Author + information
- Received May 27, 2010
- Revision received June 22, 2010
- Accepted July 6, 2010
- Published online February 8, 2011.
- Chris C.S. Lim, MBBS⁎,†,‡,
- William J. van Gaal, MBBS, MSc, MD†,‡,
- Luca Testa, MD∥,
- Florim Cuculi, MD⁎,
- Jayanth R. Arnold, MD⁎,
- Theodoros Karamitsos, MD¶,
- Jane M. Francis, DCR(R), DNM¶,
- Steffen E. Petersen, MD⁎,
- Janet E. Digby, PhD⁎,
- Stephen Westaby, PhD⁎,
- Charalambos Antoniades, MD, PhD⁎,
- Rajesh K. Kharbanda, PhD⁎,
- Louise M. Burrell, MD‡,§,
- Stefan Neubauer, MD¶ and
- Adrian P. Banning, MD⁎,⁎ ()
- ↵⁎Reprint requests and correspondence:
Dr. Adrian P. Banning, Consultant Cardiologist, The John Radcliffe, Headley Way, Oxford OX3 9DU, United Kingdom
Objectives We aimed to assess the differential implications of creatine kinase-myocardial band (CK-MB) and troponin measurement with the universal definition of periprocedural injury after percutaneous coronary intervention.
Background Differentiation between definitions of periprocedural necrosis and periprocedural infarction has practical, sociological, and research implications. Troponin is the recommended biomarker, but there has been debate about the recommended diagnostic thresholds.
Methods Thirty-two patients undergoing multivessel percutaneous coronary intervention and late gadolinium enhancement (LGE) cardiac magnetic resonance (CMR) imaging in a prospective study had cardiac troponin I, CK-MB, and inflammatory markers (C-reactive protein, serum amyloid A, myeloperoxidase, tumor necrosis factor alpha) measured at baseline, 1 h, 6 h, 12 h, and 24 h after the procedure. Three “periprocedural injury” groups were defined with the universal definition: G1: no injury (biomarker <99th percentile); G2: periprocedural necrosis (1 to 3 × 99th percentile); G3: myocardial infarction (MI) type 4a (>3 × 99th percentile). Differences in inflammatory profiles were analyzed.
Results With CK-MB there were 17, 10, and 5 patients in groups 1, 2, and 3, respectively. Patients with CK-MB–defined MI type 4a closely approximated patients with new CMR-LGE injury. Groups defined with CK-MB showed progressively increasing percentage change in C-reactive protein and serum amyloid A, reflecting increasing inflammatory response (p < 0.05). Using cardiac troponin I resulted in 26 patients defined as MI type 4a, but only a small minority had evidence of abnormality on CMR-LGE, and only 3 patients were defined as necrosis. No differences in inflammatory response were evident when groups were defined with troponin.
Conclusions Measuring CK-MB is more clinically relevant for diagnosing MI type 4a, when applying the universal definition. Current troponin thresholds are oversensitive with the arbitrary limit of 3 × 99th percentile failing to discriminate between periprocedural necrosis and MI type 4a. (Myocardial Injury following Coronary Artery bypass Surgery versus Angioplasty: a randomised controlled trial using biochemical markers and cardiovascular magnetic resonance imaging; ISRCTN25699844)
This work was partially supported by an unrestricted research donation from Boston Scientific. Dr. van Gaal has received research grants from Cordis and Pfizer. Dr. Banning and some of the study costs were partially funded by the National Institute for Health Research Oxford Biomedical Research Centre Programme, United Kingdom. Dr. Antoniades is funded by the European Association of Percutaneous Coronary Interventions. Prof. Neubauer, Dr. Karamitsos, and Dr. Petersen are partially funded by the Medical Research Council (United Kingdom) and British Heart Foundation. Dr. Banning has received unrestricted grants from Cordis and Boston Scientific. All other authors have reported that they have no relationships to disclose.
- Received May 27, 2010.
- Revision received June 22, 2010.
- Accepted July 6, 2010.
- American College of Cardiology Foundation