Absence of auto-antibodies against cardiac troponin I predicts improvement of left ventricular function after acute myocardial infarction

Eur Heart J. 2008 Aug;29(16):1949-55. doi: 10.1093/eurheartj/ehn268. Epub 2008 Jun 13.


Aims: 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 auto-antibodies to cTnI are present in patients with acute coronary syndrome, but little is known about the clinical relevance of detected cTnI-Ab.

Methods and results: First, anti-cTnI and anti-cTnT antibody titres were measured in sera from 272 patients with dilated- (DCM) and 185 with ischaemic- (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 titre >/=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 titre >/=1:160 was detected. Ten out of 108 patients included in the follow-up study were tested positive for cTnI-Ab with IgG Ab titres >/=1:160. TnI-Ab negative patients showed a significant increase in left ventricular ejection fraction (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.

Conclusion: 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Coronary Syndrome / blood
  • Acute Coronary Syndrome / physiopathology*
  • Animals
  • Autoantibodies / blood*
  • Cardiomyopathy, Dilated / blood
  • Cardiomyopathy, Dilated / physiopathology*
  • Female
  • Follow-Up Studies
  • Humans
  • Male
  • Mice
  • Middle Aged
  • Myocardial Infarction / blood
  • Myocardial Infarction / physiopathology*
  • Myocardial Ischemia / blood
  • Retrospective Studies
  • Stroke Volume / physiology
  • Troponin I / immunology*
  • Ventricular Dysfunction, Left / blood
  • Ventricular Dysfunction, Left / physiopathology*


  • Autoantibodies
  • Troponin I