Serum biomarkers of early stages of hypertrophic cardiomyopathy in a young population

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Serum biomarkers of early stages of hypertrophic cardiomyopathy in a young population. / Fernlund, Eva I.; Gyllenhammar, Tom; Larsson, Anders; Arnlov, Johan; Carlsson, Marcus; Jablonowski, Robert; Liuba, Petru.

In: Journal of the American College of Cardiology, Vol. 65, No. 10S, 17.03.2015, p. A787.

Research output: Contribution to journalPublished meeting abstract

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TY - JOUR

T1 - Serum biomarkers of early stages of hypertrophic cardiomyopathy in a young population

AU - Fernlund, Eva I.

AU - Gyllenhammar, Tom

AU - Larsson, Anders

AU - Arnlov, Johan

AU - Carlsson, Marcus

AU - Jablonowski, Robert

AU - Liuba, Petru

PY - 2015/3/17

Y1 - 2015/3/17

N2 - Background: Hypertrophic cardiomyopathy (HCM) is the most common monogenic cardiac disorder and the leading cause of sudden cardiac death in the young. Although in a majority of HCM cases there are gene mutations coding for sarcomere proteins, the onset for the clinical consequences of these mutations are difficult to predict, as these mutations do not show any clear relationship to the degree of myocardial hypertrophy. Hence identification of early markers for this disease is important. The aim of this study was to investigate novel serum biomarkers reflecting myocardial remodeling, microfibrosis and coronary endotheliopathy in young presymtomatic HCM patients and in individuals at risk for developing HCM. Methods: Eighty-nine participants (18 HCM patients, 14 HCM-risk individuals, and 57 healthy controls) with median age of 15 (range 0-30) years underwent assessment with echocardiography and serum analysis for myostatin, cathepsin S, endostatin, type I collagen degradation marker (ICTP), matrix metalloproteinase (MMP) 9, vascular (VCAM) and intercellular adhesion molecules (ICAM). In some individuals, myocardial perfusion was measured both at rest and after adenosine via magnetic resonance. Results: Both cathepsin S and endostatin were increased in the HCM group (p0.3) and diastolic function, expressed as E/e' (p0.3). In the HCM-risk group, myostatin was decreased (p0.1). Conclusion: To the best of our knowledge, this is the first study to suggest early onset changes in biomarkers of myoblast regulation, endothelial function and matrix remodeling in young presymptomatic HCM patients and in HCM-risk individuals.

AB - Background: Hypertrophic cardiomyopathy (HCM) is the most common monogenic cardiac disorder and the leading cause of sudden cardiac death in the young. Although in a majority of HCM cases there are gene mutations coding for sarcomere proteins, the onset for the clinical consequences of these mutations are difficult to predict, as these mutations do not show any clear relationship to the degree of myocardial hypertrophy. Hence identification of early markers for this disease is important. The aim of this study was to investigate novel serum biomarkers reflecting myocardial remodeling, microfibrosis and coronary endotheliopathy in young presymtomatic HCM patients and in individuals at risk for developing HCM. Methods: Eighty-nine participants (18 HCM patients, 14 HCM-risk individuals, and 57 healthy controls) with median age of 15 (range 0-30) years underwent assessment with echocardiography and serum analysis for myostatin, cathepsin S, endostatin, type I collagen degradation marker (ICTP), matrix metalloproteinase (MMP) 9, vascular (VCAM) and intercellular adhesion molecules (ICAM). In some individuals, myocardial perfusion was measured both at rest and after adenosine via magnetic resonance. Results: Both cathepsin S and endostatin were increased in the HCM group (p0.3) and diastolic function, expressed as E/e' (p0.3). In the HCM-risk group, myostatin was decreased (p0.1). Conclusion: To the best of our knowledge, this is the first study to suggest early onset changes in biomarkers of myoblast regulation, endothelial function and matrix remodeling in young presymptomatic HCM patients and in HCM-risk individuals.

KW - biological marker

KW - myostatin

KW - endostatin

KW - marker

KW - cathepsin S

KW - protein

KW - adenosine

KW - cell adhesion molecule

KW - gelatinase B

KW - serum

KW - hypertrophic cardiomyopathy

KW - population

KW - American

KW - college

KW - cardiology

KW - human

KW - risk

KW - patient

KW - heart muscle perfusion

KW - mutation

KW - sarcomere

KW - myoblast

KW - echocardiography

KW - heart left ventricle mass

KW - nuclear magnetic resonance

KW - gene mutation

KW - sudden cardiac death

KW - heart ventricle hypertrophy

KW - cell adhesion

KW - control group

KW - high risk population

KW - collagen degradation

KW - diseases

M3 - Published meeting abstract

VL - 65

SP - A787

JO - Journal of the American College of Cardiology

T2 - Journal of the American College of Cardiology

JF - Journal of the American College of Cardiology

SN - 0735-1097

IS - 10S

ER -