European Heart Journal Advance Access originally published online on August 8, 2005
European Heart Journal 2005 26(20):2206; doi:10.1093/eurheartj/ehi424
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Impact of the elevation of biochemical markers of myocardial damage on long-term mortality after percutaneous coronary intervention: results of the CK-MB and PCI study
Universita' Cattolica del Sacro Cuore
Roma
Italy
John Radcliffe Hospital
Headley Way
OX3 3DU
UK
Tel: +44 1865 228934
E-mail address: i.porto{at}doctors.org.uk
John Radcliffe Hospital
Oxford
UK
John Radcliffe Hospital
Oxford
UK
We read with great interest the paper ‘Impact of the elevation of biochemical markers of myocardial damage on long-term mortality after percutaneous coronary intervention: results of the CK-MB and PCI study’ by Cavallini et al.1
This large cohort follow-up study is of particular relevance for the interventional cardiologist, as it gives further data about the impact of procedure-induced myonecrosis on long-term outcome following PCI.
However, we would like to comment on the dissociation between creatine-kinase MB and troponin I elevation, with the former exhibiting an almost linear correlation with mortality (in Figure 1 of their paper), which is not apparent for the latter (Figure 2 of their paper). According to the authors, troponin I is an extremely sensitive marker that detects even reversible myocardial injury caused by procedure-induced ischaemia or very minor myocardial necrosis, which does not influence the long-term prognosis.
Although we agree with authors about the sensitivity of the troponin assay, we believe that a methodological problem might have played a role in determining their result. In a recent paper, we were able to demonstrate a strong linear correlation between the mass of new myocellular necrosis (as measured by delayed-enhancement MRI) and post-procedural (24 h) troponin I absolute elevation (r=0.84, P<0.001).2
In their study, Cavallini et al. chose to grade troponin I elevation by the peak ratio, calculated by dividing the maximum post-procedural level of the marker by its upper reference limit or by its baseline value if the baseline value was above the upper reference limit. For troponin I, the upper reference limit for cTnI was 0.15 µg/L. Thus, in a stable patient with no pre-procedural cTnI elevation, a peak ratio of 10 (at the extreme right end in Figure 2) would mean an absolute cTnI elevation of only 1.5 µg/L, whereas in a patient with a baseline cTnI of 1, the same peak ratio would mean an absolute cTnI elevation of 10 µg/L. If these two values were interpolated in the regression curve obtained from our data, they would translate to about 2 vs. 13 g of new myocardial necrosis.
Moreover, in our paper, few (four out of 50) patients, all with normal pre-procedural cTnI, showed an absolute troponin I elevation of between 0.2 and 1 µg/L (the latter being the upper limit of normal in our laboratory), and no new areas of hyperenhancement were seen by MRI, probably because troponin I is even more sensitive than MRI in detecting small, patchy necrosis. In these patients, it is very unlikely that trivial myocardial damage will alter prognosis.
This lack of relationship would be an important finding, challenging the current European Society of Cardiology/American College of Cardiology guidelines that recognize elevation of cardiac troponins within 24 h of a PCI procedure in the definition of myocardial infarction.3
References
- Cavallini C, Savonitto S, Violini R, Arraiz G, Plebani M, Olivari Z, Rubartelli P, Battaglia S, Niccoli L, Steffenino G, Ardissino D. Impact of the elevation of biochemical markers of myocardial damage on long-term mortality after percutaneous coronary intervention: results of the CK-MB and PCI study. Eur Heart J. Published online ahead of print March 1, 2005.
- Selvanayagam JB, Porto I, Channon K, Petersen SE, Francis JM, Neubauer S, Banning AP. Troponin elevation after percutaneous coronary intervention directly represents the extent of irreversible myocardial injury: insights from cardiovascular magnetic resonance imaging. Circulation 2005;111:1027–1032.
[Abstract/Free Full Text] - Antman E, Bassand J-P, Klein W, Ohman M, Lopez Sendon JL, Ryden L, Simoons M, Tendera M. Myocardial infarction redefined: a consensus document of the Joint European Society of Cardiology/American College of Cardiology committee for the redefinition of myocardial infarction: the Joint European Society of Cardiology/American College of Cardiology Committee. J Am Coll Cardiol 2000;36:959–969.
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