Abstract

Some previous studies have reported contradictory evidence about the kinetics of total prostate-specific antigen (tPSA) after an acute myocardial infarction (AMI), observing either increased or decreases value [1–3]. No information is also available on the behaviour of free PSA (fPSA) and especially on the novel prostate cancer biomarker PSA isoform p2PSA [4] in patients with AMI, to the best of our knowledge. tPSA, fPSA and p2PSA were assessed on Access2 Immunoassay System analyzer (Beckman Coulter, Brea, CA, USA) in 24 consecutive male patients admitted to the local emergency department (ED) with suspected AMI. Blood was collected at admission, 6 and 12 h afterwards. None of the patients had clinical history, sign or symptoms suggestive of prostate disorders. The significance of differences was assessed by Kruskal–Wallis test (for continuous variables), and chi-squared test with Yates's correction for continuity (for categorical variables). A final diagnosis of AMI, defined according to established criteria [5], was achieved in 5 patients (21%). No significant difference between patients with AMI and those without was observed for the mean (±standarddeviation, SD)baselinevalues of tPSA (0.82±0.43vs 1.34± 0.92 ng/ml; p=0.14), fPSA (0.24±0.14 vs 0.40±0.32 ng/ml; p=0.17) and p2PSA (2.11±1.74 vs 4.59±2.89 pg/ml; p=0.06) at ED admission. Nevertheless, when calculating the ratio between the peak value recorded in the following 12 h and the baseline value at ED admission, a significant difference between patients with AMI and those without was found for the mean (±SD) p2PSA ratio (1.8±1.1 vs 1.0±0.2; pb0.01), but not for tPSA (1.1±0.5 vs 0.9±0.1; p=0.10) and fPSA (1.0±0.6 vs 0.9±0.2; p=0.19) ratios (Fig. 1). The value of p2PSA increased in 4/5 AMI patients (80%), as compared with 8/19 in patients without AMI (42%; pb0.01). At variance with previous studies, which reported that PSA values either increase or decrease after an AMI [2,3], the results of this preliminary investigation suggest that p2PSA might increase after AMI, whereas the concentrations of both tPSA and fPSA remain mostly unchanged. Notwithstanding the limited number of subjects studied, which precludes to draw definitive conclusions on this topic, the relationship between AMI and prostate biology is an appealing area of research that merits further scrutiny in larger clinical trials.

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