Dynamic coupling between heart rate and ventricular repolarisation

Authors

HALAMEK Josef JURAK Pavel VILLA M. SOUČEK Miroslav FRÁŇA Petr NYKODYM Jiří EISENBERGER Martin LEINVEBER Pavel VONDRA Vlastimil SOMERS V.K. KÁRA Tomáš

Year of publication 2007
Type Article in Periodical
Magazine / Source Biomedizinische Technik
MU Faculty or unit

Faculty of Medicine

Citation
Doi http://dx.doi.org/10.1515/BMT.2007.044
Field Cardiovascular diseases incl. cardiosurgery
Keywords heart rate; ventricular repolarisation
Description A novel model for the coupling between ventricular repolarisation and heart rate (QT/RR) is presented. It is based upon a transfer function (TRF) formalism that describes the static and dynamic properties of this coupling, i.e., the behaviour after a sudden change in heart rate. Different TRF models were analysed by comparing their capability to describe experimental data collected from 19 healthy volunteers using several RR stimulation protocols: (i) rest with deep breathing at 0.1 Hz; (ii) tilt with controlled breathing at 0.1 and 0.33 Hz; and (iii) cycling. A search for the best TRF led to unambiguous identification of a three-parameter model as the most suitable descriptor of QT/RR coupling. Compared with established static models (linear or power-law), our model predictions are substantially closer to the experimental results, with errors similar to 50% smaller. The shape of the frequency and step responses of the TRF presented is essentially the same for all subjects and protocols. Moreover, each TRF may be uniquely identified by three parameters obtained from the step response, which are believed to be of physiological relevance: (i) gain for slow RR variability; (ii) gain for fast RR variability; and (iii) time during which QT attains 90% of its steady-state value. The TRF successfully describes the behaviour of the RR control following an abrupt change in RR interval, and its parameters may offer a tool for detecting pharmacologically induced changes, particularly those leading to increased arrhythmogenic risk.

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