Comparison of left atrial dimensions by transesophageal and transthoracic echocardiography.

Transesophageal echocardiography (TEE) is an established cardiovascular diagnostic technique. Left atrial (LA) size, as measured by transthoracic echocardiography (TTE), is associated with cardiovascular disease and is a risk factor for atrial fibrillation, stroke, death, and the success of cardioversion. Assessment of LA size has not been as well validated on TEE as on TTE. We determined LA size measurements in four standard views in 122 patients undergoing TEE and TTE at the same setting. In this study, we found that measurement of LA dimensions by TEE suffers from significant limitations in all views except the basal long-axis view (mid-esophageal level) with transducer plane at 120-150 degrees. This view had the best correlation with transthoracic LA measurements: r = 0.79 for TEE long axis (CI 0.71-0.85), P <.0001.

Phenytoin teratogenesis: correlation between embryopathic effect and covalent binding of putative arene oxide metabolite in gestational tissue.

The possibility that phenytoin (DPH) teratogenesis is due to an arene oxide (epoxide) metabolite was examined. On gestational day 11, Swiss mice were given teratogenic doses of DPH (50, 75 and 100 mg/kg) with and without a nonteratogenic dose of 1,2-epoxy-3,3,3-trichloropropane (TCPO; 100 mg/kg), an epoxide hydratase inhibitor. TCPO significantly increased the incidence of DPH-induced cleft lip and palate and enhanced the embryolethality 2-fold over DPH alone. Four hours after treatment with 14C-DPH (75 mg/kg, 80-90 muCi) the covalent binding of DPH radioactivity in fetuses and placentae was enhanced 2-fold in groups cotreated with TCPO (100 mg/kg). Enhancement was still evident in placentae 24 hours after treatment. There was no effect of TCPO on maternal plasma DPH level, which was comparable to that found in clinical therapeutics (20-30 microgram/ml). Likewise, fetal and placental DPH uptake was not increased by TCPO. DPH teratogenesis is postulated to result from DPH-epoxide formation and covalent binding of epoxide, the ultimate teratogen, to constituents of gestational tissue.