and 6 to 8 hours after CEA or CAS. Biomarkers were also assessed any time there was clinical evidence of cardiac ischemia. MI was defined as biomarker elevation plus ECG evidence of ischemia or chest pain. Cardiac biomarkeronly elevation was defined as elevation of cardiac biomarkers without chest pain or ECG abnormalities. Among the 2502 patients randomized in CREST, 14 MIs were associated with CAS and 28 MIs were associated with CEA (HR, 0.5; 95% CI, 0.26-0.94; P ϭ .032). The median biomarker ratio in patients with MIs was 40 times the upper limit of normal. Eight additional CAS patients and 12 additional CEA patients had biomarker-only events (HR, 0.66; 95% CI, 0.27-1.61; P ϭ 0.36). Median biomarker ratio compared with normal was 14 times the upper limit of normal for the patients with biomarker-only elevation. When comparing patients with MI vs those without biomarker elevation, mortality was higher over 4 years (HR, 3.4; 95% CI, 1.67-6.92). Mortality was also higher for those patients with biomarkers-only end points compared with those with no biomarker elevations (HR, 3.57; 95% CI, 1.46-8.68). Adjustments for baseline risk factors indicated that MI and biomarker-only elevations were still independent risk factors for increased mortality. Comment: Even a small MI after a noncardiac intervention is associated with increased late mortality. The data do not imply a cause-and-effect relationship. It is reasonable to postulate a periprocedural MI or biomarkeronly elevations are likely markers of more extensive atherosclerotic disease. One cannot determine whether an ischemic event itself, in relationship to performance of a procedure, increases the late risk of this elevated atherosclerotic burden. The data do suggest that one should think twice about performing any form of carotid artery revascularization in patients felt to be at increased cardiac risk because of likely decreased long-term survival in such patients.

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