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Serum Matrix Metalloproteinases as Quantitative Biomarkers for Myocardial Fibrosis and Sudden Cardiac Death Risk Stratification in Patients With Hypertrophic Cardiomyopathy

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Serum Matrix Metalloproteinases as Quantitative Biomarkers for Myocardial Fibrosis and Sudden Cardiac Death Risk Stratification in Patients With Hypertrophic Cardiomyopathy. / Münch, Julia; Avanesov, Maxim; Bannas, Peter; Säring, Dennis; Krämer, Elisabeth; Mearini, Giulia; Carrier, Lucie; Suling, Anna; Lund, Gunnar; Patten-Hamel, Monica.

In: J CARD FAIL, Vol. 22, No. 10, 10.2016, p. 845-50.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Münch, J, Avanesov, M, Bannas, P, Säring, D, Krämer, E, Mearini, G, Carrier, L, Suling, A, Lund, G & Patten-Hamel, M 2016, 'Serum Matrix Metalloproteinases as Quantitative Biomarkers for Myocardial Fibrosis and Sudden Cardiac Death Risk Stratification in Patients With Hypertrophic Cardiomyopathy', J CARD FAIL, vol. 22, no. 10, pp. 845-50. https://doi.org/10.1016/j.cardfail.2016.03.010

APA

Münch, J., Avanesov, M., Bannas, P., Säring, D., Krämer, E., Mearini, G., Carrier, L., Suling, A., Lund, G., & Patten-Hamel, M. (2016). Serum Matrix Metalloproteinases as Quantitative Biomarkers for Myocardial Fibrosis and Sudden Cardiac Death Risk Stratification in Patients With Hypertrophic Cardiomyopathy. J CARD FAIL, 22(10), 845-50. https://doi.org/10.1016/j.cardfail.2016.03.010

Vancouver

Münch J, Avanesov M, Bannas P, Säring D, Krämer E, Mearini G et al. Serum Matrix Metalloproteinases as Quantitative Biomarkers for Myocardial Fibrosis and Sudden Cardiac Death Risk Stratification in Patients With Hypertrophic Cardiomyopathy. J CARD FAIL. 2016 Oct;22(10):845-50. https://doi.org/10.1016/j.cardfail.2016.03.010

Bibtex

@article{af0c7b49810740c09de2fbeab404f22b,
title = "Serum Matrix Metalloproteinases as Quantitative Biomarkers for Myocardial Fibrosis and Sudden Cardiac Death Risk Stratification in Patients With Hypertrophic Cardiomyopathy",
abstract = "BACKGROUND: Hypertrophic cardiomyopathy (HCM) is associated with an increased risk of sudden cardiac death due to ventricular tachycardia (VT), and myocardial fibrosis reflects an important risk factor. Several matrix metalloproteinases (MMPs) and procollagen N-terminal propeptides (PNPs) are involved in collagen turnover and discussed as fibrosis biomarkers. We aimed to identify biomarkers that correlate with myocardial fibrosis in late-gadolinium-enhancement cardiac magnetic resonance imaging (LGE-CMR) and/or cardiac events (syncope, VT) in HCM patients.METHODS AND RESULTS: In 54 HCM patients (age 55.9 ± 14.3 y, 50% female) fibrosis was quantified by LGE-CMR. Serum concentrations of MMP-1, -2, -3, -9, and tissue inhibitor of MMP (TIMP) 1 were analyzed by means of enzyme-linked immunosorbent assay and PINP, PIIINP, and type I collagen C-terminal telopeptide (ICTP) concentrations by radioimmunoassay. MMP-9 was associated with fibrosis in LGE-CMR (mean increase 0.66 g/unit MMP9 [95% confidence interval [CI] 0.50-0.82]; P < .001) and with cardiac events in women (odds ratio [OR] 1.07 [1.01-1.12], P = .01) but not in men. Increased MMP-2 levels in women were associated with lower fibrosis (0.05 [-0.09 to -0.01]; P = .015). MMP-3 levels were positively associated with cardiac events (OR 1.13 [1.05-1.22]; P = .001) independently from fibrosis and sex. No association was detected for MMP-1, TIMP-1, PNPs, and ICTP.CONCLUSIONS: These data suggest that MMP-9 is a useful biomarker for fibrosis and cardiac events in female HCM patients, whereas MMP-3 is associated with a higher event rate independent from fibrosis and sex.",
keywords = "Journal Article",
author = "Julia M{\"u}nch and Maxim Avanesov and Peter Bannas and Dennis S{\"a}ring and Elisabeth Kr{\"a}mer and Giulia Mearini and Lucie Carrier and Anna Suling and Gunnar Lund and Monica Patten-Hamel",
note = "Copyright {\textcopyright} 2016 Elsevier Inc. All rights reserved.",
year = "2016",
month = oct,
doi = "10.1016/j.cardfail.2016.03.010",
language = "English",
volume = "22",
pages = "845--50",
journal = "J CARD FAIL",
issn = "1071-9164",
publisher = "Churchill Livingstone",
number = "10",

}

RIS

TY - JOUR

T1 - Serum Matrix Metalloproteinases as Quantitative Biomarkers for Myocardial Fibrosis and Sudden Cardiac Death Risk Stratification in Patients With Hypertrophic Cardiomyopathy

AU - Münch, Julia

AU - Avanesov, Maxim

AU - Bannas, Peter

AU - Säring, Dennis

AU - Krämer, Elisabeth

AU - Mearini, Giulia

AU - Carrier, Lucie

AU - Suling, Anna

AU - Lund, Gunnar

AU - Patten-Hamel, Monica

N1 - Copyright © 2016 Elsevier Inc. All rights reserved.

PY - 2016/10

Y1 - 2016/10

N2 - BACKGROUND: Hypertrophic cardiomyopathy (HCM) is associated with an increased risk of sudden cardiac death due to ventricular tachycardia (VT), and myocardial fibrosis reflects an important risk factor. Several matrix metalloproteinases (MMPs) and procollagen N-terminal propeptides (PNPs) are involved in collagen turnover and discussed as fibrosis biomarkers. We aimed to identify biomarkers that correlate with myocardial fibrosis in late-gadolinium-enhancement cardiac magnetic resonance imaging (LGE-CMR) and/or cardiac events (syncope, VT) in HCM patients.METHODS AND RESULTS: In 54 HCM patients (age 55.9 ± 14.3 y, 50% female) fibrosis was quantified by LGE-CMR. Serum concentrations of MMP-1, -2, -3, -9, and tissue inhibitor of MMP (TIMP) 1 were analyzed by means of enzyme-linked immunosorbent assay and PINP, PIIINP, and type I collagen C-terminal telopeptide (ICTP) concentrations by radioimmunoassay. MMP-9 was associated with fibrosis in LGE-CMR (mean increase 0.66 g/unit MMP9 [95% confidence interval [CI] 0.50-0.82]; P < .001) and with cardiac events in women (odds ratio [OR] 1.07 [1.01-1.12], P = .01) but not in men. Increased MMP-2 levels in women were associated with lower fibrosis (0.05 [-0.09 to -0.01]; P = .015). MMP-3 levels were positively associated with cardiac events (OR 1.13 [1.05-1.22]; P = .001) independently from fibrosis and sex. No association was detected for MMP-1, TIMP-1, PNPs, and ICTP.CONCLUSIONS: These data suggest that MMP-9 is a useful biomarker for fibrosis and cardiac events in female HCM patients, whereas MMP-3 is associated with a higher event rate independent from fibrosis and sex.

AB - BACKGROUND: Hypertrophic cardiomyopathy (HCM) is associated with an increased risk of sudden cardiac death due to ventricular tachycardia (VT), and myocardial fibrosis reflects an important risk factor. Several matrix metalloproteinases (MMPs) and procollagen N-terminal propeptides (PNPs) are involved in collagen turnover and discussed as fibrosis biomarkers. We aimed to identify biomarkers that correlate with myocardial fibrosis in late-gadolinium-enhancement cardiac magnetic resonance imaging (LGE-CMR) and/or cardiac events (syncope, VT) in HCM patients.METHODS AND RESULTS: In 54 HCM patients (age 55.9 ± 14.3 y, 50% female) fibrosis was quantified by LGE-CMR. Serum concentrations of MMP-1, -2, -3, -9, and tissue inhibitor of MMP (TIMP) 1 were analyzed by means of enzyme-linked immunosorbent assay and PINP, PIIINP, and type I collagen C-terminal telopeptide (ICTP) concentrations by radioimmunoassay. MMP-9 was associated with fibrosis in LGE-CMR (mean increase 0.66 g/unit MMP9 [95% confidence interval [CI] 0.50-0.82]; P < .001) and with cardiac events in women (odds ratio [OR] 1.07 [1.01-1.12], P = .01) but not in men. Increased MMP-2 levels in women were associated with lower fibrosis (0.05 [-0.09 to -0.01]; P = .015). MMP-3 levels were positively associated with cardiac events (OR 1.13 [1.05-1.22]; P = .001) independently from fibrosis and sex. No association was detected for MMP-1, TIMP-1, PNPs, and ICTP.CONCLUSIONS: These data suggest that MMP-9 is a useful biomarker for fibrosis and cardiac events in female HCM patients, whereas MMP-3 is associated with a higher event rate independent from fibrosis and sex.

KW - Journal Article

U2 - 10.1016/j.cardfail.2016.03.010

DO - 10.1016/j.cardfail.2016.03.010

M3 - SCORING: Journal article

C2 - 27018569

VL - 22

SP - 845

EP - 850

JO - J CARD FAIL

JF - J CARD FAIL

SN - 1071-9164

IS - 10

ER -