Diagnostische und therapeutische Implikationen der Troponinerhöhung bei akut exazerbierter chronisch obstruktiver Lungenerkrankung

Zusammenfassung

Ziel der Studie: Kardiovaskuläre Komorbiditäten sind überproportional häufig bei Patienten mit chronisch obstruktiver Lungenerkrankung (COPD) und bestimmen maßgeblich Morbidität und Mortalität der COPD. Im Rahmen akuter COPD-Exazerbationen finden sich bei bis zu 74 % der Patienten erhöhte Troponinspiegel, die Ausdruck einer begleitenden myokardialen Schädigung sind und primär auf systemische inflammatorische Prozesse zurückgeführt werden können. Die Mechanismen, die zur Troponinfreisetzung führen, sind mannigfaltig und umfassen sowohl die primäre Myokardischämie (Myokardinfarkt Typ 1), das KHK-unabhängige Ungleichgewicht zwischen Sauerstoffangebot und -bedarf (Myokardinfarkt Typ 2) sowie die akute Rechts- und Linksherzbelastung. Aufgrund ihrer multifaktoriellen Ätiologie wird das therapeutische Vorgehen, insbesondere die Indikation und der Zeitpunkt der invasiven Koronardiagnostik, bislang uneinheitlich gehandhabt.

Methodik: Auf Grundlage der aktuellen Literatur wird ein diagnostischer und therapeutischer Algorithmus zum Vorgehen bei Troponinelevation im Rahmen der akuten COPD-Exazerbation empfohlen.

Ergebnisse: Zur Differenzialdiagnose des Typ 1-Myokardinfarktes, der infolge intrakoronarer Thrombusformation einer Koronarangiografie zugeführt werden muss, dient die kardiologische Basisdiagnostik aus klinischem Beschwerdebild, Ruhe-EKG, Echokardiografie und Troponinspiegel bzw. -dynamik. Anhand der hierbei erhobenen Befunde sind Indikation und Zeitpunkt der invasiven Koronardiagnostik ableitbar.

Schlussfolgerung: Die Notwendigkeit zum standardisierten Vorgehen bei akuter COPD-Exazerbation mit erhöhtem Troponinspiegel erwächst aus der häufig begleitenden koronaren Herzkrankheit und dem Risiko, eine thrombotisch bedingte primäre Myokardischämie zu übergehen.

Abstract

Aims: Cardiovascular comorbid conditions are frequent in chronic obstructive pulmonary disease (COPD) and substantially influence morbidity and mortality. Elevated plasma levels of cardiac troponin have been detected in up to 74 % of patients with acute exacerbated COPD (AECOPD), pointing at concomitant myocardial damage that can primarily be ascribed to systemic inflammatory processes. The mechanisms promoting troponin release in AECOPD are manifold and comprise: type 1 myocardial infarction as a consequence of intraluminal thrombus formation, type 2 myocardial infarction due to an imbalance between myocardial oxygen supply and demand, as well as right and left heart failure. Given its multifactorial aetiology, no standardized diagnostic and therapeutic approach are as yet available.

Material and methods: On the basis of current literature, we propose a potential diagnostics and therapeutics algorithm for AECOPD patients with elevated troponin levels.

Results: Clinical presentation, electro- and echocardiogram, as well as cardiac troponin levels and their dynamics represent sufficient risk stratifiers that permit evaluation and timing of invasive coronary strategy.

Conclusion: The necessity for a standardized approach to elevated troponin during AECOPD arises from the frequent presence of concomitant coronary heart disease and the potential risk of oversight of type 1 myocardial infarction.

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