Abstract
The early outcomes after coronary intervention have improved remarkably, particularly in the stent era. Patients previously at risk for acute closure and possibly urgent bypass surgery now go home the next day. The risk of bypass surgery is likewise markedly reduced. Nonetheless, subgroups of patients remain at increased risk for adverse outcomes, both short-term and over subsequent follow-up. Predictors of adverse outcome include slow or no reflow, side branch occlusion, diffuse multivessel disease, and preprocedure thrombotic or unstable lesions, as determined by angiography and clinical history. Furthermore, the risk of embolic complications seems to increase with the use of nonballoon devices.1 Importantly, the risk of short-term and late adverse outcomes seems partially related to the presence and extent of the release of creatine kinase (CK)-MB2 or other markers3 after the intervention. However, many of the patients at increased risk on the basis of CK-MB release were previously defined as successes because of the lack of a recognized, acute, in-laboratory event with no electrocardiographic changes. Although initially controversial, the importance of CK-MB release in terms of short-term and late outcome is now convincing.4 5 6 7 8 Overall, there seems to be an up to 30% risk of increased CK-MB release after a “successful” coronary intervention,2 particularly in complex interventional procedures, often involving nonballoon devices.9 Coincident with the data regarding CK-MB release, the use of IIb/IIIa platelet antagonists …
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