Troponin and Anti-Troponin Autoantibody Levels in Patients with Ventricular Noncompaction

Hatice Betül Erer,Nurten Sayar,Tolga Sinan Güvenç,Servet Altay,Yüksel Kaya,Ahu Sarbay Kemik,Mehmet Eren,Şeref Kul ,Hale Yılmaz

doi:10.1371/journal.pone.0057648

Abstract

Ventricular hypertrabeculation/noncompaction is a morphologic and functional anomaly of myocardium characterized by prominent trabeculae accompanied by deep recessus. Dilated cardiomyopathy with left ventricular failure is observed in these patients, while the cause or pathophysiologic nature of this complication is not known. Anti-troponin antibodies are formed against circulating cardiac troponins after an acute coronary event or conditions associated with chronic myocyte necrosis, such as dilated cardiomyopathy. In present study, we aimed to investigate cardiac troponins and anti troponin autoantibodies in ventricular noncompaction/hypertrabeculation patients with/without reduced ejection fraction. A total of 50 patients with ventricular noncompaction and 23 healthy volunteers were included in this study. Noncompaction/hypertrabeculation was diagnosed with two-dimensional echocardiography using appropriate criteria. Depending on ejection fraction, patients were grouped into noncompaction with preserved EF (LVEF >50%, n = 24) and noncompaction with reduced EF (LVEF <35%, n = 26) groups. Troponin I, troponin T, anti-troponin I IgM and anti-troponin T IgM were measured with sandwich immunoassay method using a commercially available kit. Patients with noncompaction had significantly higher troponin I (28.98±9.21 ng/ml in NCNE group and 28.11±10.42 ng/ml in NCLE group), troponin T (22.17±6.97 pg/ml in NCNE group and 22.78±7.76 pg/ml in NCLE group) and antitroponin I IgM (1.92±0.43 µg/ml in NCNE group and 1.79±0.36 µg/ml in NCLE group) levels compared to control group, while antitroponin T IgM and IgG were only elevated in patients with noncompaction and reduced EF (15.81±6.52 µg/ml for IgM and 16.46±6.25 µg/ml for IgG). Elevated cardiac troponins and anti-troponin I autoantibodies were observed in patients with noncompaction preceding the decline in systolic function and could indicate ongoing myocardial damage in these patients.

Highlights

Venricular hypertrabeculation/noncompaction (NC/HT) is a primarily genetic cardiomyopathy characterized by prominent trabeculae with deep recessus separating trabeculations [1]
Patients with left ventricular noncompaction were separated in two groups based on their ejection fraction: those with a left ventricular EF of less than 35% (NCLE group) and those with a left ventricular EF of equal to or more than 50% (NCNE group)
Left ventricular end diastolic and end systolic volumes were higher in NCLE group compared to other groups (170.25640.86 ml vs. 140.99653.05 ml and 97.35626.75 ml; p,0.05 for LVEDv and 121.45632.01 ml vs. 71.58646.49 ml and 27.4567.46 ml; p,0.001 for LVESv), and in NCNE group compared to healthy controls (p,0.01 for LVEDv and p,0.001 for LVESv)

Summary

Introduction

Venricular hypertrabeculation/noncompaction (NC/HT) is a primarily genetic cardiomyopathy characterized by prominent trabeculae with deep recessus separating trabeculations [1]. Left ventricular systolic dysfunction and development of idiopathic cardiomyopathy are the most important consequences of NC/HT [1,2]. The cause for transformation to a dilated cardiomyopathy (DCM) phenotype remains unknown despite being a topic of active research. Both cardiac troponin I (cTnI) and cardiac troponin T (cTnT) are components of myocardial troponin-tropomyosin complex and elevated serum levels are observed in dilated cardiomyopathy (DCM) patients due to myocardial necrosis, apoptosis or myocardial leakage. Antibodies against various myocardial components, including cardiac troponins, were observed in patients with left ventricular systolic dysfunction and in normal individuals [6,7]

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