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Nihon Naika Gakkai Zasshi 01/2008; 96(12):2836-7, 2858-9.
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ABSTRACT: We tested our hypothesis that, in atrial flutter (AFL) dependent on the cavotricuspid isthmus (CTI), lower loop reentry is the common pathway route at the coronary sinus posterior site, and thus, dual loop reentry is a common circular pattern.
We studied 25 patients with CTI-dependent AFL, 16 with chronic counterclockwise atrial flutter (CCW-AFL) and 9 with clockwise atrial flutter (CW-AFL) and determined the precise reentry circuitry, especially for conduction patterns around the coronary sinus orifice, using electroanatomical mapping. We measured post pacing interval and tachycardia cycle length during entrainment from sites within the flutter circuit. The coronary sinus anterior pacing site was within the AFL circuit in 16 of the 25 CCW-AFL patients, and in 6 of the 9 CW-AFL patients. Both the coronary sinus anterior and posterior sites were within the AFL circuit in 8 of 16 CCW-AFL and 8 of the 9 CW-AFL patients. Results of 3-dimensional activation mapping suggest that all of these patients have a dual loop reentry circuit, and that coronary sinus posterior conduction broke through the eustachian valve/ridge.
Coronary sinus posterior conduction consisted of the flutter circuit and appeared to be critical for maintaining AFL.
Journal of Cardiology 08/2007; 50(1):1-10. · 1.28 Impact Factor
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ABSTRACT: The objective of the present study was to investigate the differential activation of protein kinase C between ischemic (IPC) and pharmacological preconditioning (PPC) in the rabbit heart. Control, IPC, diazoxide (Diaz), and chelerythrine (Chel)+IPC groups underwent prolonged coronary artery occlusion (CAO) for 30 minutes followed by 180 minutes' reperfusion (protocol I). In protocol II, sham, IPC-only, Diaz-only, and Chel+IPC-only groups did not undergo prolonged CAO. IPC was induced with 4 cycles of 5-min regional ischemia and 10-min reperfusion before prolonged CAO. Diaz (5 mg/kg) was administered 30 min before prolonged CAO. Chel (5 mg/kg) was administered 5 min before the IPC procedure. Infarct size was determined by tetrazolium staining. Assessment of protein kinase C (PKC) isoforms from a left ventricular (LV) sample was conducted by western blotting. Apoptosis in situ was determined by TUNEL assay. The infarction area in the IPC (11.6 +/- 1.0%) and Diaz (19.5 +/- 3.8%) groups was reduced significantly (p< 0.01, p< 0.05) relative to the control group (40.0 +/- 3.8%). The reduction by IPC was abolished by pretreatment with Chel. Apoptosis was significantly decreased (p< 0.01) in the IPC and diazoxide groups compared with the control and Chel+IPC groups (control: 4.78 +/- 0.56% vs. IPC: 2.00 +/- 0.38% vs. Diaz: 2.20 +/- 0.32% vs. Chel+IPC: 4.32 +/- 0.41%) and DNA laddering was attenuated in the IPC and Diaz groups. Membrane PKC-epsilon levels in the IPC and Diaz groups increased significantly relative to the control and Chel+IPC groups. Membrane PKC-epsilon levels in the IPC-only group showed greater increases than the Diaz-only and Chel+IPC-only groups. These findings suggest that whereas PPC suppresses apoptosis when diazoxide opens mitochondrial K(ATP) channels and then activates PKC-epsilon through ischemia-reperfusion, IPC activates PKC-epsilon in the particulate fraction prior to continuous ischemia-reperfusion. We concluded that the difference between IPC and PPC appears to consist in the difference in the timing of PKC-epsilon activation, though both IPC and PPC provide the cardioprotection in ischemia-reperfusion injury.
The Japanese Journal of Physiology 06/2003; 53(3):173-80. · 1.04 Impact Factor
