Myocardial damage can be marked by knowing cardiac troponins levels in blood. Normally, they can’t be found in blood circulation until there are even small cardiac lessions. Otherwise, after a myocardial injury and the troponins enter 
blood circulation, this condition can be used for diagnosing Acut Coronary Syndromes.
The fact that they are normally not found in the circulation provides a high level of clinical sensitivity and specificity even when cardiac lesions are small. Thus, the cardiac troponins are parameter for disease classification and risk stratification, according to the one of article of American Heart Association Journal medio October 2006.
However, little is known about the long-term effects of the released troponins on cardiac function. Retrospective studies reported that PD-1 receptor–deficient mice developed autoantibodies to cardiac troponin I (TnI) and severe Dilated Cardiomyopathy (DCM). The researchers further found that administration of monoclonal antibodies to cardiac TnI induced heart dysfunction and dilation by chronic stimulation of Ca2+ influx in cardiomyocytes.
Ziya Kaya, MD and colleagues from Department of Internal Medicine III, Cardiology, University of Heidelberg, Germany took animal model experiment to study the effects on production of troponin-specific autoantibodies, cross-reactivity of autoantibodies, troponin-specific cellular response, inflammation, and expression of inflammatory cytokines, chemokines, fibrosis, heart function, ischemia/reperfusion injury, myocardial remodeling, and survival of the animals.
The results they obtained from their study suggest that the presence of autoantibodies against cardiac TnI in patients with acute coronary syndrome refers to an early induction of an autoimmune response to cardiac TnI, this condition means these patients may have a higher risk of heart failure due to inflammation in the myocardium. In other words, the titer of autoantibodies against cardiac TnI may be an additional risk indicator for heart failure.
Find complete information about Cardiac Tn I Induces Severe Autoimmune Inflammation in the Myocardium in the following PDF filetype (source: ahajournals.org).
