PMID- 1283888
OWN - NLM
STAT- MEDLINE
DCOM- 19930325
LR  - 20190824
IS  - 0021-4868 (Print)
IS  - 0021-4868 (Linking)
VI  - 33
IP  - 5
DP  - 1992 Sep
TI  - Mexiletine and disopyramide suppress ventricular premature contractions (VPC) 
      irrespective of the relationship between the VPC and the underlying heart rate.
PG  - 665-78
AB  - The effects of mexiletine (300 mg/day, 24 patients) and disopyramide (300 mg/day, 
      20 patients) on ventricular premature contractions (VPCs) were studied using a 
      24-hour ambulatory electrocardiogram. The VPC frequency was evaluated as a 
      function of the underlying heart rate (HR). The VPC-HR correlation was classified 
      into 2 major types, depending on whether the frequency of the VPC increased with 
      the increased HR (positive type) or not (nonpositive type). The effects of the 
      drugs were assessed based on the VPC-HR correlation and on the percent reduction 
      of the VPC frequency. Mexiletine and disopyramide significantly decreased the 
      frequency of the VPCs of both the positive and nonpositive types. Each drug was 
      assumed to be effective when the percent reduction of the VPC frequency exceeded 
      70%. Mexiletine (300 mg/day) was 58.5% effective in positive type patients and 
      33.3% effective in nonpositive type patients, with a total efficacy of 45.8%. 
      Disopyramide was effective in 50% of total cases with 44.4% in positive type 
      patients and 54.5% in nonpositive type patients. However, the efficacy of these 
      drugs on the 2 different types of VPCs was the same statistically. The findings 
      strikingly contrasted those obtained with diltiazem and atenolol, which 
      predominantly suppressed VPCs of the positive type which share similar 
      characteristics with a triggered activity in vitro. We conclude that the mode of 
      action of class I antiarrhythmics on the VPCs differs from that of class II or IV 
      antiarrhythmics, as viewed from the VPC-HR relationship, and that the difference 
      probably comes from the different arrhythmogenesis for positive and nonpositive 
      types of VPCs, in addition to the different electrophysiological actions of 
      mexiletine and disopyramide.
FAU - Saikawa, T
AU  - Saikawa T
AD  - Department of Medicine, Oita Medical University, Japan.
FAU - Nakagawa, M
AU  - Nakagawa M
FAU - Takahashi, N
AU  - Takahashi N
FAU - Ishida, S
AU  - Ishida S
FAU - Fujino, T
AU  - Fujino T
FAU - Ito, M
AU  - Ito M
FAU - Shimoyama, N
AU  - Shimoyama N
FAU - Hara, M
AU  - Hara M
FAU - Yonemochi, H
AU  - Yonemochi H
FAU - Maeda, T
AU  - Maeda T
AU  - et al.
LA  - eng
PT  - Clinical Trial
PT  - Comparative Study
PT  - Journal Article
PT  - Randomized Controlled Trial
PL  - Japan
TA  - Jpn Heart J
JT  - Japanese heart journal
JID - 0401175
RN  - 1U511HHV4Z (Mexiletine)
RN  - GFO928U8MQ (Disopyramide)
SB  - IM
MH  - Cardiac Complexes, Premature/diagnosis/*drug therapy/physiopathology
MH  - Disopyramide/*therapeutic use
MH  - Electrocardiography, Ambulatory/methods
MH  - Female
MH  - Heart Rate/*physiology
MH  - Humans
MH  - Male
MH  - Mexiletine/*therapeutic use
MH  - Middle Aged
MH  - Signal Processing, Computer-Assisted
EDAT- 1992/09/01 00:00
MHDA- 1992/09/01 00:01
CRDT- 1992/09/01 00:00
PHST- 1992/09/01 00:00 [pubmed]
PHST- 1992/09/01 00:01 [medline]
PHST- 1992/09/01 00:00 [entrez]
AID - 10.1536/ihj.33.665 [doi]
PST - ppublish
SO  - Jpn Heart J. 1992 Sep;33(5):665-78. doi: 10.1536/ihj.33.665.