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


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.


CONCLUSIONS
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.
Leuschner
Florian
F
Department of Internal Medicine III, Cardiology, University of Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany.
Li
Jin
J
Göser
Stefan
S
Reinhardt
Lars
L
Ottl
Renate
R
Bride
Peter
P
Zehelein
Jörg
J
Pfitzer
Gabriele
G
Remppis
Andrew
A
Giannitsis
Evangelos
E
Katus
Hugo A
HA
Kaya
Ziya
Z
D054058:Acute Coronary Syndrome / Q000097:blood / Q000503:physiopathology*; D000818:Animals; D001323:Autoantibodies / Q000097:blood*; D002311:Cardiomyopathy, Dilated / Q000097:blood / Q000503:physiopathology*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D051379:Mice; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000503:physiopathology*; D017202:Myocardial Ischemia / Q000097:blood; D012189:Retrospective Studies; D013318:Stroke Volume / Q000502:physiology; D019210:Troponin I / Q000276:immunology*; D018487:Ventricular Dysfunction, Left / Q000097:blood / Q000503:physiopathology*
D001323:Autoantibodies; D019210:Troponin I