Cardiac and Inflammation Biomarker Profile after Initiation of Adjuvant Trastuzumab Therapy
Author(s) -
Sukhbinder DhesyThind,
Vikaash Kumar,
Aidan Snider-McNair,
Colleen Shortt,
Som D. Mukherjee,
Peter Ellis,
Gregory R. Pond,
Peter A. Kavsak
Publication year - 2012
Publication title -
clinical chemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.705
H-Index - 218
eISSN - 1530-8561
pISSN - 0009-9147
DOI - 10.1373/clinchem.2012.192419
Subject(s) - trastuzumab , cardiotoxicity , medicine , troponin complex , troponin , biomarker , troponin i , heart failure , inflammation , cardiology , ejection fraction , troponin t , cancer , breast cancer , myocardial infarction , chemotherapy , biochemistry , chemistry
To the Editor:Liebetrau and colleagues have reported mechanistic data indicating that cardiac biomarkers appear rapidly in the blood upon induction of myocardial cell necrosis (1). Interestingly, concentrations of cardiac troponin T (cTnT)1 in both high-sensitivity (hs-cTnT) and fourth-generation assays continue to increase up to 1 day after the onset of necrosis. These data support the argument that irreversible myocardial injury causes prolonged release of cardiac troponin into the blood. Many anticancer therapies produce myocardial injury. Accordingly, measurement of blood cardiac biomarkers 1 day after therapy initiation may be necessary to assess whether irreversible myocardial injury has occurred. That may be important in the setting of trastuzumab treatment for human epidermal growth factor receptor 2–positive breast cancers, in which data have shown that this agent may cause cardiotoxicity, specifically a decrease in the left ventricular ejection fraction, which could lead to heart failure (2). Recent data have also suggested that inflammation (as assessed by C-reactive protein measurement) might be better than cardiac troponin I (cTnI) and the natriuretic peptides as a prognostic factor for the development of trastuzumab-mediated cardiotoxicity, although the cTnI assay used in that study was not a high-sensitivity assay (2). Moreover, earlier and additional inflammation biomarkers (as opposed to C-reactive protein) have also been demonstrated to identify the patients …
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