Can we assess an acute myocardial infarction in patients with acute coronary syndrome according to diagnostic accuracy of heat shock proteins?

Heat shock proteins (HSPs) have changed very little with evolution, suggesting that they play important role(s) in cellular survival. Specifically, HSPs protect cells from induced cell death. Their expression is triggered by heat or other stress, such as ischemia. HSPs provide protection against protein denaturation, although they slightly differ with respect to group affiliation. Release of HSPs from necrotic and ischemic cardiomyocytes into the intercellular space and plasma may correlate with the intensity of the pro-inflammatory response observed during and immediately after myocardial infarction. We hypothesized that the plasma concentration of particularly inducible forms of HSPs from different groups (HSP 90, HSP 70, HSP 60 and/or HSP 20) can be used as early specific markers for diagnosing myocardial infarction in patients with acute coronary syndrome. Our hypothesis is supported by the following data: (I) HSP expression occurs very early after acute coronary events; (II) HSP concentrations increase rapidly in the peripheral blood; (III) HSP concentrations correlate with markers of myocardial necrosis and pro-inflammatory biochemical parameters. The magnitude of the increase in plasma HSP concentrations over initial concentrations during the period of highest sensitivity and specificity of the assay could be important for early detection of myocardial infarction and distinguishing it from unstable angina. We suggest that these parameters, along with close observation of patients with chest pain, will assist providers who must differentiate between acute myocardial damage and other organ diseases.