• Mojca Remskar, Matija Horvat, Sergej Hojker, and Marko Noc.
• Center for Intensive Internal Medicine, University Medical Center, Ljubljana, Slovenia. marko.noc@mf.uni-lj.si
• Wien. Klin. Wochenschr. 2002 Mar 28; 114 (5-6): 205-10.

AbstractAcute myocardial infarction induces an inflammatory reaction. We related conventional inflammatory parameters including C-reactive protein, erythrocyte sedimentation rate, white blood cell count and axillary temperature to plasma concentrations of procalcitonin in patients with acute myocardial infarction. In a prospective-descriptive study, we evaluated 54 patients with acute myocardial infarction. During a time period of 8 days following myocardial infarction, C-reactive protein, erythrocyte sedimentation rate, white blood cell count and axillary temperature as well as the plasma concentrations of procalcitonin were measured. Maximal procalcitonin remained normal (below 0.5 microgram/L) in patients with uncomplicated acute myocardial infarction. This contrasted with results obtained from patients additionally afflicted by pulmonary edema and cardiogenic shock, in whom maximal procalcitonin increased up to 5.24 micrograms/L. Resuscitation after cardiac arrest and/or concomitant bacterial infection increased procalcitonin to a maximal value of 134 micrograms/L, which was independent of the severity of left heart failure. Conventional inflammatory parameters were all significantly increased even in the absence of cardiac and non-cardiac complications of acute myocardial infarction. In conclusion, procalcitonin increases in patients with acute myocardial infarction only if associated with severe left heart failure, resuscitation after cardiac arrest or in the presence of bacterial infections. Thus, procalcitonin may help to elucidate the etiology of systemic inflammatory response during the early course of acute myocardial infarction.

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