Early appearance of MB-creatine kinase activity in nontransmural myocardial infarction detected by a sensitive assay for the isoenzyme

Shell, William E.; DeWood, Marcus A.; Kligerman, Miriam; Ganz, William; Swan, H.J.C.

doi:10.1016/0002-9343(81)90126-1

Cited by 33 publications

(3 citation statements)

References 21 publications

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“…Interestingly, how ever, the time from symptom onset to peak CK measurements was significantly shorter in the reperfusion group (16.8 ± 7.5 vs. 23.8 ± 7.9 h; p < 0.001), confirming the findings of Shell et al [70] who described accelerated washout of CK. Furthermore, this supports the hypothesis described by the same workers that perfusion to the /one of infarction is associated with early appearance of CK [72].…”

Section: Randomized Studiessupporting

confidence: 91%

Value and Limitations of Thrombolytic Therapy in Early Acute Transmural Myocardial Infarction

DeWood

Amsterdam

1985

Cardiology

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Since coronary thrombosis is the final common pathway by which acute transmural myocardial infarction occurs, intracoronary thrombolytic reperfusion has taken on new significance. The goals of early restoration of coronary blood flow are to reduce mortality as well as to demonstrate improvement of markers of success or failure associated with thrombolytic therapy relative to nonreperfused patients. This paper examines clinical studies from multiple centers and the results derived from these studies. Mortality, left ventricular function, electrocardiographic indices of necrosis, laboratory studies, enzymatic indices of myocardial infarction size, thallium perfusion, and scintigraphic studies from controlled randomized and nonrandomized studies are presented. Overall, it appears that thrombolytic reperfusion is beneficial if applied early, although the markers of success or failure do not necessarily correlate with short-term mortality.

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Section: Randomized Studiessupporting

confidence: 91%

Value and Limitations of Thrombolytic Therapy in Early Acute Transmural Myocardial Infarction

DeWood

Amsterdam

1985

Cardiology

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“…For example, CK and LDH activities increase < 60-fold and < 10-fold, respectively. [19][20][21] Another disadvantage of cytosolic enzymes is their short persistence in the serum after AMI. CK and LDH serum concentrations decrease to normal concentrations within 3-6 days and 6-15 days, respectively.…”

Section: Discussionmentioning

confidence: 99%

Troponin T concentrations 72 hours after myocardial infarction as a serological estimate of infarct size

Licka

Zimmermann²,

Zehelein³

et al. 2002

Heart

129

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Background: After acute myocardial infarction, the structural protein T is released considerably longer than cytosolic creatine kinase (CK), CK MB isoenzyme (CK-MB), or lactate dehydrogenase (LDH) and late troponin T release (> 48 hours after onset of chest pain) appears to be less affected by early coronary reperfusion. Objective: To investigate the precision of a single measurement of circulating troponin T concentrations 72 hours after onset of chest pain compared with standard scintigraphic and enzymatic estimates of myocardial infarct size. Methods: Quantitative single photon emission computed tomography thallium-201 scintigraphy at rest was performed in 37 patients 2-3 weeks after myocardial infarction (group 1: 14 patients without early coronary reperfusion; group 2: 23 patients with early reperfusion achieved by thrombolytic therapy, by percutaneous transluminal coronary angioplasty, or by both). Results: In both groups, the number of myocardial segments with abnormal thallium-201 uptake indicating the individual extent of irreversible myocardial damage correlated significantly with the troponin T concentrations 72 hours after infarction as well as with peak concentrations of CK, CK-MB, and LDH. Conclusion: The data show that a single measurement of circulating troponin T 72 hours after onset of chest pain-independent of reperfusion-is superior for the estimation of myocardial infarct size to measurement of peak CK, CK-MB, or LDH, which require serial determinations and depend on coronary reperfusion.

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“…Therefore, CKMB determinations are generally regarded asthe reference standard for diagnostic tests forAMl. Yet variable normal serum levels of CKMB (20)(21)(22) and its brief elevation in serum during the course of myocardial infarction (23)(24)(25), limit the diagnostic value of CKMB determinations. In practice, physicians are sometimes left with patients in whom definitive diagnosis of myocardial infarction cannot be made by CKMB measurements and an alternative test of even greater sensitivity and specificity is needed.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of clinical utility of serum enzymes and troponin—T in the early stages of acute myocardial infarction

Shah¹,

Haridas

2003

Indian J Clin Biochem

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Laboratory infarction diagnostics are based on the detection of elevated serum activities of total Creatine Kinase (CK), Creatine Kinase isoensyme MB,(CKMB), Lactate dehydrogenase (LDH), isoenzyme forms of LDH and transaminases. Determination of these cardiac marker enzymes permits a highly sensitive diagnosis of transmural myocardial infarction. In such patients the diagnosis of acute myocardial infarction can be confirmed by the clinical symptoms, and changes in the ECG in addition to the enzyme assays. The 50 AMI patients selected in the present study were those admitted to the ICCU of Shri Krishna Hospital, Karamsad. The blood samples were taken at the time of admission (ie. within four hours of the start of chest pain). The samples were analyzed for CK, CKMB, SGOT,(Serum glutamate oxaloactate transaminase) (~HBDH o~ -hydroxybutyrate dehydrogenase and troponin T. The serum CKMB activity in AMI showed an increase only 5-6 hours after the commencement of chest pain. The elevation in SGOT and ocHBDH was still delayed. At the same time we could observe that the cardiac Troponin T (cTnT) was elevated at the time of admission of the patient itself. This increase of cTnT in AMI patients was 20 times higher than the normal blood donors. The controls included 25 normal blood donors and 25 patients with polytraumatic injuries with no chest contusion. The study shows that cTnT estimation could serve in the early diagnosis of AMI. The increase of cardiac troponin T in AMI patient was 20 times higher than the normal blood donors in AMI patients at the time of admission. Cardiac troponin T in serum appears to be a more sensitive indicator of myocardial cell injury than CKMB activity and its detection in the circulation may be a useful prognostic indicator in patients with unstable angina as well. When the blood of normal blood donors or that of patients with polytraumatic injury was analysed the troponin T values were well within the normal range in both the above categories showing that cardiac troponin T is highly specific for heart tissue .Although CKMB and cardiac troponin T are released soon after the myocardial injury, the release of cardiac troponin T is much earlier than CKMB thereby invalidating the important role of cardiac troponin T in diagnosing AMI. Cardiactroponin T has been shown to be highly sensitive for cardiac injury and not elevated in any other trauma, heavy exercise or skeletal muscle injury.Cardiac troponin T is ordinarily undetectable in healthy individuals, and so its measurement can serve as a powerful tool in the diagnosis of AMl. KEY WORDSCardiac Troponin T, alpha hydroxybutyrate dehydrogenase, Lactate dehydrogenase, myocardial infarction

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Early appearance of MB-creatine kinase activity in nontransmural myocardial infarction detected by a sensitive assay for the isoenzyme

Cited by 33 publications

References 21 publications

Value and Limitations of Thrombolytic Therapy in Early Acute Transmural Myocardial Infarction

Value and Limitations of Thrombolytic Therapy in Early Acute Transmural Myocardial Infarction

Troponin T concentrations 72 hours after myocardial infarction as a serological estimate of infarct size

Evaluation of clinical utility of serum enzymes and troponin—T in the early stages of acute myocardial infarction

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