Changes in incidence of rotablation-induced coronary perforation by modifying practice over time: experiences at a high-volume center

Figures

• 

  Figure 1. Favorable bias cutting and exception lesions. RA can be utilized to ablate thick calcium plates or calcified nodules located at the inner corner of acute bends (arrows, panel A). Using normal frame rate, normal field of vision (FOV), and fluoroscopic setting is encouraged, with careful attention to the relationship between the burr/wire and the vessel wall calcium. During the procedure, thinning of the calcium plate by RA can be observed (arrows, panel B). The operator should stop further rotablation when a majority of the calcium is sequentially taken out by the burr and a minimal amount of calcium is left (arrows, panel C). Overdoing rotablation could lead to the burr cutting through the vessel wall and perforating the vessel (arrows, panel D). However, in extreme cases, the calcium chunk could be too thick, solid, and hard to be taken out by RA (**, panel E). In this case, the burr could slide over the calcium chunk and cut into the outer corner of the downstream acute bend (arrow, panel E) and precipitate vessel perforation (arrow, panel F).

• 

  Figure 2. Unfavorable RA bias cutting. When RA bias cutting is utilized to treat thick calcium at inner corners of acute bends, the burr may go too far down and reach the calcification-free inner corner of the downstream bend (arrow, panel A) or travel though a similar lesion at an upstream bend (arrow, panel C) before it reaches the intended target lesion. Because there is no calcium at those sites, unfavorable bias cutting occurs, potentially leading to vessel perforation at these sites (arrows, panels B,D). Unfavorable bias cutting also occurs when RA is intended to treat calcified lesions located at the outer corners of acute bends, where the burr can easily cut through the non-calcified inner corners, leading to perforation (arrows, panels E,F).

• 

  Figure 3. An example case of complex and heavily-calcified lesions which could be treated by RA using favorable bias cutting. The calcified lesions involved LM bifurcation, ostial-proximal-middle-distal LAD (panels A,B) and proximal LCX (panel A), which was well treated with rotablation plus DES for all above lesions as the patient definitely defied CABG. Given all the thick calcifications were located at inner corners of curvatures (black arrows) which were best appreciated when the extrasupport RA wire was in place, they were RA bias cutting favorable and comfortably treated (panels C,D), leading to well acceptable angiographic results (panel E).

• 

  Figure 4. A patient with heavily calcified CAD involving the distal LM bifurcation, mid-distal LAD, and proximal LCX (panel A). Thick calcification was eccentric in distribution and located at the outer corners of acute bends in the distal LAD (black arrows, panels B,C), while the inner corners of the corresponding bends were free of thick calcium and prone to RA bias cutting through the vessel wall (white arrows, panel C). Because of safety reasons, RA was not considered and CABG was chosen instead.

• 

  Figure 5. A patient with RA-induced CP at distal RCA. The patient had occlusive ISR at mid-RCA, followed by a CTO lesion (panel A). After the wire was passed, no device could be advanced. Therefore, RA was considered and the wire was placed. However, there was acute angulation with a small radius at the mid-distal junction of the RCA and a large/thick calcium at the inner corner (arrows, panels B,C). The RA burr could not ablate the thick calcium but slid over it to a downstream segment (arrowheads, panels D,E) and bias cut through the non-calcified vessel wall after multiple RA runs, leading to perforation (arrows, panel F, and arrowheads, panel G). This mechanism is explained in panels E,F of Figure 1.

• 

  Figure 6. Incidences of major adverse effects during RA. There was a significant reduction in the incidence of acute slow/no flow and total RA-induced CP in Period II.