This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Bhatt, D. L. Search for Related Content PubMed PubMed Citation Articles by Bhatt, D. L. Related Collections Catheter-based coronary interventions: stents Coronary imaging: angiography/ultrasound/Doppler/CC Chronic ischemic heart disease

(Circulation. 2006;114:1898-1900.)
© 2006 American Heart Association, Inc.

Editorial

Shifting the Diagnosis of Periprocedural Myocardial Infarction Upstream

Deepak L. Bhatt, MD

From the Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio.

Correspondence to Dr Deepak L. Bhatt, Cleveland Clinic, Department of Cardiovascular Medicine, Cleveland Clinic Foundation, 9500 Euclid Ave, Desk F25, Cleveland, OH 44195. E-mail bhattd@ccf.org

Key Words: Editorials • angioplasty • catheterization • electrocardiography • ischemia • myocardial infarction • stents

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

Prevention of periprocedural myocardial infarction (MI) has been the target of substantial research effort.^1,2 Even routine, elective, uncomplicated percutaneous coronary intervention (PCI) has been demonstrated to produce embolization.³ The greater the patient acuity is, such as with ST-segment elevation myocardial infarction, the larger is the degree of embolization and the more apparent the clinical consequences. Although the exact threshold of PCI-related myonecrosis that is clinically relevant remains a matter of debate, few would challenge the central concept that myonecrosis is best avoided if possible.^1,2

Article p 1948

Detection of periprocedural MI rests largely on the use of creatine kinase myocardial isoform (CK-MB) measurement. The problem with this approach is that by the time the myonecrosis is detected, the proverbial horse is out of the barn. Troponin measurements are more sensitive though less validated in this setting and still give information regarding myonecrosis only after the fact, though, at least in some study populations, have been shown to provide incremental information.⁴ Newer imaging modalities such as cardiac magnetic resonance imaging are able to detect microinfarctions,⁵ though, once more, the diagnosis is being made after the damage is done.

Biomarkers, particularly those associated with inflammation, also seem to predict subsequent myonecrosis.⁶ Diminished response to antiplatelet therapy has also been linked to increased degrees of post-PCI myonecrosis, including in elective PCI.^7–9 Although heightened inflammatory status or relative antiplatelet resistance may predispose to plaque embolization and subsequent platelet aggregatory response during PCI, other procedural factors that predispose to embolization such as plaque burden caused . . . [Full Text of this Article]