CORRESPONDENCE: LETTER TO THE EDITOR
Reply
Gregg W. Stone, MD*,
Abhiram Prasad, MD and
Bernard J.. Gersh, MB, ChB, DPhil
* Center for Interventional Vascular Therapy, New York-Presbyterian Hospital, Columbia University Medical Center, The Cardiovascular Research Foundation, 111 East 59th Street, 11th Floor, New York, New York 10022 (Email: gstone{at}crf.org).
We thank Dr. Lim and colleagues for their interest in our paper (1). While agreeing with the principal finding of our study (1) that spontaneous myocardial infarction (SMI) portends a worse prognosis than periprocedural myocardial infarction (PMI), Lim and colleagues remain concerned that we have underestimated the importance of PMI. We agree with many of the suppositions in their communication (as clearly stated throughout our report [1]), namely that "even small periprocedural troponin rises reflect new areas of myocardial necrosis on MRI imaging," and "there is little doubt about the influence of large periprocedural enzyme rises ... ." We disagree, however, that "debate persists about the influence on prognosis of these small/moderate enzyme rises ... ." Whereas the literature is replete with prior studies examining the influence of PMI, the largest studies in the stent era have shown that only truly large PMI as evidenced by elevation of peak creatine kinase-myocardial band to >8x or >10x normal or the development of new Q-waves significantly influences subsequent survival (2,3). Other studies that have used a low threshold for PMI have found that such infarctions have no long-term prognostic significance (4). Smaller enzyme elevations are a marker for more diffuse atherosclerosis (5), but do not have per se a great enough influence on left ventricular function or arrhythmogenesis to directly impair survival. Other studies have suggested that biomarker elevations after percutaneous coronary intervention are of no clinical relevance unless associated with a failed procedure or angiographic complications (6). We also agree with Dr. Lim and colleagues that the prognostic implications of troponin elevations after percutaneous coronary intervention are uncertain, with questionable clinical relevance (7).
The data from the ACUITY (Acute Catheterization and Urgent Intervention Triage Strategy) trial are consistent with these previous studies; when considering all PMI (defined as creatine kinase-myocardial band >3x normal, the most widely used definition) in a time-updated, covariate-adjusted multivariable model, PMI was not an independent correlate of 1-year survival. However, large PMI (such as Q-wave myocardial infarction), was a predictor. Our study was not meant to minimize the role of large PMI, which clearly reduce early and late survival. Rather, most small PMI may be disregarded as clinically inconsequential, whereas SMI, even using a sensitive threshold for detection (any troponin elevation greater than the local laboratory normal), is a powerful independent predictor of subsequent mortality. These data emphasize the fact that SMI and PMI deserve different thresholds for diagnosis and should prompt suitably different therapeutic responses.
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1. Prasad A, Gersh BJ, Bertrand ME, et al. Prognostic significance of periprocedural versus spontaneously occurring myocardial infarction after percutaneous coronary intervention in patients with acute coronary syndromes: an analysis from the ACUITY trial J Am Coll Cardiol 2009;54:477-486.[Abstract/Free Full Text]2. Stone GW, Mehran R, Dangas G, et al. Differential impact on survival of electrocardiographic Q-wave versus enzymatic myocardial infarction after percutaneous intervention: a device-specific analysis of 7,147 patients Circulation 2001;104:642-647.[Abstract/Free Full Text] 3. Brener SJ, Ellis SG, Schneider J, Topol EJ. Frequency and long-term impact of myonecrosis after coronary stenting Eur Heart J 2002;23:869-876.[Abstract/Free Full Text] 4. Hirsh A, Windhausen F, Tijssen JGP, et al. Long-term outcome after an early invasive versus selective invasive treatment strategy in patients with non–ST-elevation acute coronary syndrome and elevated cardiac troponin T (the ICTUS trial) Lancet 2007;369:827-835.[CrossRef][Web of Science][Medline] 5. Mehran R, Dangas G, Mintz GS, et al. Atherosclerotic plaque burden and CK-MB enzyme elevation after coronary interventions: intravascular ultrasound study of 2,256 patients Circulation 2000;101:604-610.[Abstract/Free Full Text] 6. Jeremias A, Baim DS, Ho KKJ, et al. Differential mortality risk of postprocedural creatine kinase-MB elevation following successful versus unsuccessful stent procedures J Am Coll Cardiol 2004;44:1210-1214.[Abstract/Free Full Text] 7. Prasad A, Rihal CS, Singh M, et al. Significance of periprocedural myonecrosis for outcomes following percutaneous coronary intervention. An analysis of pre and post intervention troponin T levels in 5487 patients. Circ Cardiovasc Interv 2008;1:10-19.[Abstract/Free Full Text]
Related Article
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Periprocedural Myocardial Injury: Not a Benign Entity
- Chris C.S. Lim, William J. Van Gaal, and Adrian P. Banning
J. Am. Coll. Cardiol. 2010 55: 503.
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