The presence of ERP heterogeneity and anisotropic conduction properties within the PV and at the PV-LA junction may be crucial to promote re-entry formation and thus might play an important role as a substrate for the maintenance of AF.

A significant shortening of P-wave duration by P-wave signal-averaged ECG can be used as an indicator for successful PV isolation. These findings suggest that activation of the PV muscle sleeves may be an important component of the terminal portion of the P-wave on surface ECG.

KUMAGAI, K., ET AL.: Role of Rapid Focal Activation in the Maintenance of Atrial Fibrillation Origi nating from the Pulmonary Veins. Most episodes of focal atrial fibrillation (AF) can be initiated by pre mature beats originating from the pulmonary veins (PV). However, the role of rapid focal activation in the maintenance of AF is unclear. Thirty-two patients with focal AF who underwent focal ablation of trigger ing ectopic beats were studied. Bipolar electrograms from all four PVs were recorded simultaneously.The cycle length (CL) of RFA at sites that triggered AF was measured at AF onset, after 5 minutes of sustained AF, and just before the spontaneous termination of 32 episodes of nonsustained AF. Fifteen episodes of sustained AF (> 10 minutes) and 17 episodes of nonsustained AF (5-120 seconds, mean 56 ± 59 seconds) were analyzed. In sustained AF, the mean CL of RFA in the PV from which it originated was not signifi cantly different than in the other PVs, and RFA was continuously observed. In nonsustained AF, the mean CL of RFA in a PVfrom which it originated was significantly shorter than in other PVs and, when RFA dis appeared, AF terminated. RFA in 1 PV induced RFA in another PV. In conclusion, widespread conduc tion of RFA from a PV at its source to the other sites may be necessary for the sustenance of AF. A PV in teraction, a RFA triggering another, may be involved in the maintenance of AF. RFA arising from PVs is important not only as a trigger of onset, but also in the maintenance of

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Aims: Amino acids, especially branched chain amino acids (BCAAs), have important regulatory roles in protein synthesis. Recently studies revealed that BCAAs protect against ischemia/reperfusion (I/R) injury. We studied the signaling pathway and mitochondrial function affecting a cardiac preconditioning of BCAAs.Main methods: An in vivo model of I/R injury was tested in control, mTOR +/+ , and mTOR +/-. Mice were randomly assigned to receive BCAAs, rapamycin, or BCAAs + rapamycin. Furthermore, isolated cardiomyocytes were subjected to simulated ischemia and cell death was quantified.Biochemical and mitochondrial swelling assays were also performed. Key findings: Mice treated with BCAAs had a significant reduction in infarct size as a percentage of the area at risk compared to controls (34.1 ± 3.9% vs. 44.7 ± 2.6%, P = 0.001), whereas mice treated with the mTOR inhibitor rapamycin were not protected by BCAA administration (42.2 ± 6.5%, vs. control, P = 0.015). This protection was not detected in our hetero knockout mice of mTOR. Western blot analysis revealed no change in AKT signaling whereas activation of mTOR was identified. Furthermore, BCAAs prevented swelling which was reversed by the addition of rapamycin. In myocytes undergoing simulated I/R, BCAA treatment significantly preserved cell viability (71.7 ± 2.7% vs. 34.5 ± 1.6%, respectively, p < 0.0001), whereas rapamycin prevented this 4 BCAA-induced cardioprotective effect (43.5 ± 3.4% vs. BCAA, p < 0.0001).Significance: BCAA treatment exhibits a protective effect in myocardial I/R injury and that mTOR plays an important role in this preconditioning effect.