Section: Research Program

General methodology

Every signal conveys, as a measure experiment, information on the physical system whose signal is an acquisition of. As a consequence, it seems natural that signal analysis or compression should make use of physical modelling of phenomena: the goal is to find new methodologies in signal processing that goes beyond the simple problem of interpretation. Physics of disordered systems, and specifically physics of (spin) glasses is putting forward new algorithmic resolution methods in various domains such as optimization, compressive sensing etc. with significant success notably for NP hard problem heuristics. Similarly, physics of turbulence introduces phenomenological approaches involving multifractality. Energy cascades are indeed closely related to geometrical manifolds defined through random processes. At these structures’ scales, information in the process is lost by dissipation (close to the lower bound of inertial range). However, all the cascade is encoded in the geometric manifolds, through long or short distance correlations depending on cases. How do these geometrical manifold structures organize in space and time, in other words, how does the scale entropy cascades itself ? To unify these two notions, a description in term of free energy of a generic physical model is sometimes possible, such as an elastic interface model in a random nonlinear energy landscape : This is for instance the correspondence between compressible stochastic Burgers equation and directed polymers in a disordered medium. Thus, trying to unlock the fingerprints of cascade-like structures in acquired natural signals becomes a fundamental problem, from both theoretical and applicative viewpoints.

To illustrate the general methodology undertaken, let us focus on an example conducted in the study of physiological time series: the analysis of signals recorded from the electrical activity of the heart in the general setting of Atrial Fibrillation (AF). AF is a cardiac arrhythmia characterized by rapid and irregular atrial electrical activity with a high clinical impact on stroke incidence. Best available therapeutic strategies combine pharmacological and surgical means. But when successful, they do not always prevent long-term relapses. Initial success becomes all the more tricky to achieve as the arrhythmia maintains itself and the pathology evolves into sustained or chronic AF. This raises the open crucial issue of deciphering the mechanisms that govern the onset of AF as well as its perpetuation. We have developed a wavelet-based multi-scale strategy to analyze the electrical activity of human hearts recorded by catheter electrodes, positioned in the coronary sinus (CS), during episodes of chronic AF. We have computed the so-called multifractal spectra using two variants of the wavelet transform modulus maxima method, the moment (partition function) method and the magnitude cumulant method (checking confidence intervals with surrogate data). Application of these methods to long time series recorded in a patient with chronic AF provides quantitative evidence of the multifractal intermittent nature of the electric energy of passing cardiac impulses at low frequencies, i.e. for times ($>\sim 0.5$ s) longer than the mean interbeat ($\simeq {10}^{-1}$s). We have also reported the results of a two-point magnitude correlation analysis which infers the absence of a multiplicative time-scale structure underlying multifractal scaling. The electric energy dynamics looks like a “multifractal white noise” with quadratic (log-normal) multifractal spectra. These observations challenge concepts of functional reentrant circuits in mechanistic theories of AF. A transition is observed in the computed multifractal spectra which group according to two distinct areas, consistently with the anatomical substrate binding to the CS, namely the left atrial posterior wall, and the ligament of Marshall which is innervated by the ANS. These negative results challenge also the existing models, which by principle cannot explain such results. As a consequence, we go beyond the existing models and propose a mathematical model of a denervated heart where the kinetics of gap junction conductance alone induces a desynchronization of the myocardial excitable cells, accounting for the multifractal spectra found experimentally in the left atrial posterior wall area (devoid of ANS influence).