These results indicate that AF itself enhances platelet aggregation and coagulation, which are influenced by the duration of AF. The acceleration of platelet activity and coagulability occurred 12 h after the occurrence of AF.

No abstract

SUMMARYTo clarify whether inflammation is a cause or consequence of atrial fibrillation (AF), we measured high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-α) before and after pharmacological cardioversion in 15 patients with paroxysmal AF. Levels of hs-CRP, IL-6, and TNF-α after cardioversion were significantly higher than those in controls (P < 0.05). Furthermore, the levels of these indices did not differ significantly even at 24 hours and 2 weeks after cardioversion. These results suggest that inflammation is a causative agent of paroxymal AF. (Jpn Heart J 2004; 45: 441-445)

His-bundle pacing gives a more physiological ventricular contraction in comparison to right ventricular apical pacing. However the problems of lead fixation and stability of long-term His-bundle pacing are yet unsolved. We used six adult beagles, in which a screw-in lead was anchored in the His-bundle region for observation of the pacing conditions and histopathologic changes of the conduction system over the course of 2 months. In the results, a satisfactory fixation was obtained using a conventional screw-in lead and no histological influence on the conduction system was observed. The pacing threshold at the time of implantation was 1.15 +/- 0.69 V (3.23 +/- 3.08 mA) in the pulse width of 0.5 ms. R wave amplitude, the impedance and slew rate were 7.28 +/- 2.04 mV, 409 +/- 102 Ohm, and 0.65 +/- 0.41 V/s, respectively. Two months later, these parameters changed to 2.83 +/- 1.06 V (10.4 +/- 5.71 mA), 5.63 +/- 1.62 mV, 310 +/- 71.3 Ohm, and 0.49 +/- 0.22 V/s, respectively. These results suggest the feasibility of clinical application of permanent His-bundle pacing.

To examine both of the target vessels and the optimal time of their endothelial denudation to study vascular restenosis after balloon injury in cholesterol-loaded rabbits, we made 36 atherosclerotic rabbits by feeding a hypercholesterol diet, and histologically examined the onset time and the development of atherosclerosis. Atheromatous changes were observed first after the 5th week in the thoracic aorta from the start of the diet, and then extended to the abdominal aorta, coronary artery with time. The atherosclerotic lesions in the thoracic aorta and the proximal portion of the coronary artery showed high-grade concentric intimal thickening with luminal stenosis. The abdominal aortic lesion mildly progressed. In the renal, carotid and femoral arteries, in contrast, slight atheroscleromatous changes developed during the diet period. These results suggest that the thoracic and abdominal aortas and the coronary artery would be suitable as target vessels to study vascular restenosis after balloon injury, and the endothelial denudation of these vessels should be performed between the 8th and 15th week in this diet protocol for an accurate analysis.