The effect of thrombolytic therapy on QT dispersion in acute myocardial infarction and its role in the prediction of reperfusion arrhythmias.

PURPOSE: We aimed to determine the effect of intravenous thrombolytic therapy on QT dispersion (QTd) and its role in the prediction of reperfusion arrhythmias. MATERIALS AND METHODS: Twenty patients with acute myocardial infarction (MI) were enrolled in the study. Measurements of QTd were carried out prior to thrombolytic therapy and before discharge. The patients were examined for ventricular arrhythmias with 24-h Holter electrocardiography monitoring after treatment and the relationship between ventricular arrhythmias and the QTd values in the early phase of MI was investigated. RESULTS: The values of QTd were significantly higher during the early phase of MI (60 ± 5.32 ms) than those in the late phase (53.35 ± 4.07 ms) (P = 0.032). There was no correlation between isolated, bigeminal, trigeminal and total ventricular premature beats, accelerated idioventricular rhythm (AIVR) with QTd values. However, the patients with sustained ventricular tachycardia (VT), prolonged VT and sustained AIVR had higher corrected QTd (92 ms 1/2 , 97.8 ms 1/2 , 81.7 ms 1/2 , respectively) than the patients without these arrhythmias (74 ms 1/2 , 56.3 ms 1/2 , 58.28 ms 1/2 , respectively) (P = 0.022, 0.013, 0.018). CONCLUSION: The values of QTd may be significantly reduced in the 1 st week of acute MI and measurement of QTd in the early phase of MI may have a correlation with the following reperfusion arrhythmias: Sustained VT, prolonged VT and AIVR.

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.