- Poster presentation
- Open Access
Elevated high-sensitivity cardiac troponin is associated with hypertrophy and fibrosis assessed with CMR in patients with hypertrophic cardiomyopathy
© Gommans et al; licensee BioMed Central Ltd. 2013
- Published: 30 January 2013
- Cardiovascular Magnetic Resonance
- Body Surface Area
- Late Gadolinium Enhancement
- Hypertrophic Cardiomyopathy
- Lower Detection Limit
High-sensitivity (hs) cardiac troponin is a valuable biomarker of myocardial injury and frequently elevated in patients with hypertrophic cardiomyopathy (HCM). Using cardiovascular magnetic resonance (CMR) the HCM phenotype can be characterized in great detail with fibrosis as a key finding with prognostic impact. Therefore, our aim was to investigate whether elevated troponin levels in patients with clinical HCM were associated with LV hypertrophy and fibrosis as assessed with CMR.
In 62 clinical HCM patients (58% males, mean age 51 ± 15 years) hs-troponin T was determined with a high-sensitivity assay (Roche Diagnostics). The lower detection limit is 0.003 pg/l and an elevated hs-troponin is defined as a concentration ≥ the 99th percentile reference limit (≥ 0.014 pg/l). CMR with late gadolinium enhancement (LGE) was performed (Philips Achieva 1.5T) to assess LV mass indexed to body surface area, maximal wall thickness (MWT) and fibrosis. LV mass, MWT and the presence and extent of LGE were assessed (QMass 7.0, Medis) and compared between HCM patients with and without an elevated hs-troponin using Mann Whitney U or Fisher exact testing.
Total N = 62
Troponin not elevated N = 46
Troponin elevated N = 16
LV mass indexed to BSA (g/m2) (median; IQR)
Maximal LV wall thickness (mm) (median; IQR)
Fibrosis present n (%)
Fibrosis extent in LGE positive patients (%) (median; IQR)
Elevated troponin levels assessed with a high-sensitivity assay are common in HCM patients and associated with specific features of HCM such as hypertrophy and maximal wall thickness. Our findings are indicative of troponin as a potential surrogate marker of myocardial injury in the form of fibrosis. Future studies will have to address this issue more elaborately especially with regard to the potential prognostic value of troponin in these patients.
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.