Rapid estimation of myocardial infarct size.

See article by de Groot et al. [9] (pages 315 –324) in this limitation of enzymatic infarct size [7]. Earlier, we demonissue. strated that thrombolytic therapy had no influence on the relation between infarct size estimated with aHBDH and Although the use of biochemical markers of acute left ventricular performance, indicating that coronary remyocardial infarction started in 1954 [1], their value in perfusion has no influence on the recovery of myocardial estimating myocardial infarct size was demonstrated aHBDH in plasma [8]. roughly 20 years later. The groups of Hermens and Although the benefits of enzymatic infarct size estimacolleagues [2] and Sobel and colleagues [3] independently tion have been demonstrated in several randomized trials, reported methods to calculate infarct size on the basis of the method has the drawback that the data of infarct size of serial serum enzyme activities, such as creatine kinase the individual patient becomes available relatively late, i.e. (CK) and a-hydroxybutyrate dehydrogenase (aHBDH). too late to have influence on acute care. The article of de The methods employed were based on the same principle: Groot and colleagues describes modifications of the methan input of marker (e.g. an enzyme) from the infarcted od to estimate infarct size [9]. The first modification is the myocardium into the circulation is calculated by correction use of concentration-vs-time curves of relatively small of the enzyme’s activity-vs-time curve for the output proteins (15-20 kD) that are rapidly cleared from the (clearance) of that marker from the circulation. To that circulation, such as fatty acid-binding protein (FABP) and purpose Sobel and colleagues used the late linear decline myoglobin. These proteins are cleared by the kidneys, of CK’s logarithmic activity-vs-time curve [3]. Hermens whereas proteins like CK and aHBDH (or LDH) are and colleagues stressed the fact that the use of slowly cleared by the reticuloendothelial system, particularly the cleared enzymes, such as aHBDH, greatly diminished the liver. The second modification is the use of individual influence of error in estimated clearance rates [4]. Howclearance rates for FABP and myoglobin, instead of the ever, for slowly cleared enzymes it appeared that their use of mean clearance rates for large proteins like CK and longer presence in the circulation causes extravasation of aHBDH (or LDH). Individual clearance rates for FABP the enzyme (and back), so that incorporation of efflux to and myoglobin are calculated using glomerular filtration and from the extracellular space had to be taken into rates (estimated from plasma creatinine concentrations and account in the biophysical model. corrected for age and gender) and plasma volume (corThese classical methods to estimate enzymatic infarct rected for age and gender). size have proven their value when used to assess novel By employing these modifications, de Groot et al. have therapies of acute myocardial infarction, such as thromdemonstrated that infarct size as estimated from FABP and bolytic therapy. Early thrombolytic therapy in patients with myoglobin in the first 24 hours after onset of symptoms acute myocardial infarction was associated with limitation equalled the enzymatic infarct size as estimated by CK and of enzymatic infarct size by 30%, leading to less impairaHBDH in the first 72 hours after onset of symptoms. ment of regional and global left ventricular function and Therefore, the obvious benefit of using serum FABP or less mortality [5]. The slogan ‘‘time is myocardium’’ was myoglobin concentrations to estimate infarct size is the substantiated by showing that the earlier thrombolysis was marked shortening of the sampling procedure: 24 hours applied, the greater the limitation of infarct size [6]. with FABP and myoglobin as opposed to 72 hours with Likewise, recent improvements in therapy of acute CK and aHBDH. That implies that, if FABP and myoglomyocardial infarction by inducing rapid reperfusion using bin are assayed rapidly, a reliable estimate of infarct size primary PTCA were observed to be associated with further will become available while the patient is still in the acute