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January 1, 2003Circulation Journal1 citationsOpen Access

Effects of Flecainide on the Electrophysiological Properties of Atrial Vulnerability in Humans

YYYasuhiro YoshigaASAkihiko ShimizuTYToshihiko Yamagata

Key Result

Intravenous flecainide significantly prolonged the effective refractory period of the right atrium (202 to 238 ms, p<0.001) in patients with baseline repetitive atrial firing.

Study Design

Type

Observational (n=38)

Structured PICO

Does intravenous flecainide alter the electrophysiological properties of atrial vulnerability in humans?

P
Population
38 patients undergoing electrophysiological measurements, divided into 2 groups based on whether repetitive atrial firing (RAF) was induced at baseline.
I
Intervention
Intravenous flecainide (2 mg/kg per 10 min)
C
Comparator
Baseline measurements (before flecainide administration)
O
Outcome
Changes in electrophysiological characteristics of the right atrium (effective refractory period, maximum conduction delay, repetitive atrial firing zone, fragmented atrial activity zone, and conduction delay zone)surrogate

Flecainide alters atrial electrophysiological properties, preferentially affecting patients with baseline repetitive atrial firing by prolonging the effective refractory period and reducing vulnerability zones.

Main Result

Absolute Event Rate: 238% vs 202%

p-value: p=<0.001

Abstract

The aims of this study were to evaluate the changes in the electrophysiological characteristics of the right atrium after the administration of flecainide and to clarify whether flecainide has a selective effect on human atrial tissue. Electrophysiological measurements were made in 38 patients, before and after intravenous administration of flecainide (2 mg/kg per 10 min). The effective refractory period of the right atrium (ERP-A), maximum conduction delay (Max.CD), repetitive atrial firing zone (RAFZ), fragmented atrial activity zone (FAAZ), and conduction delay zone (CDZ) were studied in the patients who were divided into 2 groups based on whether repetitive atrial firing (RAF) was induced in the baseline study. Flecainide significantly prolonged the ERP-A (202+/-22 to 238+/-33 ms, p<0.001) and shortened Max.CD (77+/-17 to 63+/-32 ms, p<0.05) in the patients with RAF, but not in those without RAF in the baseline study. After flecainide administration, there were significant reductions in the RAFZ (43+/-22 to 13+/-19 ms, p<0.0001), FAAZ (51+/-22 to 28+/-26 ms, p<0.001) and CDZ (70+/-21 to 48+/-30 ms, p<0.01) in the patients with RAF. However, atrial fibrillation (AF) was induced by stimulation after flecainide in 2 patients without RAF in the baseline study. There was a significant negative correlation between the ERP-A in the baseline study and the change in the ERP-A upon flecainide administration (r=0.45, p<0.01). Flecainide may preferentially activate the substrate for AF and RAF, but that action is mainly based on the electrophysiological characteristics found in the baseline study.

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Cite This Study

Yoshiga et al. (2003) conducted an observational in Patients undergoing electrophysiological study (n=38). Flecainide vs. Baseline was evaluated on Effective refractory period of the right atrium (ERP-A) in patients with RAF (p=<0.001). Intravenous flecainide significantly prolonged the effective refractory period of the right atrium (202 to 238 ms, p<0.001) in patients with baseline repetitive atrial firing.

synapsesocial.com/papers/6a16c2081375058a29054bebhttps://doi.org/10.1253/circj.67.437
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