Comparison of enzymatic and anatomic estimates of myocardial infarct size in man.

Hackel, D B; Reimer, Keith A.; Ideker, Raymond E.; Mikat, Eileen M.; Hartwell, Tyler; Parker, CharlesW.; Braunwald, Eugene; Buja, Maximilian; Gold, Herman K.; Jaffe, Allan S.

doi:10.1161/01.cir.70.5.824

Cited by 143 publications

(38 citation statements)

References 46 publications

(12 reference statements)

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“…Several clinical studies have produced convincing correlations between enzymatic and histologic estimates of infarct size. n - 27 In our study, the correlation between the cumulative cytoplasmic HBDH and cumulative CK release is higher (r=0'96, n=21, P<O·OOOI) compared to the correlation between the cumulative HBDH and cumulative troponin-T release (r=0'84, n=21, P<O·OOOI). Recently, Omura 28 showed a good correlation between the late troponin-T peak and left ventricular ejection fraction (r=0'68), injury extent score (r=0'71) and severity score (r = 0'66).…”

Section: Discussioncontrasting

confidence: 52%

Cardiac Troponin T Release into Plasma after Acute Myocardial Infarction: Only Fractional Recovery Compared with Enzymes

1996

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SUMMARY. After acute myocardial infarction (AMI) cardiac enzymes and proteins are released into plasma and are used as biochemical markers of cardiac muscle injury. We studied the completeness of the release of troponin T, a cardiac protein that is largely bound to myofibrillar structures and compared it with the release of cytoplasmic cardiac enzymes in 22 patients with AMI, who were treated with thrombolytic therapy.Creatine kinase (CK; EC 2.7.3.2), hydroxybutyrate dehydrogenase (HBDH), lactate dehydrogenase (LDH; EC 1.1.1.27) and troponin T were assayed serially in plasma samples obtained frequently and for at least 168 h after the start of thrombolytic therapy. Cumulative release of enzymes and troponin T in plasma were calculated by using a two-compartment model for circulating proteins.In order to express the cumulative plasma releases in gram equivalents (g-eq) healthy myocardium per litre plasma (infarct size), we determined HBDH, LDH and total troponin T contents per gram net weight of tissue in 17 human hearts obtained post-mortem from patients who died from non-cardiac causes. Mean (SD) tissue contents per gram wet weight of, respectively, l56±25 Ujg, 385±59 Ujg and 234 ± 65 Ji.gjg were found.For the cardiac enzymes CK, HBDH and LDH the mean (SEM, n = 22) total release over 72 h, was, respectively, 5·9 ± 1'5, 5·9 ± 1·6 and 6·1 ± 1·7 g-eqjL. There was no further increase after 72 h and the differences between enzymes were not significant. The mean (SEM) cumulative troponin T release, expressed in gram equivalents of myocardium per litre of plasma was only O· 30 ± 0·09 g-eqjL after 72 h and O' 51 ± 0·61 g-eq/L after 168 h. After 72 h total recovery of troponin T in g-eqjL was only 5% and after 168 h only 8·5% of the total recovery of cytoplasmic cardiac enzymes after 72 h.Cumulative troponin T release after 72 h and after 168 h correlates well with infarct size, estimated from cumulative cytoplasmic enzyme release. However, quantification of infarct size should preferably be performed from plasma release curves of cytoplasmic cardiac enzymes or proteins in order to prevent underestimation of infarct size, caused by incomplete release of the non-cytoplasmic proteins. Additional key phrases: compartmental model; reperfusion; intracellular compartmentation; quantification of tissue damage

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Section: Discussioncontrasting

confidence: 52%

Cardiac Troponin T Release into Plasma after Acute Myocardial Infarction: Only Fractional Recovery Compared with Enzymes

1996

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“…The maximum concentration of CK-MB is related to the grade of myocardial damage, [23][24][25][26] and the present study showed a close relationship between the maximum concentrations of M and CK-MB. The study data suggested that the maximum concentration of M, which was obtained at 6-12 h after onset, could be related to the grade of myocardial damage.…”

Section: Relationship Between Maximum Concentrations Of Serum Myoglobsupporting

confidence: 77%

Usefulness of Rapid Quantitative Measurement of Myoglobin and Troponin T in Early Diagnosis of Acute Myocardial Infarction

Yamamoto

Komiyama

Koizumi

et al. 2004

Circ J

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“…The MB heterodimer has been found to comprise between 1% and 22% of the total creatine kinase activity present in human myocardium (3), but is absent from extracts of normal skeletal muscle or brain (4). Accordingly, analysis of plasma MB creatine kinase activity has been used extensively for detection of acute myocardial infarction and quantification of the extent of myocardial injury in patients (5).…”

Section: Introductionmentioning

confidence: 99%

“…Isoelectric points of MB isoforms were determined with the PhastSystem and PhastGel (both Pharmacia Fine Chemicals) containing ampholytes in the pH range of4.0-6.5. Purified isoforms and standards (0.5 Mg) with known pI were prefocused at 2,000 V, 2.0 mA constant power for 5 min, and separated at 2,000 V, 5.0 mA for 20 min at 150C.…”

Section: Introductionmentioning

confidence: 99%

Characterization of MB creatine kinase isoform conversion in vitro and in vivo in dogs.

Billadello¹,

Fontanet²,

Strauss³

et al. 1989

J. Clin. Invest.

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Time-dependent removal of the COOH-terminal lysine residue from each subunit of tissue MM creatine kinase by plasma carboxypeptidase N produces two additional isoforms that are readily separated, thereby permitting sensitive, early detection of acute myocardial infarction. Only two isoforms of MB creatine kinase have been detected in plasma leading to speculation that the COOH-terminal lysine on the B subunit is resistant to hydrolysis. To define the biochemical changes resulting in MB creatine kinase isoform conversion, we incubated highly purified MB creatine kinase from canine myocardium with plasma carboxypeptidase N. Quantitative anion-exchange chromatography of incubation mixtures and serial plasma samples from dogs subjected to coronary occlusion revealed a second, more acidic form evolved with time that was separated from the tissue isoform. Cyanogen bromide digestion of the two isoforms followed by amino acid sequencing of COOH-terminal peptides showed that MB creatine kinase undergoes removal of the COOH-terminal lysine residue from both M and B subunits. An intermediate form lacking lysine on the M subunit was delineated during incubations by the combined use of anion-exchange chromatography and conventional electrophoretic techniques. Thus, sequential cleavage of lysine from subunits of MB creatine kinase produces an intermediate isoform that has not been detected previously because of difficulties separating it from the tissue and fully converted isoforms.

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Comparison of enzymatic and anatomic estimates of myocardial infarct size in man.

Abstract: Enzymatic estimates of myocardial infarct size based on plasma levels of MB creatine kinase (MB-CK) were

Cited by 143 publications

References 46 publications

Cardiac Troponin T Release into Plasma after Acute Myocardial Infarction: Only Fractional Recovery Compared with Enzymes

Cardiac Troponin T Release into Plasma after Acute Myocardial Infarction: Only Fractional Recovery Compared with Enzymes

Usefulness of Rapid Quantitative Measurement of Myoglobin and Troponin T in Early Diagnosis of Acute Myocardial Infarction

Characterization of MB creatine kinase isoform conversion in vitro and in vivo in dogs.

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