for evaluating patients

Background: The prognosis of pulmonary hypertension (PH) is not satisfactory, even though several speciﬁc drugs have been available. Although noninvasive techniques such as echocardiography and MRI are widely used for assessing the severity of PH, there are still data lacking on the relation between noninvasive testings and prognostic factors. Purpose: We aimed to clarify potential relationship between hemodynamics at rest or exercise capacity and echocardiographic parameter in patients with PH. Methods and results: We performed transthoracic echocardiography, right heart catheterization, and cardiopulmonary exercise testing in 53 PH patients. Left ven- tricular end-diastolic dimension (LVDd), early diastolic velocity of the septal mitral annulus (septal e (cid:8) ), tricuspid regurgitation peak gradient (TRPG), and tricuspid annular plane systolic excursion (TAPSE) were signiﬁcantly complications (such as acute stroke). It was shown a signiﬁcant increase in risk (p=0.0295) for the PAPS carriers of the mutant allele of methylenetetrahydrofolate gene, consistent with the data that DNA polymorphisms in folate cycle lead to hyperhomocysteinemia signiﬁcant risk factor of thrombosis including arterial. Conclusion: The presence of mutations in the hemostatic system causes the development of a hypercoagulable syndrome, the formation of heart valves disease and development of thromboembolic complications. Carriage C677T mutation in methylenetetrahydrofolate signiﬁcantly increases the risk of PAPS. The introduc- tion of genetic testing allows you to create risk groups among PAPS patients who develop individual schemes of prevention and treatment. and cell invasion. Heparanase is also di- rectly involved in the activation of the coagulation system, interacting with tissue factor and enhancing the generation of factor Xa. Recent reports have described the procoagulant activity of heparanase in several arterial and venous thrombotic diseases. In this study, we aimed to investigate the role of heparanase in patients with prosthetic valve thrombosis (PVT) in relation to thrombus burden, throm-boembolism, and treatment success with unfractionated heparin (UFH) in these patients. Methods: This prospective and observational study enrolled 79 PVT patients (mean age:49.8±13.5 years, female:51) with a thrombus diameter more than 10 mm who were treated with UFH infusion and 82 healthy controls (mean age: 49.9±14.3 years, female:50). The diagnosis of PVT and efﬁcacy of the treatment were evaluated by serial transthoracic and transesophageal echocardiography. Patients received UFH infusion with a target activated partial thromboplastin time of 60 to 70 seconds until ﬁnal success for maximum 28 days. In order to detect heparanase, plasma samples were collected from patients at baseline and after the UFH treatment and from controls at baseline only. Plasma samples were tested for heparanase levels by heparanase enzyme-linked immunosorbent as-say. Results: The patient group included 12 aortic, 51 mitral, 13 aortic+mitral and 3 tricuspid PVT patients with 18 obstructive (OT) and 61 non-obstructive thrombosis (NOT). The patients received UFH infusion for a median time of 15 (7–20) days. The UFH treatment was successful in 37 (46.8%) patients. The baseline heparanase levels were higher in the patient group than the controls [0.29 (0.21– 0.71) vs 0.25 (0.17–0.33) pg/mL; p=0.002]. There was a signiﬁcant increase in heparanase levels after UFH treatment [0.29