Editorial note Extension of myocardial infarction and serum myoglobin

Kagen, Lawrence J.

doi:10.1016/0167-5273(84)90193-1

Cited by 3 publications

(1 citation statement)

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“…In the routine clinical chemistry laboratory, myoglobin concentrations Myoglobin is a low-molecular mass, oxygen-binding can be determined by ra dioimmunoassay (7,8) or imhaemoprotein (M r 17700) of the skeletal and cardiac munonephelometry (9) . ^ methods m sens itive but muscle (1). Elevation of the myoglobin concentration time consuming and not suitable for em er g ency testing.…”

Section: Introductionmentioning

confidence: 99%

A Rapid Assay for the Quantification of Myoglobin: Evaluation and Diagnostic Relevance in the Diagnosis of Acute Myocardial Infarction

Baum¹,

Booksteegers²,

Steinbeck³

et al. 1994

CCLM

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Summary:We evaluated a new, fast, quantitative, turbidimetric assay (TurbiTimeSystem, Behringwerke AG, Marburg, Germany) for the determination of myoglobin concentration in serum. Within-run imprecision (n = 10) was < 3.7% in controls ranging from 81.1 to 621.4 g/l and between-day imprecision (n = 50) was < 6% in controls ranging from 69.5 to 623.4 g/l. The assay is linear over the measuring ränge and interfering substances such äs bilirübin, haemoglobin or haptoglobin do not interfere but triacylglycerol-rich samples are only measureable after brief ultracentrifugation. EDTA-or citrate-treated samples display depressed myoglobin concentration when compared with serum samples. The upper reference limit for apparently healthy individuals (n = 100, 50 female and 50 male) is 61.5 g/l. Comparison with nephelometry revealed a good correlation (r = 0.982) between the two methods with the regression equation: turbidimetric assay = 5.53 4-1.02x nephelometric assay.Serial determination of myoglobin concentration and creatine kinase in 18 patients with proven acute myocardial infarction showed in general an equal diagnostic significance for both analytes. In the first 4 hours after onset of ehest pain, the determination of myoglobin can have an advantage, since it is released into the blood stream at an earlier stage, but thereafter myoglobin can lead to false negative diagnosis. Therefore, determination of creatine kinase and its isoenzyme MB is still the diagnostic strategy of choice in the diagnosis of acute myocardial infarction. Introductionnosis of acute myocardial infarction (6). In the routine clinical chemistry laboratory, myoglobin concentrations Myoglobin is a low-molecular mass, oxygen-binding can be determined by ra dioimmunoassay (7, 8) or imhaemoprotein (M r 17700) of the skeletal and cardiac munonephelometry (9) . ^ methods m sens itive but muscle (1). Elevation of the myoglobin concentration time consuming and not suitable for em er g ency testing. above the upper reference limit is normally caused by A latox agglutination assay (5> 10) gives only semithe injury of cardiac muscle, e. g. acute myocardial m-quantitative results and is less sensitive. The aim of our farction, provided skeletal muscle has been excluded äs study was to evaluate a new fast ^ quantitative turbidia sotirce. In addition, physical exercise (2) or decreased metric assay for det ermination of myoglobin and to renal function with subsequent decreased myoglobin test the diagil ostic relevance in the early phase of acute clearance can result in elevated myoglobin levels in myocard jai infarction. blood (3). After aoute myocardial infarction, myoglobin is rapidly released from necrotic myocardium in advance of cytoplasmic enzymes such äs creatine kinase ( (EC 2.7.3.2)

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