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Register a new userCritical Scale-invariance in Healthy Human Heart Rate
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We demonstrate the robust scale-invariance in the probability density function (PDF) of detrended healthy human heart rate increments, which is preserved not only in a quiescent condition, but also in a dynamic state where the mean level of heart rate is dramatically changing. This scale-independent and fractal structure is markedly different from the scale-dependent PDF evolution observed in a turbulent-like, cascade heart rate model. These results strongly support the view that healthy human heart rate is controlled to converge continually to a critical state.
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The CVS is composed of numerous interacting and dynamically regulated physiological subsystems which each generate measurable periodic components such that the CVS can itself be presented as a system of weakly coupled oscillators. The interactions between these oscillators generate a chaotic blood pressure waveform signal, where periods of apparent rhythmicity are punctuated by asynchronous behaviour. It is this variability which seems to characterise the normal state. We used a standard experimental data set for the purposes of analysis and modelling. Arterial blood pressure waveform data was collected from conscious mice instrumented with radiotelemetry devices over $24$ hours, at a $100$ Hz and $1$ kHz time base. During a $24$ hour period, these mice display diurnal variation leading to changes in the cardiovascular waveform. We undertook preliminary analysis of our data using Fourier transforms and subsequently applied a series of both linear and nonlinear mathematical approaches in parallel. We provide a minimalistic linear and nonlinear coupled oscillator model and employed spectral and Hilbert analysis as well as a phase plane analysis. This provides a route to a three way synergistic investigation of the original blood pressure data by a combination of physiological experiments, data analysis viz. Fourier and Hilbert transforms and attractor reconstructions, and numerical solutions of linear and nonlinear coupled oscillator models. We believe that a minimal model of coupled oscillator models that quantitatively describes the complex physiological data could be developed via such a method. Further investigations of each of these techniques will be explored in separate publications.
The overarching goal of the present work is to contribute to the understanding of the relations between fetal heart rate (FHR) temporal dynamics and the well-being of the fetus, notably in terms of predicting cardiovascular decompensation (CVD). It makes uses of an established animal model of human labor, where fourteen near-term ovine fetuses subjected to umbilical cord occlusions (UCO) were instrumented to permit regular intermittent measurements of metabolites, pH, and continuous recording of electrocardiogram (ECG) and systemic arterial blood pressure (to identify CVD) during UCO. ECG-derived FHR was digitized at the sampling rate of 1000 Hz and resampled to 4Hz, as used in clinical routine. We focused on four FHR variability features which are tunable to temporal scales of FHR dynamics, robustly computable from FHR sampled at $4$Hz and within short-time sliding windows, hence permitting a time-dependent, or local, analysis of FHR which helps dealing with signal noise. Results show the sensitivity of the proposed features for early detection of CVD, correlation to metabolites and pH, useful for early acidosis detection and the importance of coarse time scales (2.5 to 8 seconds) which are not disturbed by the low FHR sampling rate. Further, we introduce the performance of an individualized self-referencing metric of the distance to healthy state, based on a combination of the four features. We demonstrate that this novel metric, applied to clinically available FHR temporal dynamics alone, accurately predicts the time occurrence of CVD which heralds a clinically significant degradation of the fetal health reserve to tolerate the trial of labor.
An example of phase transition in natural complex systems is the qualitative and sudden change in the heart rhythm between sinus rhythm and atrial fibrillation (AF), the most common irregular heart rhythm in humans. While the system behavior is centrally controlled by the behavior of the sinoatrial node in sinus rhythm, the macro-scale collective behavior of the heart causes the micro-scale behavior in AF. To quantitatively analyze this causation shift associated with phase transition in human heart, we evaluated the causal architecture of the human cardiac system using the time series of multi-lead intracardiac unipolar electrograms in a series of spatiotemporal scales by generating a stochastic renormalization group. We found that the phase transition between sinus rhythm and AF is associated with a significant shift of the peak causation from macroscopic to microscopic scales. Causal architecture analysis may improve our understanding of causality in phase transitions in other natural and social complex systems.
Human heart rate is known to display complex fluctuations. Evidence of multifractality in heart rate fluctuations in healthy state has been reported [Ivanov et al., Nature {bf 399}, 461 (1999)]. This multifractal character could be manifested as a dependence on scale or beat number of the probability density functions (PDFs) of the heart rate increments. On the other hand, scale invariance has been recently reported in a detrended analysis of healthy heart rate increments [Kiyono et al., Phys. Rev. Lett. {bf 93}, 178103 (2004)]. In this paper, we resolve this paradox by clarifying that the scale invariance reported is actually exhibited by the PDFs of the sum of detrended healthy heartbeat intervals taken over different number of beats, and demonstrating that the PDFs of detrended healthy heart rate increments are scale dependent. Our work also establishes that this scale invariance is a general feature of human heartbeat dynamics, which is shared by heart rate fluctuations in both healthy and pathological states.
How do you use imaging to analyse the development of the heart, which not only changes shape but also undergoes constant, high-speed, quasi-periodic changes? We have integrated ideas from prospective and retrospective optical gating to capture long-term, phase-locked developmental time-lapse videos. In this paper we demonstrate the success of this approach over a key developmental time period: heart looping, where large changes in heart shape prevent previous prospective gating approaches from capturing phase-locked videos. We use the comparison with other approaches to in vivo heart imaging to highlight the importance of collecting the most appropriate data for the biological question.
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