fig. 3). Long tapered segment replaced by blunt stump.

Fig. (5)

Still from coronary angiogram recorded during PCI in 2013 from patient in whom angina recurred 18 years post CABG. The occlusion of the RCA was reported on coronary angiography in 1993.

Fig. (6)

Coronary angiography of final result following successful PCI. 20 year old lesion crossed by antegrade wire escalation techniques.