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Identification and characterization of new biomarkers that can predict the development of heart failure in hypertrophic cardiomyopathy
Author(s) -
Altara Raffaele,
Hessel Marleen H.M.,
Hermans Rob J.J.,
Janssen Ben J.A.,
Blankesteijn Matthijs W.
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1033.3
Subject(s) - hypertrophic cardiomyopathy , identification (biology) , heart failure , cardiology , medicine , cardiomyopathy , computational biology , biology , botany
In a subpopulation of patients long standing left ventricular hypertrophy (LVH) may lead to a deterioration of cardiac function and development of heart failure (HF). To determine if cytokines can serve as biomarkers for the in vivo progression from LVH to HF a feasibility study in experimental animals has been conducted. For this purpose, LVH was induced in mice by transverse aortic constriction (TAC) to trigger LVH. Blood was collected from the mice at 4 and 8 weeks after TAC. The serum levels of >40 analytes were assessed semi‐quantitatively using a membrane‐bound antibody technique (ProteomeProfiler TM ). Circulating levels of at least 4 analytes show differences between TAC and SHAM. Analyte A increased up to 12‐fold after 8 weeks of TAC, whereas the other 3 analytes increased up to 5‐fold. To confirm these results, we used serum obtained from rats that were subjected to myocardial infarction. We observed increases of the same 4 analytes in the serum and heart tissue homogenates. To confirm the potential cardiac origin of these analytes we could demonstrate the presence of TIMP‐1, a circulating inhibitor of matrix metalloproteinases, in both serum and tissue obtained from the infarcted area. These first sets of data in rats and mice prove the feasibility of the current approach to screen for novel circulating biomarkers for HF and to confirm their cardiac origin.