Comparison of computed tomography imaging with intraprocedural contrast esophagram: implications for catheter ablation of atrial fibrillation.

BACKGROUND: Computed tomography (CT) has been used to localize the esophagus before radiofrequency ablation (RFA) of atrial fibrillation (AF). OBJECTIVE: The purpose of this study was to compare esophageal imaging by CT versus esophagram. METHODS: CT imaging of the left atrium was performed in 57 patients 1 week before RFA and was imported into the CARTO mapping system. The electrophysiologist created a virtual shell of the left atrium and pulmonary veins (PVs) that was merged with the CT image; however, the CT-defined location of the esophagus was not displayed. The patient was then given 10 mL of oral contrast. Using fluoroscopy, an electroanatomic catheter tagged the esophageal borders outlined by esophagram. The CT-defined esophagus was then imported, and the borders were tagged on the merged map. In this manner, the esophagus borders by esophagram versus those by CT were compared. RESULTS: The maximum diameter of the esophagus by esophagram versus CT was not different (16.3 +/- 3.4 vs. 16.5 +/- 3.1 mm; P = .7). The esophagus was near the left PVs in 34 (62%), center in 13 (24%), and near the right PVs in eight (15%) patients. There was concordance between CT and esophagram in 48 of 55 patients (87%; P = .2). Ye, in 21 (44%) of 48 patients with concordant location, the CT-defined esophageal borders were separated from the esophagram-defined borders by >or=50% of the esophagus diameter. CONCLUSIONS: Reliance on remotely acquired CT images does not ensure adequate intraprocedural localization of the esophagus or enhance recognition of esophageal motility.

Tissue-specific pyruvate dehydrogenase complex deficiency causes cardiac hypertrophy and sudden death of weaned male mice.

Pyruvate dehydrogenase complex (PDC) plays an important role in energy homeostasis in the heart by catalyzing the oxidative decarboxylation of pyruvate derived primarily from glucose and lactate. Because various pathophysiological states can markedly alter cardiac glucose metabolism and PDC has been shown to be altered in response to chronic ischemia, cardiac physiology of a mouse model with knockout of the alpha-subunit of the pyruvate dehydrogenase component of PDC in heart/skeletal muscle (H/SM-PDCKO) was investigated. H/SM-PDCKO mice did not show embryonic lethality and grew normally during the preweaning period. Heart and skeletal muscle of homozygous male mice had very low PDC activity (approximately 5% of wild-type), and PDC activity in these tissues from heterozygous females was approximately 50%. Male mice did not survive for >7 days after weaning on a rodent chow diet. However, they survived on a high-fat diet and developed left ventricular hypertrophy and reduced left ventricular systolic function compared with wild-type male mice. The changes in the heterozygote female mice were of lesser severity. The deficiency of PDC in H/SM-PDCKO male mice greatly compromises the ability of the heart to oxidize glucose for the generation of energy (and hence cardiac function) and results in cardiac pathological changes. This mouse model demonstrates the importance of glucose oxidation in cardiac energetics and function under basal conditions.