Application of antibodies against cardiac troponin I (cTnI-Ab) can induce dilation and dysfunction of the heart in mice. Recently, we demonstrated that immunization with cTnI induces inflammation and fibrosis in myocardium of mice. Others have shown that autoanti-bodies to cTnI are present in patients with acute coronary syndrome. But little is known about the clinical relevance of detected cTnI-Ab. First, anti-cTnI and anti-cTnT antibody titers were measured in sera from 272 patients with dilated- (DCM) and 185 with ischemic- (ICM) cardiomyopathy. Secondly, 108 patients with acute myocardial infarction (AMI) were included for a follow-up study. Heart characteristics were determined by magnetic resonance imaging 4 days and 6 –9 months after AMI. Altogether, in 7,0% of patients with DCM and in 9,2% with ICM an anti-cTnI IgG antibody titer ≥1:160 was measured. In contrast, only in 1,7% of patients with DCM and in 0,5% with ICM an anti-cTnT IgG antibody titer ≥1:160 was detected. Ten out of 108 patients included in the follow-up study were tested positive for cTnI-Ab with IgG Ab titers ≥1:160. TnI-Ab negative patients showed a significant increase in LVEF and stroke volume 6 –9 months after AMI. In contrast, there was no significant increase in LVEF and stroke volume in TnI-Ab positive patients. We demonstrate for the first time that the prevalence of cTnI-Abs in patients with AMI has an impact on the improvement of the LVEF over a study period of 6 –9 months.
Does the rest electrocardiogram after myocardial infarction determine the predictive value of exercise-induced st depression? A 2 year follow-up study in a veteran population
