Alternation of QRS Morphology and Effect of Radiofrequency Ablation in Idiopathic Ventricular Tachycardia

We performed electrophysiological studies in 13 patients with idiopathic VT and attempted radiofrequency (RF) catheter ablation in 4 of them.Results: VT was induced by programmed stimulation in all patients and the mean cycle length was 363 ± 58 msec. In 8 of 13 patients (62%), alternation of either the cycle length and/or morphology of VT was observed. Transient entrainment was achieved in all patients by rapid pacing from the right ventricular outflow tract so reentry was considered the underlying mechanism of VT. The site of earliest activation (EAS) during VT was located at the apicoposterior portion of the left ventricular septum and used as the target site for RF catheter ablation. Spikelike presystolic activity was detected 20–40 msec prior to the large deflection of the local electrogram in four patients. VT was terminated by a few seconds of RF current in all four patients, but subsequently new VTs with a slightly different morphology were induced in three of them and re-mapping showed a shift of the EAS. After additional RF ablation at the new EAS, VT was no longer induced. No complication was noted and VT did not recur during a follow-up period for a mean of 9.3 ± 5.2 months.Conclusion: RF catheter ablation seems useful and safe for idiopathic VT. The alternation of QRS morphology and the findings at the time of catheter ablation suggest that an alternative pathway or multiple exits may be present in some patients with idiopathic VT, because the change in VT morphology was associated with a shift of the EAS.     

A Case of Rectal Carcinoma with Elevated Serum Alpha-Fetoprotein

A gradual increase in serum alpha-fetoprotein (AFP) had beenobserved in a patient with liver cirrhosis and the complicationof rectal carcinoma was disclosed 18 months later. The concentrationof serum AFP decreased rapidly after removal of the tumor andreached a normal value within a month. The level of serum AFP has remained normal and the patient hasbeen well since the operation. There has been no clinical evidenceof the existence of a liver tumor and the production of AFPby the rectal carcinoma cells was suggested.     

PPARα activator irbesartan suppresses the proliferation of endometrial carcinoma cells via SREBP1 and ARID1A

Endometrial carcinoma (EMC) is associated with obesity; however, the underlying mechanisms have not yet been elucidated. Peroxisome proliferator-activated receptor alpha (PPARα) is a nuclear receptor that is involved in lipid, glucose, and energy metabolism. PPARα reportedly functions as a tumor suppressor through its effects on lipid metabolism; however, the involvement of PPARα in the development of EMC remains unclear. The present study demonstrated that the immunohistochemical expression of nuclear PPARα was lower in EMC than in normal endometrial tissues, suggesting the tumor suppressive nature of PPARα. A treatment with the PPARα activator, irbesartan, inhibited the EMC cell lines, Ishikawa and HEC1A, by down-regulating sterol regulatory element-binding protein 1 (SREBP1) and fatty acid synthase (FAS) and up-regulating the tumor suppressor genes p21 and p27, antioxidant enzymes, and AT-rich interaction domain 1A (ARID1A). These results indicate the potential of the activation of PPARα as a novel therapeutic approach against EMC.