Cardiovascular Diseases & Diagnosis

Natriuretic Peptides and Troponin I Do Not Predict Chemotherapy-Induced Cardiac Toxicity

Abstract

Katja Jungandreas, Alexander Vogt, Wieland Voigt, Karin Jordan, Hans-Georg Strauß, Christoph Thomssen, Henning Ebelt, Karl Werdan, Jürgen Schwamborn and Axel Schlitt

Background/Aims: Cytostatics and human antibodies are successfully being used to treat oncological diseases. Despite the beneficial effects of these potent drugs, cardiotoxicity represents one of the most relevant side effects and limits their usage. It is very important to detect cardiotoxicity at an early stage particular in patients under curative chemotherapy to avoid long-term side effects and impairment of quality of life. The aim of this prospective study was to investigate the value of natriuretic peptides and troponin for early detection of cardiotoxicity.

Patients and Methods: In this single-center study, 99 cancer patients under treatment with anthracyclines, taxanes, and/or trastuzumab were prospectively included. Clinical examination, echocardiography, and blood sampling (brain natriuretic peptide (BNP), N-terminal-proBNP, and troponin I) were performed at baseline and at 3 and 12 months, respectively. Cardiotoxicity was defined as clinical or echocardiographic signs of heart failure as defined by an increment in New York Heart Association (NYHA) class by more than one and a decline in left ventricular ejection fraction (LVEF) depending on baseline situation. 

Results: During the 12-month follow-up, 27 patients presented with at least one predefined endpoint. Neither BNP, nor NT-proBNP, nor troponin I was related to the incidence of cardiotoxicity as defined by the combined endpoint. In post-hoc analysis a significant association between an increasing NYHA stage and a decrease in LVEF was found (negative predictive value of 91%). 

Conclusion: The occurrence of cardiotoxicity could not be detected either by natriuretic peptides or troponin. However, we hypothesize that an increase of more than one NYHA stage as a marker for dyspnea may be an indicator of cardiotoxicity.

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