Abstract
The pathogenesis of ascending aortic aneurysm (AAA) involves many factors; elastin degradation could lead to initial dilation, and changes in the collagen structure predispose the aneurysm to rupture. Prolidase is an enzyme that catalyzes the final step of collagen breakdown by liberating free proline for collagen recycling. The enzyme activity may be a step-limiting factor in the regulation of collagen biosynthesis. Consequently, in this study we sought to determine serum prolidase activity in AAAs. Eighty consecutive patients with the diagnosis of hypertension or chest pain, referred for echocardiographic examination in the outpatient cardiology clinic, were included in the study. The subjects were grouped into three categories according to the aortic diameter; control group without aortic dilatation (≤ 3.7 cm, n = 20), medium (3.8-4.3 cm, n = 36), and large (≥ 4.4 cm, n = 24) group. We assessed the association of serum prolidase activity with the presence and severity of AAAs, clinical characteristics and laboratory parameters. Serum prolidase activity was significantly higher in the patients without aortic dilatation (1386.3 ± 320.5 U/L) compared to medium group (1212.0 ± 282.5 U/L) and large group (1072.2 ± 192.3 U/L): control group vs. medium group (P = 0.023) and control group vs. large group (P < 0.001). Ascending aortic diameter was inversely correlated with serum prolidase activity and in multivariate analysis, serum prolidase activity was the only independent predictor of aortic dilatation (β = −0.44, P = 0.006). In conclusion, the presence of AAAs is associated with low serum prolidase activity.
