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 Larose, E. Search for Related Content PubMed PubMed Citation Articles by Larose, E. Related Collections Catheter-based coronary interventions: stents Coronary imaging: angiography/ultrasound/Doppler/CC CT and MRI Acute myocardial infarction

(Circulation. 2006;114:620-622.)
© 2006 American Heart Association, Inc.

Editorial

Below Radar

Contributions of Cardiac Magnetic Resonance to the Understanding of Myonecrosis After Percutaneous Coronary Intervention

Eric Larose, DVM, MD, FRCPC

From the Cardiac Magnetic Resonance Laboratory and Cardiac Catheterization Laboratory, Department of Cardiology, Quebec Heart Institute at Laval Hospital and Laval University Medical School, Quebec City, Canada.

Correspondence to Eric Larose, DVM, MD, Quebec Heart Institute at Laval Hospital, 2725 Chemin Sainte-Foy, Quebec, QC, Canada G1V4G5. E-mail emjlarose@videotron.ca

Key Words: Editorials • magnetic resonance imaging • myocardial infarction • ultrasonics

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

With >900 000 procedures performed annually in North America, percutaneous coronary intervention has dramatically altered the landscape of cardiology since its inception in 1977. Despite procedural success rates now exceeding 90%, biomarker rise indicating myonecrosis has been reported after up to 30% of otherwise successful procedures.¹ Most agree with the Joint European Society of Cardiology/American College of Cardiology Committee for the Redefinition of Myocardial Infarction recommendation that the same biochemical marker cutoffs be applied regardless of the clinical circumstances.² However, available data suggest that mild periprocedural marker rise may not confer substantial risk in an otherwise successful procedure. Several reports have identified non–Q-wave infarctions with creatine kinase (CK)–MB elevations 3 to 5 times the upper limit of normal as having clinical significance, whereas others suggest that increased risk may become apparent only for large non–Q-wave (CK-MB rise >5 to 8 times the upper limit of normal) and Q-wave myocardial infarctions,³ which are largely related to procedural complications.⁴ Troponin T and I elevation occurs more frequently than CK-MB increase after percutaneous coronary intervention and does not appear to have prognostic value unless a marked increase (>5 times the upper limit of normal) occurs.⁵ A notable exception comes from saphenous vein grafts in which even mild CK-MB rise after successful intervention predicts mortality.⁶

Article p 662

Mechanisms of cardiac enzyme release after percutaneous coronary intervention include procedure-related factors (side-branch occlusion, dissection, embolization, and no reflow), lesion-related factors (thrombus burden, plaque volume, plaque composition), and patient-related factors (prothrombotic state, systemic inflammatory state). In . . . [Full Text of this Article]