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Circulation. 2005;112:906-922
doi: 10.1161/CIRCULATIONAHA.104.483297
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(Circulation. 2005;112:906-922.)
© 2005 American Heart Association, Inc.


Controversies in Cardiovascular Medicine

Does creatinine kinase-MB elevation after percutaneous coronary intervention predict outcomes in 2005?

Periprocedural Cardiac Enzyme Elevation Predicts Adverse Outcomes

Deepak L. Bhatt, MD; Eric J. Topol, MD

From the Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio (D.L.B., E.J.T.); and the Harvard Clinical Research Institute, Division of Cardiology, Beth Israel Deaconess Medical Center, Division of Cardiology, Brigham and Women’s Hospital, and Harvard Medical School, Boston, Mass (D.E.C., R.E.K.).

Correspondence to Deepak L. Bhatt, MD, Dept of Cardiovascular Medicine, The Cleveland Clinic Foundation, 9500 Euclid Ave, Desk F25, Cleveland, OH 44195 (e-mail bhattd@ccf.org); or Donald E. Cutlip, MD, Interventional Cardiology Section, Beth Israel Deaconess Medical Center, 185 Pilgrim Rd, Baker 4, Boston, MA 02215 (e-mail dcutlip@bidmc.harvard.edu).


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 


*    Introduction
 
Extensive clinical investigation throughout the 1990s validated periprocedural myonecrosis as a powerful predictor of adverse outcomes, so it is surprising that this remains a contentious point. Originally derided as "enzyme leaks" or "myocardial infarctlets," periprocedural myocardial infarction (MI) has now been definitively linked in large data sets to long-term adverse outcomes, most notably mortality. It is not, however, always directly contributory or causative. For example, a large creatine kinase (CK) elevation caused by closure of a major side branch resulting in chest pain and development of new Q waves is obviously undesirable and causally related to the interventional procedure. Alternatively, even small, asymptomatic CK elevations have been clearly associated with worse long-term outcome, and although this may in part be causally related to the procedure, it is more likely that the relationship is caused by the underlying predisposing factors that led to the periprocedural MI, such as arterial inflammation predilecting to the occurrence of embolization or to a large degree of atheroma burden leading to more myonecrosis. Under these circumstances, it is likely that the heightened inflammatory state and the diffuse disease that is present are the real causative factors for worse long-term outcomes. Recently, aspirin resistance has been demonstrated to predict periprocedural myonecrosis. Thus, both through direct causation and also as an epiphenomenon, embolization and attendant periprocedural myonecrosis are associated with short, intermediate, and long-term adverse outcomes (Table 1). This review details this evolution in thought.


View this table:



 
TABLE 1. Mechanisms Behind Periprocedural Myonecrosis


*    Periprocedural Myonecrosis and Outcome
 
Periprocedural myonecrosis is a frequent . . . [Full Text of this Article]




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