About this Research Topic
Oscillatory properties of cardiac and cardiovascular regulation such as the high and low frequency components of heart rate variability (HRV) and blood pressure oscillations in the low frequency range (Myer waves) have long been recognised. HRV has been the focus of extensive research in view of its link with pathophysiology and clinical outcome. While the HF component of HRV is generally considered to represent parasympathetic activity the role of the low frequency component and its relation to sympathetic nerve activity has remained controversial. In fact, evidence for any low frequency oscillatory cardiac control mechanisms relevant to cardiac physiology or clinical outcome linked to sympathetic activity has been lacking.
However, in the space of a few years evidence has emerged for the existence of low frequency oscillations of ventricular action potential duration in humans. These occur at the sympathetic nerve frequency, are unrelated to respiration and are increased during increased sympathetic activity. Oscillation in ventricular repolarization have been observed from the T wave vector of the ECG at a similar frequency which are also increased by sympathetic activity. When enhanced in post MI patients, these oscillations portend a high risk of arrhythmia and sudden death. Computational modelling studies have identified likely cellular mechanisms for LF ventricular APD oscillations during enhanced sympathetic activity, and a mechanism for the generation of arrhythmia. LF oscillations of APD have been shown in humans to interact with beat to beat variability of APD and a mechanistic basis identified by computational modelling.
These exciting new developments are addressed in this Research Topic along with several related contributions on the neurophysiology of the low frequency component of sympathetic nerve activity, and the frequency components of heart rate variability.
However, in the space of a few years evidence has emerged for the existence of low frequency oscillations of ventricular action potential duration in humans. These occur at the sympathetic nerve frequency, are unrelated to respiration and are increased during increased sympathetic activity. Oscillation in ventricular repolarization have been observed from the T wave vector of the ECG at a similar frequency which are also increased by sympathetic activity. When enhanced in post MI patients, these oscillations portend a high risk of arrhythmia and sudden death. Computational modelling studies have identified likely cellular mechanisms for LF ventricular APD oscillations during enhanced sympathetic activity, and a mechanism for the generation of arrhythmia. LF oscillations of APD have been shown in humans to interact with beat to beat variability of APD and a mechanistic basis identified by computational modelling.
These exciting new developments are addressed in this Research Topic along with several related contributions on the neurophysiology of the low frequency component of sympathetic nerve activity, and the frequency components of heart rate variability.
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