Mechanisms of periprocedural myocardial necrosis following Rotablator® and saphenous vein graft PCI

Objective: Rotational atherectomy device (Rotablator®) or saphenous vein graft (SVG) percutaneous coronary intervention (PCI) commonly results in elevated creatinine kinase-MB (CK-MB) levels and is associated with worse outcome. We have assessed the prevalence and mechanistic causes of procedural myocardial necrosis (PMN) following Rotablator® or SVG PCI. Methods: We assessed 46 cases of Rotablator® and 230 cases involving SVG PCI among the 7,700 total PCIs observed during a 12-year period (1996-2007). Following analysis of angiogram results, procedural data, and the delay between PCI and necrosis, we mechanistically classified PMN as follows: cryptogenic, immediate failure, side branch occlusion, stent thrombosis, prolonged ischemia, delayed failure, or none to communicate. Results: The incidence of elevated CK-MB greater than the upper limit of normal (ULN) after Rotablator® and SVG PCI was 19% and 7%, respectively. Important periprocedural myocardial infarction (important PMI; CK-MB >5 times ULN) was significant for both Rotablator® (56%) and SVG (70%) PCI. Also, we found that the mechanisms contributing to PMN in Rotablator® (n=9) were most often cryptogenic (56%), followed by immediate failure (22%) and prolonged ischemia (22%). For SVG PCI (n=17), cryptogenic (47%) was also the most common mechanism, followed by prolonged ischemia (29%), immediate failure (12%), stent thrombosis (6%), and none to communicate (6%). Conclusions: Rotablator® and SVG PCI led to increased risk for PMN and important PMI in comparison to the standard population. Also, we observed that the main mechanism of PMN for both Rotablator® and SVG PCI was cryptogenic, with micro-embolization likely acting as the primary etiology