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J Am Coll Cardiol, 2006; 48:2192-2194, doi:10.1016/j.jacc.2006.06.002
(Published online 8 November 2006). © 2006 by the American College of Cardiology Foundation |
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* Abteilung Innere Medizin III, Medizinische Klinik, Universitätsklinikum Heidelberg, Heidelberg, Germany
Herzzentrum Ludwigshafen, Institut für Biometrie, Ludwigshafen, Germany.
Manuscript received January 3, 2006; revised manuscript received July 19, 2006, accepted July 23, 2006.
* Reprint requests and correspondence: Dr. Evangelos Giannitsis, Abteilung Innere Medizin III, Medizinische Klinik, Universitätsklinikum Heidelberg, 69120 Heidelberg, Germany. (Email: evangelos_giannitsis{at}med.uni-heidelberg.de).
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Abstract |
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BACKGROUND: We examined the ability of a single value of cardiac troponin T (cTnT) 96 h after onset of ST-/non–ST-segment elevation myocardial infarction (STEMI/NSTEMI) to estimate absolute infarct mass.
METHODS: Functional and CE-MRI were conducted on a 1.5-T whole-body system 4 days after STEMI/NSTEMI using gadolinium (0.2 mmol/kg/bw). Infarct sizes were measured employing a specified software (Philips Medical Systems, Best, the Netherlands) and correlated with TnT measurements 96 h after onset of STEMI/NSTEMI.
RESULTS: We enrolled 23 STEMI and 21 NSTEMI patients. Median time delay from onset of symptoms to balloon angioplasty was 6.25 and 9.9 h for STEMI/NSTEMI patients, respectively. Contrast-enhanced magnetic resonance imaging (median 4 days) revealed an absolute mean infarct size of 16.2 g (7.7 to 30.1 g) with a mean ejection fraction of 58% (53% to 63%) and mean stroke volume of 84 ml (75 to 107 ml). Absolute infarct sizes and median cTnT values were larger in STEMI than in NSTEMI (29.3 g [interquartile range (IQR) 16.0 to 53.0] and 1.88 µg/l [IQR 0.7 to 2.57] vs. 8.8 g [IQR 3.3 to 16.4] and 0.83 µg/l [IQR 0.4 to 1.3], both p < 0.02). Linear regression analysis was excellent for STEMI (r = 0.910) and moderate albeit still significant for NSTEMI (r = 0.575).
CONCLUSIONS: A single 96-h cTnT value provides an accurate estimate of absolute infarct mass in myocardial infarction. The ability to quantify and the potential to distinguish effects of novel drug regimens on infarct size make cTnT attractive for routine practice and as a clinical end point.
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We hypothesized that a single cTnT measurement at 96 h could represent an ideal estimate for infarct size. To test this hypothesis, we quantified infarct size and left ventricular function by contrast-enhanced cardiac magnetic resonance imaging (CE-MRI).
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Methods |
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Measurement of cTnT. Blood samples were taken on admission and 96 h after onset of ischemic symptoms. Cardiac troponin T was measured quantitatively using electrochemiluminescence technology (3rd generation cTnT, Elecsys 2010, Roche, Mannheim, Germany). The lower detection limit of this assay is 0.01 µg/l with a recommended diagnostic threshold of 0.03 µg/l.
Cardiac MRI. Cardiac MRI was performed in a 1.5-T whole-body MRI scanner (Philips Medical Systems, Best, the Netherlands). Assessment of resting left ventricular function was determined by cine images using a steady-state free precession sequence in continuous short-axis planes covering the whole left ventricle from base to apex as well as 2- and 4-chamber views. Ten minutes after gadolinium contrast injection (Gd = 0.2 mmol/kg body weight of gadopentetate dimeglumine [Schering, Berlin, Germany]), 3 volume stacks of delayed contrast-enhanced images covering the whole left ventricle were planned on previous short-, 2-, and 4-chamber axis.
End-diastolic and -systolic volumes with resulting ejection fraction were generated manually using short-axis volumetry. Infarct size was visually defined as area of delayed hyperenhancement on short-axis views and determined manually by delineation of hyperenhanced versus normally saturated dark myocardium.
Magnetic resonance imaging analysis included quantification of absolute infarct size (grams) and left ventricular function in all patients.
Statistics. Plasma concentrations of cTnT are described as median values with the corresponding interquartile range (IQR). The baseline characteristics of patients with STEMI and non–ST-segment elevation myocardial infarction (NSTEMI) were compared using the Student t test or chi-square test. For all analyses, a value of p < 0.05 was regarded as statistically significant.
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Results |
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Magnetic resonance imaging was performed after a median of 4 days. Mean infarct size was 16.2 g (7.7 to 30.1 g). The left ventricular performance revealed a mean ejection fraction of 58% (53% to 63%) with a mean stroke volume of 84 ml (75 to 107 ml).
Absolute infarct sizes were larger in STEMI than in NSTEMI (29.3 g [IQR 16.0 to 53.0] vs. 8.8 g [IQR 3.3 to 16.4], p < 0.0002). Correspondingly, median cTnT values were higher in STEMI than in NSTEMI (1.88 µg/l [IQR 0.7 to 2.57] vs. 0.83 µg/l [IQR 0.4 to 1.3], p = 0.015).
Linear regression analysis showed a strong significant correlation between cTnT and infarct size (Figs. 1A and 1B). Correlation between cTnT and infarct size was excellent for STEMI (Fig. 1A) and moderate, albeit still significant, for NSTEMI (Fig. 1B).
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Discussion |
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Infarct size is a valuable surrogate outcome measure for clinical trials in patients with acute coronary syndromes and can either be measured non-invasively by employing electrocardiographic criteria or by using more advanced, but less available, radionuclide techniques (1). As an alternative and due to limited availability and high costs of imaging techniques, serologic tests are frequently utilized measuring cardiac non-structural cytoplasmatic enzymes such as CK or CK-MB, LDH, or HBDH. Unfortunately, there are 2 major shortcomings with these markers. First, the lack of cardiospecificity sometimes allows more sources to be responsible for the rise of these markers (2). Second, measurement of infarct size by cardiac enzymes is hampered by the need to collect blood repeatedly so as not to miss the peak of marker release. In contrast, cTnT is an exclusively cardiac and predominantly structural protein of the myofilament.
Cardiac MRI has become the gold standard for quantification of ventricular function and determination of infarct size (1). Constrast-enhanced MRI has been shown to allow quantification of spontaneous or post-procedural MI of <1 g of infarcted myocardium per image (5) and has a better sensitivity for detection of small myocardial infarcts than single photon emission tomography (6). These and other advantages including the ability to detect infarct-related complications such as microvascular obstruction, papillary muscle necrosis, or extension of infarct to the right ventricle outweigh the potential shortcoming of overestimating infarct size by approximately 10% during the acute phase (7).
Generally, infarct sizes for NSTEMI patients were significantly smaller and could, in some cases, be below the MRI detection threshold for myocardial infarcts. Moreover, due to relatively low image resolution of CE-MRI images, small infarct areas could also be missed due to partial volume effect. Furthermore, in our approach, we performed scar imaging 10 min after administration of gadolinium. This could be either too early for clear visualization of small infarcts, or small infarcts potentially have different contrast agent wash-in and wash-out kinetics when compared with larger infarcts with edema and more pronounced microvascular obstruction.
However, it is tempting to speculate that patients with small infarcts have different cTnT release time curves than patients with large myocardial infarction. Therefore, it cannot be excluded that, in patients with NSTEMI, an earlier cTnT sampling time point would have resulted in a better correlation with infarct size or left ventricular function.
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