Thrombin activatable fibrinolysis inhibitor : its role in slow coronary flow.

BACKGROUND: The slow coronary flow (SCF) phenomenon is characterized by slow progression of angiographic contrast medium in the coronary arteries in the absence of stenosis in the epicardial vessels. The pathophysiological mechanisms of SCF phenomenon remain uncertain. Several hypotheses, however, have been suggested for SCF phenomenon, including an early form of atherosclerosis, small vessel dysfunction, dilatation of coronary vessels, imbalance between vasoconstrictor and vasodilatory factors, platelet function disorder, and inflammation. Atherosclerosis and inflammation are the most accepted mechanisms for the pathogenesis of SCF. Thrombin activatable fibrinolysis inhibitor (TAFI) was described as a new inhibitor of fibrinolysis recently and plays an important role in coagulation and fibrinolysis. In previous studies, the role of TAFI was associated with inflammation and evolution of atherosclerosis in coronary artery disease. There are no data available about TAFI levels in patients with SCF phenomenon investigated by angiography. Our goal was to evaluate TAFI antigen (Ag) levels in patients with SCF and to determine the association of the TAFI Ag level with traditional cardiovascular risk factors in our study. METHODS: The study group constituted 41 patients with angiographically confirmed SCF and 46 patients with normal coronary flow as the control group. The TAFI Ag levels of each patient were determined. RESULTS: Between the control and study group, a statistical difference in the levels of TAFI Ag (p < 0.05) was observed. The TAFI Ag level was significantly higher in the SCF group than the control group (132.21 ± 21.14 versus 122.15 ± 21.59). CONCLUSION: We have demonstrated that TAFI might be a risk factor for the development of SCF independently of conventional cardiovascular risk factors. In addition, TAFI Ag levels were positively correlated with C-reactive protein (CRP) known as an acute phase reactant. Our findings support the reports of previous studies that increased TAFI levels may be associated with inflammation. Further large studies are required to evaluate the importance of TAFI antigen levels in relation to the development of SCF.

Ocular pulse amplitude and retrobulbar blood flow change in dipper and non-dipper individuals.

PURPOSE: To evaluate ocular pulse amplitude (OPA), IOP values, and hemodynamic changes in the ophthalmic artery, central retinal artery, and short posterior ciliary artery in dipper and non-dipper patients. METHODS: A total of 59 right eye measurements of healthy subjects with normotensive were included to the study. Ambulatory blood pressure (BP) monitoring measurement (ABPM), Doppler imaging, and OPA measurements were performed in the same day. The patients in which systolic BP decreased during the nocturnal time by 10% of the diurnal BP or more were called dippers. A patient whose nocturnal systolic BP fell by <10% or even rose was defined as non-dipper. Color Doppler imaging was used for blood flow velocity assessment of ophthalmic, central retinal, and posterior ciliary arteries. For each artery, peak systolic and end-diastolic velocities (PSV and EDV, respectively), resistive index (RI), and pulsalite index (PI) were automatically calculated by the machine. Mean IOP and OPA values were calculated after three consecutive measurements. RESULTS: The mean OPA in non-dipper patients was significantly lower compared with that of dipper patients (P=0.011). There was no significant difference in IOP levels between groups. There was no significant difference in the PSV, EDV, RI, and PI in the ophthalmic, posterior ciliary, and central retinal arteries between the groups. CONCLUSION: Our study demonstrated that OPA level in non-dippers is lower than dippers. This may give additional information about the effect of BP changes on OPA values.

QT dispersion. Is it an independent risk factor for in-hospital mortality in patients with intracerebral hemorrhage?

Electrocardiographic repolarization changes, comprising QT prolongation, are most commonly seen after intracerebral hemorrhage. In this study in patients with intracerebral hemorrhage (ICH), QT dispersion and its daily changes were examined and the relation between QT dispersion and in-hospital mortality assessed. In 28 patients with intracerebral hemorrhage, diagnosed by computerized tomographic scanning, an ECG was obtained on the day of admission to hospital and then serial ECGs were recorded on the following four consecutive days. Blood electrolytes (K, Ca, Mg) were also analysed. The patients with intracerebral hemorrhage were followed until discharge or death (mean 14 +/- 4 days). QT, QT peak, and QT-QT peak dispersion were measured on simultaneous twelve lead electrocardiograms. Also, in 29 healthy subjects as a control group, five consecutive day serial electrocardiograms were recorded. There were no statistically significant differences between the study and control groups in terms of gender and age. During the five days, QT, QT peak, and QT-QTpeak dispersion values were significantly higher in patients with intracerebral hemorrhage than in the control subjects (p < 0.001). There were no statistically significant differences in two patient groups with intracerebral hemorrhage who died and who were discharged in terms of mean QT, QTpeak, and QT-QTpeak dispersion values. In conclusion, QT, QT peak, and QT-QTpeak dispersion values were significantly greater in patients with intracerebral hemorrhage than in the control subjects, but QT, QT peak, and QT-QT peak dispersions were not independent risk factors for in-hospital mortality in patients with intracerebral hemorrhage.