They could be observed in very low quantities in normal individuals and detected more frequently in patients after a myocardial Therefore while creating an algorithm we sought to maximize the differences while minimizing variance infarction and dilated cardiomyopathy. Experimentally, anti-troponin I autoantibodies are capable of altering calcium currents in cultivated myocardial cells and could produce “dilated cardiomyopathy-like” lesions. In another study, exposure to anti-troponin I antibodies caused inflammatory myocarditis in mice. Clinical studies had indicated a worse prognosis for patients with positive cTnI antibodies after an acute myocardial infarction. Patients with iDCM who are positive for anti-cTnI antibodies had a trend towards increased left ventricular volume and heightened sympathetic activity. In contrast, another study indicated that cell-mediated immune response against troponins could act to reduce immune response. So far, only an association with anti-cTnI antibodies and cardiomyopathy could be demonstrated. Anti-cTnT antibodies were incapable of inducing myocardial damage, possibly due to sarcoplasmic location of cTnT. We have shown that anti-cTnI IgM antibodies are elevated in patients with NC/HT, regardless of initial ventricular function. This finding is compatible with high cTnI levels in patients with NC/HT with or without reduction of ejection fraction. Since anticTnI antibodies are capable of inducing myocardial damage, it is possible that observed anti-cTnI antibody levels could initiate or progress systolic dysfunction in NC/HT patients. However, this hypothesis remains as a deduction and remains to be proven. In contrast, we observed that anti-cTnT IgM and IgG antibodies were elevated only in a subgroup of patients with NC/HT and reduced EF. Despite the fact that anti-cTnT antibodies could be produced after immunization with cTnT in mice, no damage to myocardial cells could be demonstrated. While we observed higher anti-cTnT IgM and IgG in patients with NC/HT and reduced EF, no increase was observed in patients with NC/HT and normal systolic function. Based on previous experimental data, we assume that the effect of anti-cTnT antibodies on systolic dysfunction could be minimal. Despite intense concern, left ventricular noncompaction remains an enigmatic disease. NC/HT can be observed in isolation or accompanying congenital anomalies or muscular dystrophies. This condition is thought to arise from an embryonic arrest in myocardial compaction process, while acquired NC/HT was also reported. More importantly, the cause of ventricular dilatation and decline in systolic function is still not known. Our data shows that elevation in troponins and anti-troponin I autoantibodies, along with changes in ventricular geometry precede reduction in systolic function. However, our data is insufficient to reveal the nature of ventricular damage before appearance of heart failure or whether autoimmunity plays a role in cardiac dysfunction. A rise in antitroponin autoantibodies is not specific to NC/HTrelated ventricular failure and was previously shown to be related with other causes of dilated cardiomyopathy. Therefore, a rise in anti-troponin antibody levels could be anticipated in patients with reduced EF, regardless of initial etiologic factor. Nevertheless, our results did show a rise in autoantibody levels before development of systolic dysfunction, which diverts our study with previously conducted studies on DCM.