Quantifying the MB isoenzyme of creatine kinase with the Abbott "IMx" immunoassay analyzer

Genser

et al. 1995

Med. Pediatr. Oncol.

Anthracyclines (doxorubicin, daunorubicin, and derivatives) are among the most effective antineoplastic drugs for pediatric cancer with dose-limiting acute and long-term cardiotoxicity. The exact mechanism of the development of cardiomyopathy is still not clear. Anthracyclines may induce subclinical acute myocardial injury leading to lysis of a limited number of myocytes. Alternatively, myocytes may experience a transient loss of cytoplasmic membrane integrity. Both conditions may lead to a transient efflux of small amounts of cytoplasmic enzymes and other proteins specific to the heart muscle fibers. To test these hypotheses we assayed plasma creatine kinase (CK) MB mass and cardiac specific troponin T (TnT). CKMB may be released even in case of reversible cell membrane injury, while prolonged elevation of TnT is the most sensitive and specific marker of limited myocardial necrosis. Thirty-five anthracycline-containing chemotherapy courses in 22 children with cancer were analyzed. CKMB mass and TnT concentrations were within the normal range in all children before anthracycline therapy. Within 72 hours from anthracycline therapy no increment of one of these two marker proteins was detected (ANOVA for repeated measures, P = 0.94 [TnT] and 0.25 [CKMB]). We conclude that only minimal if any acute necroses of cardiac myocytes occur after anthracycline therapy. Even membrane integrity appears to be maintained within the first 3 days after anthracycline therapy, in the absence of electrocardiographic or echocardiographic signs of acute cardiotoxicity.

“…CKMB mass concentrations were determined using an enzyme immunoassay (Abbott, Chicago, IL). The upper limit of the reference interval is 5 pg/L [28,29].…”

Section: Assays For Troponin T and Ckmb Massmentioning

confidence: 99%

Cardiac troponin T and creatine kinase MB mass concentrations in children receiving anthracycline chemotherapy

Genser

et al. 1995

Med. Pediatr. Oncol.

Annals of Translational Medicine

“…In 1990, rapid enzyme immunoassays for direct mass measurement of CK-MB mass as μg/L were developed (75,76).…”

Section: : Ck-mb Massmentioning

confidence: 99%

An historical approach to the diagnostic biomarkers of acute coronary syndrome

Danese

Montagnana

2016

151

Suspected acute myocardial infarction (AMI) is one of the leading causes of admission to the emergency departments in Western countries but also an increasing cause in many other nations. The diagnosis of AMI involves the evaluation of clinical signs and symptoms, electrocardiographic assessment, and measurement of cardiac circulating biomarkers. In the last sixty years, the use of laboratory markers has changed considerably. Early biomarkers assessment has entailed testing for total enzyme activity of aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and creatine kinase (CK). Advances in electrophoresis allowed the identification of more cardio-specific isoenzymes of both CK and LDH, thus leading to the introduction of the CK-MB and LDH-1 activity assays. Soon thereafter, the development of immunoassays, as well as technical advances in automation, allowed the measurements of the CK-MB in mass rather than in activity and myoglobin. Currently, cardiac troponins have the highest sensitivity and specificity for myocardial necrosis and represent the biochemical gold standard for diagnosing AMI. This review provides a chronology of the major events which marked the evolution of cardiac biomarkers testing and the development of the relative assays from the first introduction of AST in the 1950s to the last high sensitivity troponin immunoassays in the 2010s.

“…Creatine kinase MB isoenzjme (CK-MB) was determined by mass concentration using the Abbott IMX system (30).…”

Section: Ufhmentioning

confidence: 99%

Systemic Thrombin Generation and Activity Resistant to Low Molecular Weight Heparin Administered Prior to Streptokinase in Patients with Acute Myocardial Infarction

Nilsen¹,

Gøransson²,

Larsen³

et al. 1997

Thromb Haemost

SummaryOne hundred patients were included in a randomized open trial to assess the systemic factor Xa (FXa) and thrombin inhibitory effect as well as the safety profile of low molecular weight heparin (LMWH) given subcutaneously in conjunction with streptokinase (SK) in patients with acute myocardial infarction (MI). The treatment was initiated prior to SK, followed by repeated injections every 12 h for 7 days, using a dose of 150 anti-Xa units per kg body weight. The control group received unfractionated heparin (UFH) 12,500 IU subcutaneously every 12 h for 7 days, initiated 4 h after start of SK infusion. All patients received acetylsalicylic acid (ASA) initiated prior to SK.Serial blood samples were collected prior to and during the first 24 h after initiation of SK infusion for determination of prothrombin fragment 1+2 (Fl+2), thrombin-antithrombin III (TAT) complexes, fibrinopeptide A (FPA) and cardiac enzymes. Bleeding complications and adverse events were carefully accounted for.Infarct characteristics, as judged by creatine kinase MB isoenzyme (CK-MB) and cardiac troponin T (cTnT), were similar in both groups of patients.A comparable transient increase in Fl+2, TAT and FPA was noted irrespective of heparin regimen. Increased anti-Xa activity in patients given LMWH prior to thrombolytic treatment had no impact on indices of systemic thrombin activation.The incidence of major bleedings was significantly higher in patients receiving LMWH as compared to patients receiving UFH. However, the occurrence of bleedings was modified after reduction of the initial LMWH dose to 100 anti-Xa units per kg body weight.In conclusion, systemic FXa- and thrombin activity following SK-infusion in patients with acute MI was uninfluenced by conjunctive LMWH treatment.