Prostate-specific antigen (PSA) is an established marker for the detection of
prostate cancer. Both elevated and diminished PSA have been reported during acute
myocardial infarction. It seems that when elevation of PSA occurs during acute
myocardial infarction (AMI), coronary lesions are frequent and often more severe than when a diminution of PSA occurs. PSA has been identified as a member of the human
kallikrein family of
serine proteases. In recent years, numerous observations have suggested that the activity of the kallikrein-kinin system is related to
inflammation and to
cardiovascular diseases. PSA
kallikrein, however, does not seem to have
kinin-generating activity. The inactive precursor form of PSA, proPSA, is converted rapidly to active PSA by Human
kallikrein 2 (hK2), suggesting an important in vivo regulatory function byhK2 on PSA activity. However, it has been reported that hK2 might not alone be able to activate proPSA in vivo, but there are also other
protease/
proteases involved in this event. Moreover, it seems that when elevation of
prostate-specific antigen occurs during AMI, it seems to relate to a higher occurrence of
major adverse cardiac events in the first 8 days after AMI than when a diminution of PSA occurs. It confirms a possible new intriguing scenario of the role of the PSA in AMI. Although these preliminary observations are suggestive, large studies need to be done to confirm these preliminary results.