We reported for the first time OCT images of RA induced white thrombosis of severely calcified coronary lesions.
RA played an important role in pre-treat of severely calcified lesions before stenting. Complications of RA included coronary dissection (10.5%), severe coronary spasm (1.6-6.6%), acute vascular occlusion (3.1%), slow-flow/no-reflow (1.2-7.6%) and coronary artery perforation (0-2%) [14.15]. Among these complications, no-reflow phenomenon remains serious and common. Potential mechanisms of no-reflow during RA included atheromatous debris embolism, platelet activation, microcirculatory vasospasm and so on [16]. A previous study had proved the effect of RA on platelet activation in an in vitro model [8]. To our knowledge, this is the first report about the effect of RA on platelet aggregation in vivo indirectly proved by OCT imaging of white thrombosis. In one article (Kini et al.) which assessed of the mechanistic effects of rotational and orbital atherectomy in severely calcified coronary lesions by OCT (RA details: burr size 1.68±0.11mm, rotation speed 150,000rpm) [17], the authors found the similar phenomenon, also in all the lesions treated by RA. They defined this phenomenon as small intimal nodules. But according to the OCT image characteristics (different transmissivity and the clear boundary from intima), combined with the results of the in vitro test, we think it is white thrombus. Future histological studies will be necessary to prove this hypothesis.
In our research, only white thrombus was found after RA, which was same to Kini’s article[17]. Red thrombus was not found. The reasons may be that red thrombogenesis was usually be seen after the mixed thrombus completely block the lumen. it often composes the tail of the continuous thrombus. During the RA procedure, there was no enough times to generate red thrombus.
The thrombotic load is influenced by several factors. In our study, we found bigger burr size and higher number of rotation would result in higher thrombotic load. In invitro model study, Reisman et al. tested freshly collected heparinized blood, which was exposed to a 2.0 mm Rotablator burr rotating at one of three speeds: 180,000, 140,000, or 0 rpm. There were significantly more platelet aggregates of >20-microm diameter at higher RA speeds, compared with high-speed RA (180,000rpm), low-speed RA (140,000rpm) can reduce the platelet aggregation [8]. In our study, we did not find the influence of rotation speed on platelet aggregation. The reason may be that in our center, we use low-medium rotation speed (140,000-160,000rpm) in all the patients in clinical practice, so the relation of rotation speed and thrombotic load can’t be found in the Pearson Correlation Analysis.
The mechanism of RA induced platelet aggregation is not entirely clear. It may be caused by heat generated by RA and RA induced cell damage [18]. These data suggest a proper RA strategy (burr size, rotation speed and ablation numbers) should be used to avoid no-reflow during RA. Williams et al. showed that pretreating platelet-rich plasma with abciximab could decrease the RA induced platelet aggregation [9]. Future work is necessary to the potential of therapeutic options, including additional pharmacotherapy agents with RA to mitigate this effect.
This work was an observational study. We generated a hypothesis from the observations. There were several limitations of our research. First, the study sample number was small. Second, the presence of white thrombus does not directly prove platelet aggregation. Future histological studies and randomized controlled study using different RA strategies will be needed to prove this hypothesis.