SUMMARY OBJECTIVE: Different parameters on electrocardiograms (ECG) have been investigated to predict arrhythmia and mortality in patients with acute pulmonary embolism (APE). The acute effect of thrombolytic therapy (TT) on these parameters has not been investigated yet. METHODS: We examined the data of 83 patients who were evaluated as high-risk APE and discharged from the hospital after TT. First, the high-risk APE patients’ ECGs were compared with healthy control subjects (n = 55). After their admission and 24 hours later, the ECGs of patients with APE were compared. Heart rate, P-wave morphology, QRS duration, QT distance, Tp-e, and the index of cardiac electrophysiological balance (iCEB) were analyzed. RESULTS: Although P maximum was not different between the groups’ ECGs, heart rate, QT, QTc (corrected QT) interval, Tp-e intervals, Tp-e/QT ratio, and P wave dispersion were significantly higher in the APE group ( P values < 0.031). iCEB or iCEBc (corrected iCEB) values were lower in APE group ( P < 0.001). After TT, we determined a decrease in heart rate, Tp-e interval, and Tp-e/QT ratio ( P < 0.001). Although we detected a decrease in the QT and QTc interval and QT dispersion (QTd), QTd had no statistical significance (respectively P -value 0.013, 0.029, and 0.096). The iCEB and iCEBc levels were lower after TT ( P -value was 0.035 and 0.044 respectively). CONCLUSION: The QT, QTc, Tp-e interval, Tp-e/QTc ratio, iCEB, and iCEBc values significantly decreased after TT. It may be thought that effective TT causes partial improvement in ventricular repolarization in an early period.

Objective: Heparanase (HPA) is an endo-β-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.

Background Neurologic and liver involvement in Wilson's disease (WD) is well-documented, however, few reports demonstrated cardiac involvement. Tpe and Tpe/QT are new measures of ventricular repolarization which were recently suggested as predictor of arrythmogenesis. We aimed to evaluate ventricular depolarization and repolarization parameters including QT, QTc, Tpe intervals, Tpe/QT, Tpe/QTc ratios, and QT dispersion (QTd) in patients with WD. Materials and methods Thirty-five patients with WD and 30 healthy controls were included in the study. Patients were evaluated by a neurologist in addition to MR imaging. Twenty-one of 35 patients were diagnosed as neuroWilson (NW), whereas 14 patients as non-NW. ECG recordings were obtained using a 12-lead commercial device (Cardiac Science, Burdick s500,USA). All patients underwent standard echocardiographic evaluation. These two groups of patients and healthy controls were compared. Results There were no difference between patients with WD and healthy controls in terms of age sex, BMI, liver, and kidney functions where as patients with WD were anemic and thrombocytopenic. Left atrial, ventricular dimensions, left ventricular systolic, and diastolic functions were similar between patients and healthy control. QT interval was prolonged in patient group, however, QTc, Tpe intervals, Tpe/QT, and Tpe/QTc ratios and QTd did not differ between groups. When patients with NW and non-NW were compared, both QT and QTc intervals were significantly longer in patients with NW, however, Tpe interval, Tpe/QT and Tpe/QTc ratios, and QTd did not differ. Conclusion QT and QTc intervals are prolonged in patients with Wilson's disease and neurologic involvement.