RESUMO
Bundle branch re-entry (BBR)-ventricular tachycardia (VT) is relatively rare with an incidence of about 6% in sustained monomorphic VT series. However, physicians unexpectedly encounter it in clinical practice. BBR-VT is associated with serious hemodynamic decompensation, and the clinical presentation in approximately 75% of patients with inducible BBR-VT is syncope or cardiac sudden death. Thus, precise mapping of His-Purkinje and bundle branch potentials is necessary for an accurate diagnosis and treatment of re-entrant mechanisms especially for BBR-VT. However, simultaneous recording of both the left-bundle (LB) and right-bundle (RB), as well as His-bundle (HB), potentials is often difficult during tachycardia. Here we report the clear documentation of the activation sequence of the His-Purkinje system during BBR-VT, which could be readily and completely treated by radiofrequency catheter ablation in a myotonic dystrophy patient.
Assuntos
Fascículo Atrioventricular/fisiopatologia , Eletrocardiografia , Distrofia Miotônica/complicações , Ramos Subendocárdicos/fisiopatologia , Taquicardia Ventricular/diagnóstico , Adulto , Ablação por Cateter , Eletrofisiologia , Feminino , Humanos , Taquicardia Ventricular/etiologia , Taquicardia Ventricular/cirurgia , Resultado do TratamentoRESUMO
BACKGROUND AND OBJECTIVE: Use of HMG-CoA reductase inhibitors (statins) and angiotensin II type 1 (AT(1)) receptor antagonists reduces the incidence of cardiovascular events. The cytokines macrophage colony-stimulating factor (M-CSF) and transforming growth factor (TGF)-beta may exert proatherogenic and antiatherogenic effects, respectively. In this study, we examined whether treatment with a statin or an AT(1) receptor antagonist alters M-CSF and TGF-beta levels in patients with coronary artery disease. METHODS: Twenty-seven consecutive patients with coronary artery disease were randomly assigned to the following three treatment groups for 8 weeks: simvastatin 5 mg/day (n = 10); losartan 50 mg/day (n = 9); or control (usual treatment; n = 8). Blood samples were collected before and after treatment. RESULTS: Clinical characteristics and baseline cytokine levels were comparable among the three groups. Serum levels of M-CSF were significantly decreased only in the simvastatin group (from 403 +/- 71 to 303 +/- 116 pg/mL; p = 0.009). Plasma levels of TGF-beta were significantly increased only in the losartan group (from 5.01 +/- 1.13 to 7.50 +/- 3.83 ng/mL; p = 0.021). Simvastatin decreased serum M-CSF levels independently of changes in total cholesterol or low-density lipoprotein-cholesterol. CONCLUSIONS: The results of this study indicate that simvastatin decreases serum levels of M-CSF while losartan increases plasma levels of TGF-beta, suggesting that the two drugs may have different anti-atherosclerotic properties.