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Br Heart J. Dec 1992; 68(6): 589–595.
PMCID: PMC1025690
Reappraisal of the coupling interval of ventricular extrasystoles as an index of ectopic mechanisms
Yuji Murakawa, Hiroshi Inoue, Tadashi Koide, Akira Nozaki, and Tsuneaki Sugimoto
Second Department of Internal Medicine, Tokyo University Hospital, Tokyo, Japan
Department of Cardiology, Kanto Central Hospital, Tokyo, Japan
Objective—A mathematical model of modulated ventricular parasystole based on the relation between the coupling interval and the preceding RR interval was developed in an attempt to distinguish between parasystolic automaticity and other mechanisms.
Mathematical model—The relation between the coupling interval and the preceding RR interval was examined by plotting the coupling interval of each extrasystole against the preceding RR interval (coupling interval/RR diagram). The coupling interval/RR diagrams obtained from simulations with various modulation modes suggested that the parasystolic mechanism was likely when the dots representing extrasystoles appeared as discrete clusters. In contrast, a linear horizontal accumulation of dots indicated a non-parasystolic mechanism.
Clinical observation—To verify the validity of the simulations, 24 hour electrocardiographic recordings from 60 patients with frequent ventricular extrasystoles (>1000/day) were analysed to determine whether the extrasystoles showed intrinsic periodicity. Intrinsic periodicity indicative of a parasystolic mechanism was seen in 14 (93%) of 15 patients in whom the coupling interval/RR diagram was characteristic of a parasystolic mechanism. When the coupling interval did not change (variability <200 ms) over a wide range of RR intervals (>700 ms) intrinsic periodicity was never identified (0/17). Parasystolic automaticity was the likely mechanism in 11 of the remaining 28 patients (39·3%) in whom coupling interval/RR diagrams were not definitive.
Conclusion—These data indicate that definite patterns of coupling interval/RR diagrams can be used to distinguish between parasystolic and non-parasystolic mechanisms.
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