Abstract 3377: Autoantibodies against Cardiac Troponin I and their Impact on Improvement of Left Ventricular Function after Acute Myocardial Infarction
Background: Cardiac troponins in blood are the most preferred markers of myocardial damage. It has been shown that the application of antibodies against cardiac troponin I (cTnI-Ab) can induce dilation and dysfunction of the heart in mice. Furthermore we recently demonstrated that immunization with troponin I induces severe inflammation and fibrosis in the myocardium. In the presented study we performed a clinical trial to investigate the presence of cTnI-Ab in patients with acute myocardial infarction and their effect on the improvement of left ventricular function (LVF) over a period of 6–9 month.
Methods and Results: 68 patients with acute myocardial infarction were included in this study. Every patient underwent coronary angiography and was treated according to the current guidelines. LVF was determined by magnetic resonance imaging (MRI) conducted on a 1.5-T whole-body system 4–7 days and 6–9 months after myocardial infarction. An ELISA-Assay to measure cTnI-Ab-titers was established and serum from each patient was screened for the presence of cTnI-Ab. Out of 68 tested patients 8 had positive cTnI-Ab-titers and 60 were negative. In average patients with positive cTnI-Ab-titers had no improvement of LVF over the follow up period of 6–9 month (+0,5% ±4,4). In contrast patients with negative cTnI-Ab-titers showed considerable improvement of LVF (+10,6% ±2,1; p=0,09). Overall, only 1 out of 8 (12,5%) patients with positive cTnI-Ab but 28 out of 60 patients with negative cTnI (46,7%) showed positive remodelling with a significant improvement of LVF over 10% over the follow up period of 6–9 month (p= 0,07).
Conclusion: Our results suggest that the presence of cTnI-Abs in patients with acute myocardial infarction may have an impact on the improvement of the LVF over a study period of 6–9 months. These findings may aid in initiating further (clinical) studies with more patient to investigate the role of antibodies to cTnI during acute cardiac damage in postinfarct remodelling and its role in heart failure.