Different time courses of cardiac contractile proteins after acute myocardial infarction

doi:10.1016/0009-8981(94)90253-4

Clinica Chimica Acta

Volume 231, Issue 1, November 1994, Pages 47-60

https://doi.org/10.1016/0009-8981(94)90253-4 Get rights and content

Abstract

For the first time we have compared time courses of cardiac myosin light chain-1 (MLC-1), β-type myosin heavy chain (MHC), troponin T (TnT), myoglobin, creatine kinase (CK) and CKMB in the same patients with acute myocardial infarction (AMI). Blood samples were serially collected in 23 patients with first-time AMI. All but 3 patients received intravenous thrombolytic treatment. TnT and MLC-1 time courses were biphasic in most patients and showed two distinct peaks in 13 and 8 patients, respectively. MHC time courses were usually monophasic. Only 1 patient showed a biphasic MHC time course with two distinct peak values. Although MHC and MLC were lower by about the fourth day after onset of AMI in early reperfused patients, reperfusion did not qualitatively alter MLC and MHC release (no significant influence on the first appearance in blood or on time to peak). MLC and MHC peaks correlated closely ( $r = 0.75$ , $P = 0.0001$ ), whereas TnT peaks were correlated less closely with MLC or MHC peaks ( $r = 0.58$ each, $P < 0.007$ ). Peak values of all cardiac contractile proteins correlated closely and significantly with CKMB peaks (0.75 ⩽ $r ⩽ 0.81$ , $P \ ̌ 0.0006$ ). Myoglobin was the first marker to increase in blood after AMI and showed the earliest peaks, whereas MHC increased latest showing the latest peaks. TnT increased significantly ( $P = 0.0001$ ) earlier than MLC and MHC. These results can be explained by the impact of the intracellular compartmentation of a cardiac protein on the rapidity with which it is released after AMI.

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Our present finding in a smaller cohort of patients supports this observation. Since myoglobin is traditionally believed to be the first cardiac biomarker released after myocardial infarction [28], we were not surprised to find that it had modest sensitivity and specificity in predicting AEs in our patient group when used in isolation although we stress that our patient cohort represents a group that would be loosely classified with suspected ACS in the emergency department rather than obvious MI. The small number of patients that had an MI (4.5%) supports this notion.
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Citation Excerpt :
Due to the lower tissue-specificity of myoglobin, the clinical cut-point is set relatively high; thus, elevated levels of myoglobin may indicate larger areas of infarction than detected by low-level elevations of troponins. Myoglobin differs from cTnI in that it is smaller and remains free in the cytoplasm of the cell, unbound to contractile proteins (1). As a result, the kinetics for myoglobin release differ from that for other cardiac proteins.
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1998, Emergency Medicine Clinics of North America
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^☆: We dedicate this paper to Prof. Dr. Dr. h.c. Helmut Wachter of Innsbruck, Austria, on the occasion of his 65th birthday

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Different time courses of cardiac contractile proteins after acute myocardial infarction☆

Abstract

Am Heart J

Mol Immunol

Am J Cardiol

Am J Cardiol

Am J Cardiol

Am Heart J

Biochim Biophys Acta

Biochemical markers of myocardial injury: is MB creatine kinase the choice for the 1990s?

Circulation

Estimation of infarct size in man and its relation to prognosis

Circulation

Enzymatic estimation of infarct size during reperfusion

Circulation

Development of monoclonal antibodies for an assay of cardiac troponin I and preliminary results in suspected cases of myocardial infarction

Clin Chem

Cardiac-specific immunoenzymometric assay of troponin I in the early phase of acute myocardial infarction

Clin Chem

Development and in vitro characterization of a new immunoassay of cardiac troponin T

Clin Chem

Radioimmunoassay of human cardiac tropomyosin in acute myocardial infarction

Clin Sci

A radioimmunoassay for the measurement of human cardiac myosin light chains

Am J Clin Pathol

The quantitation of human ventricular myosin light chain 1 in serum after myocardial necrosis and infarction

Clin Chim Acta