Shigeru Amitani

Atrial fibrillation activates platelets and coagulation in a time-dependent manner: A study in patients with paroxysmal atrial fibrillation

OBJECTIVES To determine whether atrial fibrillation (AF) alone affects the fibrinocoagulation system, we examined the relation between fibrinocoagulation activity and duration of AF in patients with paroxysmal AF (PAF). BACKGROUND Patients with chronic AF are at higher risk for stroke and a hypercoagulative state. It is not clear whether this hypercoagulative state is attributable to AF alone or to the underlying disease. There are no reports on the fibrinocoagulation properties in PAF. METHODS Fibrinocoagulation variables in 21 patients with PAF were measured during AF and 7 days after recovery of sinus rhythm. There were positive correlations between the duration of AF and beta-thromboglobulin, platelet factor 4, thrombin-antithrombin III complex and fibrinogen. These variables increased significantly 12 h after the occurrence of PAF; thus, patients were classified into two groups according to the duration of PAF: PAF-I group (< 12 h, n = 10), PAF-II group (> or = 12 h, n = 11). Nine age-matched, healthy subjects formed the control group. RESULTS Levels of beta-thromboglobulin and platelet factor 4 were significantly higher (p < 0.001) by two-way repeated measures analysis of variance (ANOVA), and thrombin-antithrombin III complex and fibrinogen levels tended to be but were not significantly higher (p = 0.06, ANOVA), in the PAF-II group than in the PAF-I group. There were no significant differences between groups in activated partial thromboplastin time, D-dimer or plasmin inhibitor complex. CONCLUSIONS 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.

Experimental His‐Bundle Pacing: Histopathological and Electrophysiological Examination

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 ± 0.69V (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.