Serum Heparanase Level Is Decreased in Stable Coronary Artery Disease.

OBJECTIVE: Heparanase (HPA), mammalian endo-ß-D-glu-cu-ronidase, separates heparan sulfate chains of proteoglycans and changes the structure of the extracellular matrix. We investigated whether serum levels of HPA differ in patients with stable coronary artery disease (SCAD) and subjects with normal coronary arteries. METHODS: This study enrolled 92 patients with SCAD and 34 controls with normal coronary arteries. Levels of HPA were measured by a commercially available human HPA enzyme-linked immunosorbent assay kit. RESULTS: Serum HPA levels were significantly lower in the SCAD group (137.5 [104.1-178.9] vs. 198.8 [178.2-244.9] pg/mL; p < 0.001). Serum HPA levels were significantly higher in subjects with diabetes mellitus (DM) compared to those without DM (p = 0.008). Levels of HPA were lower in the SCAD group, both in the diabetic and nondiabetic subgroups, as compared to controls (p < 0.001 for both subgroups). Levels of HPA positively correlated with fasting blood glucose (FBG) (r: 0.42; p < 0.001). In multiple logistic regression analysis, serum HPA level (odds ratio [OR]: 0.975; 95% confidence interval [CI]: 0.966, 0.985; p < 0.001) and FBG (OR: 1.028; 95% CI: 1.010, 1.047; p = 0.002) were independently associated with SCAD. The receiver operating characteristic curve showed that HPA levels less than 160.6 pg/mL predicted SCAD with 65% sensitivity and 97% specificity (AUC: 0.80; 95% CI: 0.728, 0.878; p < 0.001). CONCLUSION: Diabetes and FBG levels were closely associated with serum levels of HPA. Low serum levels of HPA may predict SCAD in both diabetic and nondiabetic populations.

Heparanase is a predictive marker for high thrombus burden in patients with ST-segment elevation myocardial infarction.

Objective: Heparanase (HPA) is an endo-ß-D-glucuronidase capable of degrading heparin sulphate (HS) and heparin side chains. HPA plays a role in tumour growth, angiogenesis, cell invasion and in activation of the coagulation system. We aimed to investigate the relationship between HPA and thrombus burden (TB) in patients with ST-Segment Elevation Myocardial Infarction (STEMI). Methods: This prospective study enrolled 187 patients with STEMI who were treated with primary percutaneous coronary intervention (pPCI). Blood samples were taken to determine serum HPA levels prior to coronary angiography and heparin administration. Serum HPA analysis was performed with a commercially available Human Elisa kit. Results: Patients were divided into two groups: high TB (n:58) and low TB (n:129) group. Serum HPA levels were significantly higher in patients with high TB than low TB [250.1 (188.5-338.1) vs. 173.6 (134.3-219.8) pg/mL] (p < 0.001). Serum HPA levels were higher in patients with no-reflow phenomenon compared with others [(409.3 (375.6-512.5) pg/mL vs. 186.2 (144.2-247.4) pg/mL, p < 0.001]. In multiple logistic regression analysis HPA was a predictor of high TB. Conclusion: Elevated HPA level in patients with STEMI is related to high TB. Furthermore, increased HPA level may be associated with thrombotic complications such as no-reflow phenomenon in patients with STEMI.