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Troponins and High-Sensitivity Troponins as Markers of Necrosis in CAD and Heart Failure

Troponine und hochsensitive Troponine als Nekrosemarker bei KHK und Herzinsuffizienz

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Abstract

For years, cardiac troponins (cTn) have been regarded as the preferred biomarkers for the diagnosis of myocardial infarction and for the risk stratification of patients with acute coronary syndromes, as well as for the selection of patients who need an early invasive strategy, and for the guidance of adjunctive pharmacological therapy. In addition, measurement of cTn has been found useful for detection of myocardial necrosis in conditions unrelated to myocardial ischemia including acute pulmonary embolism, myocarditis, heart failure, sepsis, and end-stage renal disease. In these conditions, an unfavorable prognosis is unequivocally associated with detectable concentrations of cTn.

A major limitation of most currently available cTn assays is the lack of adequate precision, i.e., to measure cTn concentrations at the 99th percentile value with a coefficient of variation < 10%. As a consequence, many manufacturers have developed more sensitive cTn assays that now comply with precision criteria required by the Joint European Society of Cardiology/ American College of Cardiology/American Heart Association/World Heart Federation Task Force for the Redefinition of Acute Myocardial Infarction.

Using assays with higher analytic sensitivity more patients will be seen in clinical practice with the high-sensitivity cardiac troponin T (TnThs) above the 99th percentile discriminator. The causes of these elevations may be due to acute, subacute and chronic cardiac disease such as heart failure or cardiomyopathies.

Zusammenfassung

Kardiale Troponine (cTn) sind seit Jahren der Referenzstandard für die Klassifikation und für die Risikostratifizierung von Patienten mit einem akuten Koronarsyndrom. Erhöhte Troponinwerte erlauben zudem, Patienten zu identifizieren, die von einer invasiven Therapiestrategie sowie einer intensiveren Antikoagulation und antithrombozytären Therapie profitieren.

Kardiales Troponin ist myokardspezifisch und tritt daher auch bei Erkrankungen des Herzens auf, die nicht durch ein akutes Koronarsyndrom bedingt sind, beispielsweise bei der akuten Lungenembolie, bei einer Myokarditis, bei einer schweren Niereninsuffizienz, bei dekompensierter Herzinsuffizienz oder hämodynamisch relevanter Aortenstenose sowie bei Kardiomyopathien. Die Höhe der Troponinfreisetzung spiegelt den Schweregrad dieser Erkrankungen wider und ist prognostisch relevant.

Eine Einschränkung der meisten kommerziell erhältlichen cTn-Assays ist die fehlende Präzision an der unteren Nachweisgrenze. So war es bislang nicht möglich, Konzentrationen an der 99. Perzentile einer gesunden Referenzpopulation mit einer Trennschärfe von < 10% Variationskoeffizient zu messen. Von einigen Herstellern werden jetzt Troponinassays angeboten, die niedrige Konzentrationen messen können (höhere analytische Sensitivität) und die Präzisionskriterien der neuen Infarktdefinition erfüllen. Andererseits ist zu erwarten, dass durch Erhöhung der Sensitivität die diagnostische Spezifität sinkt und jetzt vermehrt kardiale Erkrankungen erkannt werden, die bislang unerkannt geblieben waren.

Die Auswirkungen der Verwendung niedrigerer Troponinkonzentrationen bei Patienten mit akutem Koronarsyndrom für die Diagnose, Risikostratifizierung und Therapiesteuerung sowie die Bedeutung erhöhter Troponinwerte bei Patienten ohne akutes Koronarsyndrom, insbesondere bei Vorliegen einer Herzinsuffizienz, sind Gegenstand der vorliegenden Übersicht.

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Giannitsis, E., Katus, H.A. Troponins and High-Sensitivity Troponins as Markers of Necrosis in CAD and Heart Failure. Herz 34, 600–606 (2009). https://doi.org/10.1007/s00059-009-3306-6

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