Early assessment of reperfusion therapy using cardiac troponin T

Abe, Satoshi; Arima, Shinichi; Yamashita, T; Miyata, Masaaki; Okino, Hideki; Toda, Hitoshi; Nomoto, Kunihiro; Ueno, Masashi; Tahara, Masaki; Kiyonaga, Kazuaki; Nakao, Shoichiro; Tanaka, Hiromitsu

doi:10.1016/0735-1097(94)90381-6

Cited by 43 publications

(9 citation statements)

References 40 publications

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“…Venous blood samples of 10 ml were obtained just before starting thrombolytic therapy and 1, 2, 3, 4, 5, 6,8,10,14,18,22,28,34,46,58,70,82,94,118,142, 166 hours later. Exact sampling times were recorded and expressed as time after the onset of symptoms.…”

Section: Methodsmentioning

confidence: 99%

“…For reliable prediction of thrombolysis from initial slopes of cardiac markers, samples should be taken every 15 minutes after start of treatment to estimate the initial slope (8,10,14). Using early initial slopes of serum markers to predict reperfusion Zabel et al found the best discriminating results using myoglobin.…”

Section: Troponin T and Prediction Of Reperfusionmentioning

confidence: 99%

“…For troponin T it has been suggested in several studies that the effects of reperfusion on the troponin T plasma time-concentration curves in acute myocardial infarction can be used to non-invasively assess the effectiveness of thrombolytic therapy (6)(7)(8)(9)(10)(11)(12)(13)(14)(15). A characteristic biphasic change in plasma concentration has been described, especially in patients with early reperfusion after thrombolytic therapy (6.…”

Section: Introductionmentioning

confidence: 99%

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Cumulative Troponin T Release after Acute Myocardial Infarction. Influence of Reperfusion

Kragten¹,

Hermens²,

Dieijen-Visser³

1997

Clinical Chemistry and Laboratory Medicine

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For troponin T a characteristic biphasic change in the plasma time-concentration curve has been described, especially in patients with early reperfusion after thrombolytic therapy. As troponin T is bound to myofibrillar structures, treatment strategy or treatment outcome could influence the cumulative plasma release of this protein in a different way compared to the cumulative release of free cytoplasmic cardiac enzymes.The present study is the first study comparing the total quantity of troponin T released by the heart during the first 168 hours after acute myocardial infarction, both in patients treated with thrombolytic therapy (n = 16) and in patients not treated with thrombolytic therapy (n = 7). On the basis of clinical symptoms and coronary arteriogram within 24 hours, the patients treated with thrombolytic therapy were divided into two groups, reperfused (n = 9) and non-reperfused (n = 7). In the patients not treated with thrombolytic therapy, absence of spontaneous early reperfusion was judged only from clinical symptoms.Cumulative troponin T release into plasma was compared to the cumulative release of the cytoplasmic cardiac enzymes creatine kinase (EC 2.7.3.2) and hydroxybutyrate dehydrogenase (EC 1.1.1.27). Cumulative release, i.e., infarct size, was calculated using a two-compartment model for circulating proteins. Mean tissue contents, per gram wet weight, of 156 U/g for hydroxybutyrate dehydrogenase, 2.163 U/g for creatine kinase and 234 g/g for troponin T, were used to express infarct size in gram-equivalents of healthy myocardium per litre plasma (g-eq/1).Release rates were represented by the ratio of cumulative quantities released in 10 hours and 72 hours for creatine kinase and hydroxybutyrate dehydrogenase and in 10 hours and 168 hours for troponin T. Conclusions-Plasma time-concentration curves and release rates of troponin T in patients treated with thrombolytic therapy showing reperfusion differ significantly from those of patients not treated with thrombolytic therapy, showing no reperfusion.-Creatine kinase and hydroxybutyrate dehydrogenase release is completed within 72-100 hours in all patients, whereas troponin T release still continues after 168 hours.-Cumulative troponin T release at 168 hours is only a fraction (around 8%) of cumulative cytoplasmic enzyme release and the percentage released is not influenced by the treatment strategy or outcome, i. e., vessel patency.-Although troponin T release is only a fraction of the cumulative enzyme release (infarct size) there is a highly significant correlation between both, independent of the treatment strategy or treatment outcome.

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Section: Methodsmentioning

confidence: 99%

Section: Troponin T and Prediction Of Reperfusionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cumulative Troponin T Release after Acute Myocardial Infarction. Influence of Reperfusion

Kragten¹,

Hermens²,

Dieijen-Visser³

1997

Clinical Chemistry and Laboratory Medicine

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“…cTnT has also been studied as an indicator of reperfusion. Abe et al have demonstrated that a >0.5 ng/ml increase in cTnT over 60 minutes is predictive of recanalization with greater than 90% accuracy [29]. These authors emphasize, however, that the quantitative cTnT assay requires approximately 90 minutes; its cost is currently in the range of $70 [29].…”

Section: Biochemical Testingmentioning

confidence: 99%

ECG monitoring, biochemical testing, and anticoagulation assessment

O’Gara

1996

J Thromb Thrombol

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Although ancillary tools such as echocardiography and radionuclide imaging are available for emergency room use, clinicians continue to rely most often on the history, electrocardiogram (ECG), and serologic markers to establish the diagnosis of acute myocardial infarction (MI). A high clinical index of suspicion is necessary in situations in which the presentation might be atypical, for example, in the elderly or diabetic patient. Any chest pain should be further characterized within the context of the patient's risk profile and its particular attributes fully delineated. The ECG is then scrutinized for the presence of new ischemic changes, whereby an appropriate management strategy is initiated. Acute reperfusion therapy is to be considered for patients with pathologic STsegment elevations in two or more contiguous leads as well as for patients with new left bundle branch block. Note should also be made of the many ECG features that provide early prognostic information, such as the magnitude and extent of the ST-segment elevation, the presence of right-sided or precordial ST-segment deviations in the setting of inferior injury current [1,2], and the subsequent development of a Q-wave versus non-Q-wave pattern [3]. The amplirude of ST-segment elevations may vary considerably over the first 3 hours following thrombolytic therapy as a reflection of the competing forces of clot lysis and rethrombosis. In these settings, continuous or frequent monitoring of ECG leads corresponding to the infarct zone is highly recommended. Standard 12-lead tracings obtained at widely disparate intervals are relatively less informative [4,5].The noninvasive assessment of infarct-artery patency following thrombolytic therapy is a critical feature of early management. Failure of timely reperfusion is an indication for rescue angioplasty (PTCA) which, despite its potential shortcomings, is to be pursued, especially in the setting of hemodynamic instability, whenever appropriate thcilities are available. Early recanalization with normal (TIMI grade 3) flow is the primary goal of any reperfusion strategy. Noninvasive indices of vessel patency include resolution of chest pain, improvement in ST-segment elevation, and early serologic marker release. Because the latter phenomenon is usually appreciated retrospectively, attention is initially focused on the former two events.When examined in isolation, the improvement or resolution of chest pain is at best an imprecise gauge of vessel patency following thrombolysis. In an analysis of 386 patients from the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI 1) trial, Califf et al. reported that 87% of patients with complete and 71% of patients with partial resolution of chest pain had a patent artery at 90 minutes, as did 60% of the patients with unchanged or worsening pain [6]. Analysis of the change in ST-segment elevation proved more discriminatory than chest pain status in a logistic regression model. Indeed, 96% of patients with complete and 84% of patients with partial resolution ...

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“…These include detecting coronary reperfusion after thrombolysis, 50,51 predicting graft failure in cardiac transplantation, 52,53 identifying myocardial necrosis with doxorubicin therapy, 54 evaluating myocardial effects of thoracic radiation therapy, 55 and assessing cocaine-associated chest pain.…”

Section: Othermentioning

confidence: 99%

Acute coronary ischemia: troponin I and T

Sacks

1999

Vasc Med

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Despite advances in diagnosis and management, ischemic heart disease remains the leading cause of death in the USA. Serum cardiac enzymes, one of the three fundamental criteria for establishing the diagnosis of myocardial infarction, are not specific for cardiac muscle and have a narrow time-window. The recent development of monoclonal antibodies to cardiac troponin I and troponin T has resulted in cardiac-specific assays. Several published studies have documented the utility of troponin proteins in the evaluation of myocardial necrosis. A brief overview of the characteristics and clinical utility of troponin T and I is presented here.

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Early assessment of reperfusion therapy using cardiac troponin T

Abstract: Serial measurements of cardiac troponin T as well as of CK-MB are useful for early assessment of reperfusion therapy.

Cited by 43 publications

References 40 publications

Cumulative Troponin T Release after Acute Myocardial Infarction. Influence of Reperfusion

Cumulative Troponin T Release after Acute Myocardial Infarction. Influence of Reperfusion

ECG monitoring, biochemical testing, and anticoagulation assessment

Acute coronary ischemia: troponin I and T

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