| pubmed-article:19138808 | pubmed:abstractText | Coronary artery aneurysms are defined as coronary dilatations which exceed the diameter of normal adjacent segments by 1.5 times. Although more commonly associated with atherosclerosis, a variety of other acquired (eg, inflammatory, infectious, iatrogenic) or congenital causes have been identified that lead to impaired vessel media. A number of complications have been reported to occur during the course of the disease including thrombosis and distal embolization, myocardial ischemia and/or infarction, dissection, vasospasm, calcification, fistulization and rupture. Other complications relate to the size of the aneurysm and compression of adjacent structures. Prostate-specific antigen (PSA) is an established marker for detection of prostate cancer. Elevation of prostate-specific antigen as well as its diminution during acute myocardial infarction has also been reported. It seems that when elevation of prostate-specific antigen occurs during acute myocardial infarction, coronary lesions are frequent and often more severe than when diminution of prostate-specific antigen 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. We present a case of elevation of serum PSA concentration during acute myocardial infarction in a 64-year-old Italian man with significant coronary artery disease and coronary artery aneurysm. Also this case confirms previous findings and extends the evaluation of PSA during acute myocardial infarction. It confirms a possible new intriguing scenario of the role of the prostate-specific antigen in acute myocardial infarction. | lld:pubmed |
