Procalcitonin (PCT) levels are below the detection level in healthy subjects, while pre-procalcitonin mRNA is over expressed in human medullar thyroid carcinoma, in small cell lung tumor, and occasionally in other rare neuroendocrine tumors such as phaeochromocytoma. PCT is known as a sensitive and specific biomarker for bacterial sepsis, being produced by extra-thyroidal parenchymal tissues, mainly hepatocytes. The increase in plasma level correlates with the severity of infection and the magnitude and the time course of its increase can be strictly related to the patient's outcome, and to the bacterial load. So far, data on serum PCT levels in patients with cardiogenic shock and in those with acute coronary syndromes (ACS) are scarce and controversial. While some studies report that PCT levels are increased in ACS patients on admission, other investigations document that plasma PCT concentrations are in the normal range. We recently reported that the degree of myocardial ischemia (clinically indicated by the whole spectrum of ACS, from unstable angina to cardiogenic shock following ST-elevation myocardial infarction) and the related inflammatory-induced response are better reflected by C-reactive protein (which was positive in most acute cardiac care patients of all our subgroups) than by PCT, which seems more sensitive to a higher degree of inflammatory activation, being positive only in patients with cardiogenic shock. Few studies investigated the dynamics of PCT in cardiac acute patients, and, despite the paucity of data and differences in patients' selection criteria, an increase in PCT values seems to be associated with the development of complications. In acute cardiac patients, the clinical values of procalcitonin rely not on its absolute value, but only on its kinetics over time.