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Troponin-I concentration 72 h after myocardial infarction correlates with infarct size and presence of microvascular obstruction
Authors:Younger John F  Plein Sven  Barth Julian  Ridgway John P  Ball Stephen G  Greenwood John P
Institution:Cardiac Magnetic Resonance Unit, Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK.
Abstract:

Objectives

The aim of this study was to use late gadolinium hyper‐enhancement cardiac magnetic resonance (LGE‐CMR) imaging to determine if a 72‐h troponin‐I measurement would provide a more accurate estimation of infarct size and microvascular obstruction (MVO) than serial creatine kinase (CK) or early troponin‐I values.

Methods

LGE‐CMR was performed 3.7±1.4?days after medical treatment for acute ST elevation or non‐ST elevation myocardial infarction. Infarct size and MVO were measured and correlated with serum troponin‐I concentrations, which were sampled 12?h and 72?h after admission, in addition to serial CK levels.

Results

Ninety‐three patients, of whom 71 had received thrombolysis for ST elevation myocardial infarction, completed the CMR study. Peak CK, 12‐h troponin‐I, and 72‐h troponin‐I were related to infarct size by LGE‐CMR (r?=?0.75, p<0.0001; r?=?0.56, p?=?0.0003; r?=?0.62, p<0.0001 respectively). Serum biomarkers demonstrated higher values in the group with MVO compared with those without MVO (Peak CK 3085±1531 vs 1471±1135, p<0.001; 12‐h troponin‐I 58.3±46.9 vs 33.4±40.0, p?=?0.13; 72‐h troponin‐I 11.5±9.9 vs 5.5±4.6, p<0.005). The correlation between the extent of MVO and 12‐h troponin‐I was not significant (r?=?0.16), in contrast to the other serum biomarkers (peak CK r?=?0.44, p<0.0001; 72‐h troponin‐I r?=?0.46, p?=?0.0002).

Conclusion

A single measurement of 72‐h troponin‐I is similar to serial CK measurements in the estimation of both myocardial infarct size and extent of MVO, and is superior to 12‐h troponin‐I measurements.Prognosis after acute myocardial infarction is closely related to the extent of myocardial damage. The degree of damage can be estimated by serological testing and non‐invasive imaging methods (such as echocardiography). Measurement of cytosolic enzymes such as creatine kinase (CK) and the isoenzyme CK‐MB is still common clinical practice.1 However, the utility of these markers in determining infarct size is limited by the requirement for multiple sampling to determine the peak values or area under the curve, and their lack of specificity for myocardial damage.2Twelve‐hour serum troponin measurements are routinely used in the diagnosis of myocardial ischaemia or infarction. Although such measurements are highly specific for myocardial damage, they may provide unreliable estimates of infarct size.3 Troponin is a structural protein of the contractile apparatus which is released into the circulation in a biphasic fashion after acute myocardial infarction (AMI). An initial peak occurs in the first 24?h, due to release from the cytosolic pool. While this peak provides a reliable marker of infarct size in an animal model of non‐reperfused infarction,4 the complex release kinetics result in a high variability in early troponin concentrations following reperfusion therapy.2In AMI, the presence of microvascular obstruction (MVO) could cause impaired wash‐out of cardiac biomarkers in the early phase, so that the acute concentrations may not accurately reflect the true extent of myocardial damage. A second phase of troponin release occurs after 72?h, resulting from intramyocardial protein degradation,5 and this “plateau” value seems to be relatively unaffected by early reperfusion therapy.2 The troponin concentration at 72?h may therefore be less affected by release kinetics and coronary reperfusion, and hence provide a more reliable method to quantify myocardial damage and predict the presence of MVO.Cardiac magnetic resonance (CMR) can be used to image both acute and chronic myocardial infarction using the technique of late gadolinium hyper‐enhancement (LGE).6,7 Several animal studies have validated this technique,8,9 and in the canine model CMR quantification of infarct size has been shown to correlate closely (r?=?0.99) with histological measurements using triphenyltetrazolium chloride staining.10 Areas of severe MVO within the infarct core can also be demonstrated by LGE‐CMR in man.11 The high spatial resolution of the LGE‐CMR technique allows accurate measurement of in vivo infarct size.The aim of this study was to determine if a 72 h troponin (72‐h troponin‐I) measurement would provide a more accurate estimation of infarct size than serial CK or early troponin values.
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