RESUMO
BACKGROUND: Clinical independent predictors of inducible sustained ventricular tachycardia (VT) during electrophysiologic study (EPS) are not known in patients with chronic Chagas' heart disease. The purpose of this investigation was to fill this gap. METHODS: The medical charts of 47 patients with a positive serology for Chagas' disease who had undergone EPS between September 2006 and July 2012 at our institution were reviewed. Reasons for the EPS were the presence of unexplained syncope, non-sustained ventricular tachycardia (NSVT) on either resting ECG or 24 h-Holter monitoring as well as a LVEF < 55% and > 35% at echocardiography. A stepwise logistic regression analysis was performed to identify noninvasive predictors of inducible sustained VT/ventricular fibrillation during EPS. RESULTS: On univariate analysis, syncopal episodes (p = 0.04), amiodarone therapy (p < 0.005), diastolic blood pressure (p = 0.03), creatinine serum levels (p < 0.001), potassium serum levels (p < 0.001), and lengthening of the QRS complex (p = 0.03) were associated with inducible sustained VT during EPS. In the multivariate model, amiodarone therapy (p = 0.03; hazard ratio = 10; Wald coefficient = 4.5; 95% confidence interval 1.2 to 85.2) was the only variable retained as independent predictor of inducible sustained VT during EPS. CONCLUSION: Amiodarone therapy was the only independent variable associated with sustained VT inducibility during EPS in patients with chronic Chagas' heart disease.
RESUMO
The present study used functional and electrophysiological approaches to investigate the mechanisms by which warifteine, a bisbenzylisoquinoline alkaloid isolated from Cissampelos sympodialis Eichl., causes vasorelaxation of the rat thoracic aorta. Warifteine (1 pmol/L-10 µmol/L) induced concentration-dependent relaxation (pD(2) = 9.40 ± 0.06; n = 5) of endothelium-intact aortic rings precontracted with noradrenaline (10-100 µmol/L). The relaxation effects were not attenuated by removal of the endothelium. Warifteine also induced the relaxation of prostaglandin F(2α) (1-10 mmol/L)-precontracted rings (pD(2) = 9.2 ± 0.2; n = 8). In contrast, the relaxant activity of warifteine was nearly abolished in high K(+) (80 mmol/L)-precontracted aortic rings. In preparations incubated with 20 mmol/L KCl or with the K(+) channel blockers tetraethylammonium (1, 3 and 5 mmol/L), iberiotoxin (20 nmol/L), 4-aminopyridine (1 mmol/L) or glibenclamide (10 µmol/L), the vasorelaxant activity of warifteine was markedly reduced. However, BaCl(2) (1 mmol/L) had no effect on the relaxant effects of warifteine. In vascular myocytes, warifteine (100 nmol/L) significantly increased whole-cell K(+) currents (at 70 mV). Under nominally Ca(2+) -free conditions, warifteine did not reduce extracellular Ca(2+) -induced contractions in rings precontracted with high K(+) or noradrenaline (100 µmol/L). Together, the results of the present study indicate that warifteine induces potent concentration-dependent relaxation in the rat aorta via an endothelium-independent mechanism that involves the activation of K(+) channels.