Individual Cardiac Rhythmic Identity Recovery System
A method and apparatus for diagnosing the intrinsic rhythmic signature of an individual heart and restoring that signature through biomimetic polyrhythmic pacing derived from the patient’s own cardiac data
Inventor
Alexander Thomas Cooper-Rye
Date
15 March 2026
Classification
Medical Devices — Cardiac Pacing — Adaptive Rhythm Systems
Status
Filed
This is the complete provisional specification as filed. A condensed,
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heart to beat.
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§Abstract
This application discloses a cardiac pacing system founded on the principle that each human heart possesses an intrinsic rhythmic identity—a native pattern of inter-beat interval relationships that is individual, diagnostically recoverable, and therapeutically restorable. The system operates in two phases: first, a diagnostic phase that analyses residual intrinsic cardiac activity (pre-implantation recordings, inter-paced intrinsic beats, or historical ECG data) to reconstruct the patient’s native rhythmic signature using ethnomusicological rhythm classification methods; second, a therapeutic phase that restores the recovered signature through polyrhythmic pacing with additive-meter interval sequences, modulated in real time by respiratory phase, autonomic tone, activity level, and circadian state.
The core innovation is threefold: (1) the recognition that hearts have individual rhythmic identities rather than a universal “healthy rhythm”; (2) a diagnostic method for recovering that identity from degraded or partial cardiac data; and (3) a pacing architecture that restores the native signature rather than imposing a generic variability pattern. The system further proposes that cardiac health is measurable as adaptive rhythmic capacity—the range of tempi and interval structures the heart can fluidly transition between while maintaining haemodynamic adequacy—analogous to a skilled drummer’s ability to play in time with any musical structure.
The system is implementable as a firmware update to existing programmable pacemaker hardware.
INDIVIDUAL CARDIAC RHYTHMIC IDENTITY RECOVERY SYSTEM
§1. FIELD OF INVENTION
[0001]This invention relates to implantable cardiac pacemakers, specifically to the diagnostic and timing algorithms governing pulse interval generation. More particularly, it relates to: (a) a method of diagnosing the intrinsic rhythmic identity of an individual heart from partial or degraded cardiac data; (b) a method of cardiac pacing in which the inter-beat interval sequence is derived from the patient’s own recovered rhythmic signature; and (c) a metric of cardiac health defined as adaptive rhythmic capacity.
§2. BACKGROUND AND PRIOR ART
2.1 THE SELECTIVE INCORRECTNESS OF CURRENT INTERVAL ORGANISATION
[0002]The cardiac pacing field has operated under a fundamental organising assumption: that the therapeutic target for paced rhythm is either (a) fixed-interval regularity (conventional pacing) or (b) a generic physiological variability pattern applied uniformly across patients (e.g., respiratory sinus arrhythmia restoration). Both approaches treat the heart as a passive recipient of externally determined timing. Neither recognises the possibility that each heart has its own native rhythmic identity that is the correct therapeutic target.
[0003]This assumption is selectively incorrect. The field is correct that variability matters, correct that respiratory coupling is a component of healthy rhythm, and correct that metronomic pacing produces worse outcomes. It is incorrect in treating variability as a single-parameter phenomenon (more vs. less) rather than a structural phenomenon (which pattern, for which heart, in which state). The field has been optimising tempo when it should be optimising meter.
2.2 THE HEART RATE VARIABILITY LITERATURE
[0004]Four decades of HRV research (Task Force of the European Society of Cardiology, 1996; Piskorski and Guzik, 2007) consistently demonstrate that reduced heart rate variability predicts morbidity and mortality. High HRV—complex, non-linear, asymmetric beat-to-beat variation—characterises healthy hearts. Low HRV—regular, predictable, rigid—characterises failing hearts. This body of research has been instrumental in identifying the problem with metronomic pacing but has not yet produced a framework for individual rhythm recovery.
2.3 THE CERYX/CYSONI BIONIC PACEMAKER
[0005]The most advanced prior art in variable pacing is the Cysoni device developed by Ceryx Medical (University of Auckland), which restores respiratory sinus arrhythmia (RSA) by modulating heart rate in phase with respiration—increasing rate during inspiration, decreasing during expiration. Clinical trials commenced (Shanks et al., 2022; Ceryx Medical, 2022-2025) in New Zealand, Australia, and the UK in 2024–2025, with reported 20% improvements in cardiac output over monotonic pacing in animal models.
[0006]The Ceryx approach represents a significant advance over metronomic pacing. However, it has three structural limitations that the present invention addresses:
[0007](a) Generic pattern: RSA pacing applies the same variability pattern (sinusoidal respiratory modulation) to all patients. It does not account for individual differences in native rhythmic structure.
[0008](b) Single-axis variability: The Ceryx system modulates along one axis only (respiratory-coupled tempo). The native cardiac rhythm exhibits variability along multiple simultaneous axes: respiratory coupling, circadian phase, autonomic tone, activity state, and—critically—intrinsic additive-meter structure.
[0009](c) Imposed rather than recovered: RSA pacing imposes a physiological norm. It does not diagnose the patient’s own native rhythm and restore it. The distinction is between giving every patient the same pair of shoes versus measuring their feet and making shoes that fit.
2.4 THE ETHNOMUSICOLOGICAL EVIDENCE
[0010]Bettermann et al. (1999) demonstrated that healthy cardiac rhythm, when analysed using African musicological time-line theory and the Derler Rhythm Classification from jazz theory (Bettermann et al., 1999), reveals structured patterns that are: (a) polyrhythmic and asymmetric rather than metronomic; (b) cyclically recurrent within individuals; (c) specific to physiological state (sleep stage, activity level); and (d) individual-specific—different people exhibit different dominant rhythm classes. This last finding is the foundation of the present invention: the heart’s rhythmic structure is not merely variable, it is personal.
2.5 MILFORD GRAVES AND ADAPTIVE RHYTHMIC CAPACITY
[0011]The late Milford Graves, jazz drummer and researcher at Bennington College (Graves, 1941-2021; documented in Meginsky and Young, 2018), spent decades investigating the relationship between percussive rhythm and cardiac function. His core insight was that cardiac health is characterised not by a specific rhythm but by rhythmic adaptability—the heart’s ability to shift timing, modulate phase, and resist unwanted entrainment. A healthy heart, like a skilled drummer, can play in time with any structure. The pathological heart is the one that can only play one beat, or no beat at all. This insight informs the present invention’s metric of adaptive rhythmic capacity.
§3. SUMMARY OF THE INVENTION
The core observation underlying this invention — that each human heart possesses an intrinsic rhythmic identity that is individual, diagnostically recoverable, and therapeutically significant — is a natural phenomenon. It is not claimed as such. What is claimed is exclusively the diagnostic method, the structured characterisation system, and the therapeutic apparatus for recovering, encoding, and restoring that identity: the instruments and processes by which the natural phenomenon is made clinically actionable. The relationship between the unpatentable phenomenon and the patentable method is analogous to the relationship between light refraction (a natural phenomenon) and an optometric system for measuring an individual's refractive error and grinding a corrective lens (a patentable apparatus). The present invention is the optometrist's chair, not the physics of light.
[0012]The present invention comprises two integrated systems:
3.1 DIAGNOSTIC SYSTEM: RHYTHMIC IDENTITY RECOVERY
[0013]A method of analysing a patient’s intrinsic cardiac activity to recover their native rhythmic identity. The system takes as input any available cardiac timing data—pre-implantation ECG recordings, Holter monitor data, intra-operative recordings, or residual intrinsic beats detected between paced events—and applies ethnomusicological rhythm classification to identify the patient’s dominant rhythm classes, preferred interval ratios, characteristic asymmetry profile, and state-dependent pattern transitions.
[0014]The diagnostic output is a Rhythmic Identity Profile (RIP): a patient-specific data structure encoding the individual’s native rhythmic signature across physiological states. The RIP serves as the reconstruction target for therapeutic pacing.
[0015]Where pre-existing cardiac data is insufficient for full profile recovery, the system derives a partial RIP from available data and supplements it with age-, sex-, and condition-matched normative data, with the supplemented components flagged for progressive refinement as more intrinsic data becomes available during pacing.
[0016]A pacing architecture that generates inter-beat intervals conforming to the patient’s recovered RIP rather than a generic pattern. The therapeutic system comprises:
[0017](a) A polyrhythmic timing engine that generates inter-beat intervals according to the additive-meter ratio sequences specified in the patient’s RIP, modulated in real time by respiratory phase, autonomic tone, activity level, and circadian state;
[0018](b) A pattern library populated initially from the patient’s RIP and refined continuously as residual intrinsic rhythm data is collected during pacing;
[0019](c) An adaptive capacity optimiser that progressively increases the range of rhythmic structures the pacing system can deploy, expanding the heart’s functional rhythmic repertoire as the myocardium responds to biomimetic pacing—analogous to rehabilitation that progressively increases range of motion;
[0020](d) An asymmetry preservation function that ensures beat-to-beat interval variation maintains the deceleration-dominant asymmetry characteristic of the patient’s recovered native rhythm;
[0021](e) A safety constraint layer that bounds all interval variation within clinically safe haemodynamic parameters, with graceful degradation to conventional pacing upon constraint violation.
[0022]The system introduces a novel cardiac health metric: Adaptive Rhythmic Capacity (ARC), defined as the range of inter-beat interval structures across which the heart can maintain haemodynamic adequacy. A healthy heart has high ARC: it can transition fluidly between rhythmic states (rest, exercise, stress, sleep) without loss of output. A failing heart has low ARC: it is locked into a narrow range of interval patterns, or none at all.
[0023]ARC is measured as the effective dimensionality of the Poincaré plot of successive R-R intervals, weighted by haemodynamic output. This metric unifies multiple existing HRV parameters into a single clinically meaningful measure: not how much variability, but how much functional rhythmic range.
[0024]The therapeutic goal of the system is to increase ARC over time—not merely to impose a fixed variability pattern, but to progressively restore the heart’s ability to inhabit multiple rhythmic states. The pacemaker is a rehabilitation device, not a prosthesis.
§Definitions
The following terms, as used throughout this specification and claims, have the meanings set forth below.
"Intrinsic cardiac activity" means any cardiac electrical activity generated by the heart's own conduction system, including sinoatrial node depolarisation, atrioventricular conduction, and ventricular depolarisation, as distinguished from activity initiated by an external pacing device.
"Residual intrinsic beats" means intrinsic cardiac depolarisations that occur between paced events in a patient with an implanted pacemaker, representing fragments of the heart's native conduction that persist despite pacing dependence.
"Inter-beat interval data" means the measured time durations between successive cardiac depolarisations (R-wave to R-wave), whether derived from electrocardiographic recordings, intracardiac electrograms, or pacemaker sensing logs.
"R-R intervals" means the time intervals between successive R-waves of the electrocardiogram, representing the duration of one complete cardiac cycle.
"Symbolic sequences" means the binary or categorical representations derived from inter-beat interval data by classifying each interval as belonging to one of a discrete set of duration categories (e.g., short or long relative to the local mean), enabling pattern analysis using combinatorial methods. The term includes but is not limited to "binary symbol sequences" as described in the rhythm classification literature (Bettermann et al., 1999).
"Ethnomusicological rhythm pattern analysis" means a method of classifying temporal interval sequences using pattern taxonomies that recognise additive-meter grouping structures — rhythmic patterns composed of unequal sub-groups — rather than imposing a uniform metric grid. The term reflects the historical origin of the classification tools: the biological rhythmic structure of the human heart is natively polyrhythmic and asymmetric, and the pattern taxonomies best suited to characterising this structure were developed within non-Western musical traditions (specifically African musicological time-line theory and the Derler Rhythm Classification from jazz theory) because those traditions built classification systems for the same class of rhythmic phenomena. The analysis is biological in subject and musicological only in method: the heart does not derive its rhythm from musical traditions; rather, those traditions independently described the same category of asymmetric temporal structure that the heart already exhibits.
"Derler Rhythm Classification" means the hierarchical rhythm pattern classification system, as employed by Bettermann et al. (1999), derived from jazz theory and applicable to cardiac interval sequences, in which binary symbol sequences are classified into rhythm classes defined by their additive grouping structure.
"Additive-meter structures" means rhythmic interval patterns in which the total cycle length is composed of unequal sub-groups that sum to the whole (e.g., 3+2+3 = 8 beats, 2+3+2 = 7 beats), as distinguished from divisive meter in which a cycle is divided into equal parts. The asymmetric grouping produces non-uniform inter-beat intervals within each cycle.
"Dominant rhythm classes" means the additive-meter pattern structures that appear with the greatest frequency in a patient's intrinsic cardiac rhythm data, weighted by duration of occurrence across physiological states.
"Transition patterns" means the characteristic sequences by which a patient's cardiac rhythm shifts from one dominant rhythm class to another in response to changes in physiological state, including transitions between waking, sleep onset, deep sleep, exercise, and recovery states.
"Asymmetry profile" means the quantitative characterisation of the deceleration-to-acceleration ratio in a patient's beat-to-beat interval variation, as measured by the asymmetric properties of the Poincare plot of successive R-R intervals (Piskorski and Guzik, 2007).
"Poincare plot" means the scatterplot of each R-R interval against the immediately preceding R-R interval, a standard method for visualising the nonlinear dynamics of heart rate variability, in which the shape, dispersion, and asymmetry of the plot encode information about short-term and long-term cardiac variability.
"Rhythmic Identity Profile (RIP)" means a patient-specific data structure encoding the individual's native rhythmic signature across physiological states, comprising the patient's dominant rhythm classes, transition patterns, asymmetry profile, and baseline Adaptive Rhythmic Capacity, as defined herein.
"Polyrhythmic timing engine" means a computational timing module, implementable in pacemaker firmware, that generates inter-beat interval sequences by processing cardiac timing data in the envelope domain — extracting the percussive onset structure of the cardiac signal (when beats land and how they are spaced) while filtering spectral components that do not contribute to rhythmic identity — and outputting pacing intervals that conform to a specified rhythm template from the patient's Rhythmic Identity Profile, rather than a fixed-interval or sinusoidally-modulated timer.
"Base rhythm template" means the currently active additive-meter interval ratio sequence selected from the patient's Rhythmic Identity Profile for a given physiological state, expressed as a vector of relative interval durations [t1, t2, ... tn] that define the target inter-beat interval structure for one rhythmic cycle.
"Multi-axis modulation" means the simultaneous real-time adjustment of the base rhythm template across two or more independent physiological axes, specifically respiratory phase, autonomic tone, activity level, circadian state, and residual intrinsic rhythm feedback.
"Adaptive Rhythmic Capacity (ARC)" means the range of inter-beat interval structures across which the heart can maintain haemodynamic adequacy, measured as the effective dimensionality of the Poincare plot of successive R-R intervals weighted by haemodynamic output, as defined herein.
"Effective dimensionality" means the resolution at which an individual heart's rhythmic identity becomes distinguishable from noise in the Poincare plot of successive R-R intervals. It is not a fixed mathematical procedure but a patient-relative measure: the effective dimensionality of a given heart is whatever number of independent dimensions is required to capture that heart's specific rhythmic signature as distinct from structureless variability. The concept is analogous to optical correction — the effective dimensionality of a lens is whatever focal adjustment makes this person's vision clear, not a universal constant. In practice, effective dimensionality may be estimated by principal component analysis, correlation dimension, or other nonlinear methods appropriate to the patient's data; the specification does not constrain the estimation method because the insight is that the dimension itself is individual, not that it is computed by a particular algorithm.
"Haemodynamic output" means the volume of blood ejected by the heart per unit time, measured or estimated by stroke volume, cardiac output, or surrogate indices available to the pacing system including impedance cardiography or pulse pressure analysis.
"Haemodynamic adequacy" means the functional state in which the cardiovascular system is delivering sufficient blood flow to sustain tissue perfusion and organ function. Adequacy is defined by its absence: a system is haemodynamically adequate when it is not in haemodynamic insufficiency. The threshold is clinical and patient-specific, analogous to pulmonary adequacy (the capacity to breathe) — not a fixed numerical value but a functional boundary below which the system fails to sustain the organism. Within the pacing system, haemodynamic adequacy is monitored continuously and the boundary is programmable by the treating clinician based on the individual patient's requirements.
"Myocardium demonstrates tolerance" means that the heart maintains haemodynamic adequacy continuously for a clinically defined observation period (programmable, default not less than 72 hours) while paced with a given set of rhythmic structures, without triggering the safety constraint layer.
"Safety constraint layer" means a supervisory module within the pacing system that continuously monitors haemodynamic adequacy and enforces programmable upper and lower bounds on inter-beat intervals, overriding the polyrhythmic timing engine and reverting to conventional fixed-interval pacing upon any constraint violation.
"Entrainment resistance monitoring" means a spectral monitoring function within the pacing system that detects the emergence of pathological phase-locking between the pacing output and endogenous neural or muscular oscillatory activity, and automatically disrupts any detected entrainment pattern that threatens haemodynamic stability.
"Pathological phase-locking" means the involuntary synchronisation of cardiac pacing output with an endogenous oscillatory source (neural, muscular, or respiratory) at a coupling strength sufficient to override the intended pacing rhythm and compromise haemodynamic adequacy.
"Graceful degradation" means the automatic, progressive fallback from polyrhythmic pacing to conventional fixed-interval pacing upon detection of constraint violations, implemented as a staged reduction in rhythmic complexity rather than an abrupt mode switch.
"Diagnostic surfaces" means tissues that are (a) highly vascularised at or near the terminal vascular bed, (b) accessible to non-invasive or minimally invasive imaging, (c) mechanically compliant enough to undergo continuous remodelling in response to pulse wave forces over the patient's lifetime, and (d) observable by clinical examination, including but not limited to the retinal vasculature, cortical surface microvasculature, gingival tissue, oral mucosa, tongue vasculature, and terminal capillary beds of the hands and feet.
"Frequency-dependent remodelling patterns" means the morphological changes in vascular geometry, collagen fibre alignment, capillary branching density, and tissue inflammatory signatures that arise as a consequence of the specific temporal pattern (not merely the amplitude) of pulse wave mechanical forces acting on the diagnostic surface over the patient's lifetime, such that tissues pulsed with different rhythmic structures exhibit different remodelling signatures.
"Hemispheric phase offset" means the measurable difference in arrival time of the arterial pulse wave at the left versus right cerebral hemispheres, arising from the anatomical asymmetry of the aortic arch branching (left common carotid arising directly from the aortic arch; right common carotid arising via the brachiocephalic trunk).
"Cardiac-to-cerebral mechanical coupling" means the transmission of the cardiac pulse wave from the heart to the cerebral vasculature via the arterial tree, characterised by the pulse wave transit time, arrival phase offset between hemispheres, and the degree to which cortical neural processing gates to cardiac cycle phase (Edwards et al., 2009; Garfinkel and Critchley, 2016).
"Cumulative haemodynamic history" means the total record of pulse wave mechanical interactions between the cardiovascular system and the body's tissues over the patient's lifetime, as encoded in the morphological remodelling of diagnostic surfaces.
"Rockface Principle" means the diagnostic framework in which the morphological signatures observable on diagnostic surfaces are interpreted as recordings of the patient's cumulative haemodynamic history — analogous to the way a coastal rockface records the dominant wave patterns of the ocean that has acted upon it — enabling the recovery of cardiac rhythmic identity information from tissues that have been mechanically shaped by decades of pulse wave interaction, even when the heart's current rhythm is too degraded for direct analysis.
§4. DETAILED DESCRIPTION
4.1 DIAGNOSTIC PHASE: RECOVERING THE NATIVE SIGNATURE
4.1.1 DATA ACQUISITION
[0025]The diagnostic system accepts cardiac timing data from any available source: 24-hour Holter recordings, pre-implantation ECG, intra-operative recordings, or—critically—residual intrinsic beats detected during pacing. Even a heart that requires pacing retains residual intrinsic activity. In demand-mode pacing, intrinsic beats are routinely sensed and logged. These beats, though intermittent, carry fragments of the heart’s native rhythmic identity.
[0026]The system treats residual intrinsic activity as a degraded signal containing recoverable structural information, analogous to audio restoration of damaged recordings. The key insight is that rhythmic identity is structural, not merely statistical: the ratios between intervals persist even when absolute timing degrades. A heart that natively beats in a 3:2:3 ratio pattern will produce intrinsic beats whose interval relationships preserve that ratio even when the overall rate has changed.
[0028a]Furthermore, rhythmic identity is not encoded solely in electrical conduction patterns but in the morphological structure of the conduction pathway itself. Dendrite geometry, axonal branching patterns, and the physical architecture of neural and muscular tissue are shaped over a lifetime by the rhythmic activity that traverses them. A rhythm does not exist only as a transient electrical event; it is written into the cells that carry it. The excitatory pathways nearest to the heart possess morphological adaptations mapped to the expected voltages and timing patterns of the cardiac cycle. This structural encoding provides an additional basis for rhythmic identity recovery: the rhythm is hardcoded in tissue architecture, not merely performed in electrical activity.
4.1.2 RHYTHM CLASSIFICATION
[0027]Acquired R-R interval data is transformed into binary symbol sequences and classified using a hierarchical rhythm pattern scheme derived from African musicological time-line theory and the Derler Rhythm Classification (Bettermann et al., 1999). The classification identifies:
[0028]Dominant rhythm classes: The additive-meter structures (e.g., 3+2+3, 2+3+2, 3+2+2+3) that appear most frequently in the patient’s intrinsic rhythm, weighted by physiological state.
[0029]Transition patterns: How the patient’s rhythm classes shift between states (e.g., the characteristic progression from waking patterns to sleep-onset patterns to deep-sleep patterns).
[0030]Asymmetry profile: The patient’s characteristic heart rate asymmetry—the ratio of deceleration variability to acceleration variability in the Poincaré plot.
[0031]Adaptive range: The baseline ARC—the number and diversity of rhythm classes the heart can inhabit while maintaining adequate output.
4.1.3 RHYTHMIC IDENTITY PROFILE (RIP) CONSTRUCTION
[0032]The classification results are compiled into a Rhythmic Identity Profile: a patient-specific data structure encoding the target rhythm for each physiological state, the transition rules between states, the asymmetry parameters, and the baseline ARC. The RIP is stored in the pacemaker’s memory and serves as the reconstruction target for therapeutic pacing.
[0033]Where data is insufficient for complete profiling (e.g., no pre-implantation recordings are available), the system constructs a partial RIP from whatever intrinsic data can be captured and fills gaps with normative data matched by age, sex, body mass, and cardiac condition. The supplemented components are flagged, and the system progressively replaces normative estimates with patient-specific data as more intrinsic rhythm is observed during pacing. The RIP is a living document that improves over the lifetime of the device.
[0033a]The diagnostic system further enables prophylactic rhythmic identity recording: a patient's Rhythmic Identity Profile may be constructed from healthy cardiac data recorded at any point during the patient's life (e.g., from routine Holter monitoring or wearable ECG devices during the patient's third or fourth decade) and stored for future use. Should the patient subsequently develop conduction disease requiring pacemaker implantation, the stored healthy-state RIP provides a complete reconstruction target derived from the patient's own pre-disease cardiac rhythm, eliminating the need to recover rhythmic identity from degraded post-disease data. This prophylactic approach is analogous to cord blood banking: the biological resource is captured when abundant and stored against future therapeutic need.
4.2 THERAPEUTIC PHASE: RESTORING THE NATIVE SIGNATURE
4.2.1 POLYRHYTHMIC TIMING ENGINE
[0034]The core timing function replaces the conventional fixed-interval timer with a cyclic pattern generator that produces inter-beat intervals according to the currently active rhythm template from the patient’s RIP. Given a target rate R (beats per minute) and a rhythm template T expressing relative interval ratios [t₁, t₂, ... tₙ], the engine computes absolute intervals as:
[0035]Iᵢ = (tᵢ / Σt) × (n / R) × 60,000 ms
[0036]where n is the cycle length and the sum of all Iᵢ across one cycle equals the total time for n beats at rate R. This preserves the target rate while distributing beats according to the patient’s native interval structure.
4.2.2 MULTI-AXIS MODULATION
[0037]Unlike single-axis systems (e.g., respiratory-only modulation), the therapeutic system modulates the base rhythm template simultaneously across multiple axes:
[0038]Respiratory coupling: Interval modulation in phase with detected respiratory cycle, preserving RSA.
[0039]Autonomic tone: Pattern selection responsive to detected sympathetic/parasympathetic balance, shifting between rhythm classes as autonomic state changes.
[0040]Activity level: Rate and pattern adjustment based on accelerometer and minute ventilation data.
[0041]Circadian phase: Transition between daytime and nighttime rhythm profiles matching the patient’s RIP.
[0042]Intrinsic rhythm feedback: Continuous monitoring of residual intrinsic beats to detect changes in the native signature and update the RIP accordingly.
4.2.3 ADAPTIVE CAPACITY REHABILITATION
[0043]A key distinction from all prior art: the system does not merely impose a fixed variability pattern. It progressively expands the range of rhythmic structures deployed, increasing the heart’s functional ARC over time. The initial pacing programme uses a narrow subset of the patient’s RIP—the most stable, lowest-risk rhythm classes. As the myocardium demonstrates tolerance (measured by sustained haemodynamic output), the system progressively introduces additional rhythm classes, wider interval ratios, and more complex transitions.
[0044]The therapeutic model is rehabilitation, not prosthesis. The goal is not permanent dependence on externally imposed rhythm but progressive restoration of the heart’s own rhythmic capacity. The pacemaker functions as a scaffold that is gradually withdrawn as the heart recovers its native range. ARC is monitored continuously as the primary outcome metric.
4.3 THE TUNING FORK PRINCIPLE
[0045]The conceptual foundation of the therapeutic approach is the tuning fork principle: the pacemaker does not tell the heart what rhythm to play. It identifies the frequency at which the heart’s own system resonates and provides that frequency as a reference signal. The heart’s myocardium, like any oscillating system, has resonant modes determined by its physical structure, conduction pathways, and electrophysiological properties. Conventional pacing ignores these modes and imposes an arbitrary frequency. The present system identifies the resonant modes and paces in sympathy with them.
[0046]This principle explains why the diagnostic phase must precede the therapeutic phase. You cannot tune an instrument you have not first listened to. The diagnostic system listens to the heart’s remnant voice; the therapeutic system plays it back.
4.4 ENTRAINMENT RESISTANCE AND TOP-END ADAPTABILITY
[0047]Healthy cardiac rhythm resists pathological entrainment while maintaining the ability to entrain selectively with beneficial physiological rhythms (respiratory cycle, circadian cycle, activity demands). This mirrors the skill of an expert drummer: the ability to play in time with any musical structure while never losing one’s own time. Maximum health is not a specific rhythm but maximum adaptive range—the top end of the system’s capacity to shift between tempi, meters, and phase relationships while maintaining structural coherence.
[0048]The safety constraint layer includes spectral monitoring to detect emerging pathological phase-lock between pacing output and neural or muscular oscillatory activity, with automatic disruption of any entrainment pattern that threatens haemodynamic stability. The system resists capture by external rhythms while enabling cooperation with physiological ones.
4.5 GEOMETRIC PROPERTIES OF ADDITIVE METER
[0049]The additive-meter structures used in the rhythm templates have geometric properties that may be functionally significant. The pattern 3+2+3 (8 beats, asymmetrically grouped) traces a pentagonal path through an octagonal cycle. The 3:2 ratio is harmonically a perfect fifth—the most consonant interval after the octave. These geometric relationships suggest that the heart’s native rhythmic structures may be constrained by the same mathematical relationships that govern musical consonance and physical resonance. Further investigation of the geometric properties of individual RIPs may reveal diagnostically significant patterns.
§Claims
1A method of cardiac rhythm diagnosis comprising: (a) acquiring inter-beat interval data from a patient’s intrinsic cardiac activity; (b) transforming the interval data into symbolic sequences; (c) classifying the symbolic sequences using ethnomusicological rhythm pattern analysis to identify the patient’s dominant rhythm classes, transition patterns, and asymmetry profile; and (d) compiling the results into a patient-specific Rhythmic Identity Profile (RIP) encoding the individual’s native rhythmic signature across physiological states.
2The method of claim 1, wherein the intrinsic cardiac activity data includes residual intrinsic beats detected between paced events in a patient with an existing pacemaker, and wherein the system reconstructs rhythmic identity from partial and intermittent data by analysing interval ratios rather than absolute timing.
3The method of claim 1, wherein the ethnomusicological rhythm pattern analysis employs a hierarchical classification system derived from African time-line theory and/or the Derler Rhythm Classification, identifying additive-meter structures including but not limited to 3+2+3, 2+3+2, 3+2+2+3, and other asymmetric interval groupings.
4A cardiac pacing system comprising a polyrhythmic timing engine that generates inter-beat intervals conforming to a patient-specific Rhythmic Identity Profile derived from the patient’s own intrinsic cardiac rhythm data, rather than a generic variability pattern.
5The system of claim 4, wherein the polyrhythmic timing engine computes absolute inter-beat intervals by distributing a target heart rate across non-uniform relative interval ratios specified by the patient’s RIP, preserving the mean rate while distributing beats according to the patient’s native interval structure.
6The system of claim 4, further comprising multi-axis modulation that simultaneously adjusts the base rhythm template according to respiratory phase, autonomic tone, activity level, circadian state, and residual intrinsic rhythm feedback.
7The system of claim 4, further comprising an adaptive capacity rehabilitation function that progressively expands the range of rhythmic structures deployed as the myocardium demonstrates tolerance, with the therapeutic goal of increasing the patient’s Adaptive Rhythmic Capacity over time.
8A cardiac health metric, Adaptive Rhythmic Capacity (ARC), defined as the effective dimensionality of the Poincaré plot of successive R-R intervals weighted by haemodynamic output, measuring the range of inter-beat interval structures across which the heart can maintain haemodynamic adequacy.
9The system of claim 4, wherein the Rhythmic Identity Profile is a living data structure that is progressively refined during pacing by continuous analysis of residual intrinsic beats, replacing normative estimates with patient-specific data as it becomes available.
10The system of claim 4, further comprising a safety constraint layer that enforces clinically defined minimum and maximum inter-beat intervals, monitors cumulative haemodynamic adequacy, and provides graceful degradation to conventional pacing upon constraint violation.
11The system of claim 4, further comprising entrainment resistance monitoring that detects and disrupts pathological phase-locking between pacing output and neural or muscular oscillatory activity while permitting selective entrainment with beneficial physiological rhythms.
12The system of claim 4, wherein the core timing algorithm is implementable as a firmware update to existing programmable pacemaker hardware without modification to leads or pulse generators, utilising whatever sensor inputs (accelerometer, minute ventilation, impedance) are available on the installed hardware for the modulation axes they support.
13A method of cardiac pacing comprising: (a) diagnosing the patient’s intrinsic rhythmic identity by classifying available cardiac interval data into rhythm pattern classes using ethnomusicological analysis; (b) constructing a patient-specific Rhythmic Identity Profile; (c) generating pacing intervals that restore the patient’s native rhythmic signature; (d) modulating the pacing output across multiple simultaneous axes; (e) progressively expanding the range of deployed rhythmic structures as the myocardium demonstrates tolerance; and (f) continuously refining the Rhythmic Identity Profile from residual intrinsic rhythm data collected during pacing.
14A cardiac pacing system characterised by: (a) diagnosis of individual rhythmic identity from the patient's own cardiac data prior to therapeutic pacing; (b) simultaneous modulation of pacing intervals across respiratory, autonomic, activity, circadian, and intrinsic rhythm axes; (c) generation of inter-beat intervals according to additive-meter interval structures rather than sinusoidal tempo variation; and (d) progressive rehabilitation of the patient's adaptive rhythmic capacity as measured by the ARC metric, rather than permanent imposition of a fixed variability pattern.
The following claims extend the diagnostic system to include recovery of the patient’s native rhythmic identity from distal tissue morphology—the physical record left by decades of pulse wave interaction on terminal and surface tissues. The underlying principle is that the pulse wave does not merely pass through tissue; it mechanically deforms it with every heartbeat. Over billions of cardiac cycles, these deformations produce cumulative structural remodelling that encodes the heart’s rhythmic history in the morphology of the tissues it has been pulsing against. The body is a distributed recording medium for cardiac rhythm. The heart writes its signature on the surfaces it touches.
5A.1 THE ROCKFACE PRINCIPLE
An ocean’s movements are complex and turbulent, but the rockface it beats against records the dominant patterns with high fidelity over geological time. The smoothing, etching, and erosion patterns on a coastal rockface encode the rhythmic structure of the waves that created them. The same principle applies to the cardiovascular pulse wave and the tissues it acts upon. Vessel walls thicken or thin in response to shear stress patterns. Collagen fibres align along dominant stress vectors. Capillary beds branch in response to flow dynamics. Inflammatory markers accumulate at sites of greatest mechanical strain. These changes are frequency-dependent: a tissue pulsed at a 3:2:3 ratio for decades will exhibit different microstructural signatures than one pulsed at uniform intervals, because the asymmetric stress distribution produces asymmetric remodelling.
This principle has a critical diagnostic implication: the heart’s native rhythmic identity is recoverable even when the heart itself can no longer express it. A patient who has been in atrial fibrillation for two years still carries forty years of native rhythm encoded in the morphology of their retinal vessels, cortical vasculature, gingival tissue, and terminal capillary beds. The recording medium outlasts the instrument.
5A.2 DIAGNOSTIC SURFACES
The following tissues are identified as primary diagnostic surfaces for rhythmic imprint recovery, selected because they are: (a) highly vascularised terminal or near-terminal tissue; (b) accessible to non-invasive or minimally invasive imaging; (c) soft enough to undergo continuous remodelling in response to pulse wave forces; and (d) already the subject of existing clinical observation that detects systemic disease from local morphology, though without a mechanistic framework explaining why.
Retinal vasculature. The retina is the single best non-invasive window into microvascular morphology. Branching geometry, arterial-to-venous ratio, and tortuosity are already used as diagnostic markers Retinal microvascular changes are also independently predictive of chronic kidney disease progression and renal dysfunction (Liu et al., 2020; Kanbay et al., 2024), further demonstrating that the retina records systemic vascular history that is not accessible through the organ-specific imaging modalities used by nephrology.. Critically, the two retinas receive pulse waves via different arterial paths (ophthalmic arteries branching from the internal carotids, which themselves have asymmetric aortic origins), producing a stereo pair: two rockfaces etched by the same ocean arriving at slightly different phases. Differential analysis of left vs. right retinal vascular morphology may encode the hemispheric phase offset described elsewhere in this specification.
Cortical surface microvasculature. The leptomeningeal vessels on the brain surface are directly exposed to pulse pressure transmitted through cerebrospinal fluid. The left hemisphere, receiving the pulse wave earlier via the direct left common carotid, would exhibit different vascular remodelling patterns than the right hemisphere, which receives a phase-delayed and angle-refracted version of the same signal. High-resolution MRI or functional near-infrared spectroscopy may be able to detect these asymmetric morphological signatures.
Oral mucosa, gingival tissue, and tongue. The oral cavity is densely vascularised, with the gingival tissue and tongue among the most responsive soft tissues in the body to haemodynamic changes. Dentists routinely detect systemic cardiovascular disease, diabetes, and haematological malignancies from gingival examination—an observation that has historically lacked a mechanistic explanation beyond “shared risk factors.” The Rockface Principle provides that explanation: the gingival vasculature is a terminal recording surface with minimal barrier between the microvasculature and the observable tissue surface. Decades of pulse wave impact are directly readable as tissue morphology, colour, inflammatory patterning, and vascular geometry. The tongue, as one of the most densely innervated and vascularised structures in the body, serves a similar function.
Hands, feet, and nail beds. Terminal capillary beds at the greatest vascular distance from the heart. The pulse wave arriving at these sites has traversed the maximum path length and reflected off every upstream branch point, arriving as a complex interference pattern that encodes the full history of the arterial tree. Nail bed capillaroscopy already exists as a diagnostic tool; the present invention proposes extending this analysis to read rhythmic signatures from capillary morphology. Podiatric examination, like dental examination, detects systemic disease from local tissue observation—the Rockface Principle explains why.
5A.3 EPISTEMOLOGICAL NOTE: SCANNER MEDICINE VS. ROCKFACE MEDICINE
Medical imaging technologies (MRI, CT, ultrasound, PET) operate by sending an externally generated signal through tissue and reading what reflects back. These are active interrogation systems: they impose their own wave and measure the tissue’s response to that wave. They read structure at the moment of scanning. They do not read history.
The clinical disciplines that examine terminal and surface tissues—ophthalmology (retina), dentistry (gingiva, oral mucosa), podiatry (feet, nail beds), dermatology (skin)—operate differently. They read surfaces that have been shaped by the body’s own waves over time. They are passive recording readers: they observe the cumulative morphological record left by years or decades of endogenous pulse wave interaction. They read history, not just structure.
This distinction explains the persistent clinical observation that “peripheral” disciplines catch systemic disease early: they are not catching it early. They are reading a longer record. A gingival change reflecting cardiovascular disease is not an early marker of a new condition; it is the accumulated morphological evidence of decades of abnormal pulse wave interaction, finally becoming visible on the recording surface. The Rockface Principle reframes these disciplines from peripheral screening tools to primary diagnostic surfaces for haemodynamic history—and, for the purposes of the present invention, for cardiac rhythmic identity recovery.
5A.4 SUPPLEMENTARY CLAIMS
15A method of recovering a patient’s native cardiac rhythmic identity from the morphological signatures left by decades of pulse wave interaction on distal tissues, comprising: (a) imaging one or more diagnostic surfaces including retinal vasculature, cortical surface microvasculature, gingival tissue, oral mucosa, tongue vasculature, and/or terminal capillary beds of the hands and feet; (b) analysing the vascular geometry, branching patterns, collagen alignment, tissue remodelling patterns, and/or inflammatory signatures present in the imaged tissue; (c) extracting rhythmic structural information encoded in the frequency-dependent remodelling patterns; and (d) incorporating the extracted rhythmic information into the patient’s Rhythmic Identity Profile as described in claims 1–4.
16The method of claim 15, wherein differential analysis of bilateral diagnostic surfaces (left vs. right retinal vasculature, left vs. right cortical surface vasculature) is used to extract the hemispheric phase offset of pulse wave arrival, providing information about the patient’s cardiac-to-cerebral mechanical coupling that is not available from cardiac data alone.
17The method of claim 15, applied specifically to post-injury or post-arrhythmia patients whose current cardiac rhythm is too degraded to permit direct rhythmic identity recovery, wherein the distal tissue morphological record serves as the primary source of pre-injury rhythmic identity data, enabling reconstruction of the patient’s native rhythmic signature from the body’s distributed recording surfaces when the cardiac source signal is no longer available.
18A diagnostic framework (the Rockface Principle) for interpreting clinical observations made by medical disciplines that examine terminal and surface tissues (ophthalmology, dentistry, podiatry, dermatology) as readings of cumulative haemodynamic history rather than point-in-time structural assessment, wherein the observable morphology of these tissues is understood as a recording medium that encodes the patient’s cardiovascular rhythmic history over the lifetime of the tissue.
§6. DIFFERENTIATION FROM PRIOR ART
[0001]The present invention is distinguished from all known prior art in cardiac pacing by six structural differences. The most advanced prior art is the Cysoni bionic pacemaker developed by Ceryx Medical (University of Auckland), which restores respiratory sinus arrhythmia by modulating heart rate in phase with respiration (Shanks et al., 2022; Ceryx Medical, 2022-2025). The following summarises the differentiation across all material axes.
[0002]Variability pattern. Ceryx/Cysoni: applies a generic respiratory sinus arrhythmia pattern identically to all patients, modulating tempo sinusoidally in phase with breathing. Present invention: diagnoses the individual patient's native rhythmic identity and restores that specific signature through polyrhythmic pacing derived from the patient's own cardiac data.
[0003]Number of modulation axes. Ceryx/Cysoni: single axis (respiratory coupling only). Present invention: simultaneous modulation across five axes (respiratory phase, autonomic tone, activity level, circadian state, and residual intrinsic rhythm feedback).
[0004]Interval structure. Ceryx/Cysoni: sinusoidal tempo variation around a target rate, producing smooth acceleration and deceleration. Present invention: additive-meter interval sequences (e.g. 3+2+3, 2+3+2) derived from ethnomusicological rhythm classification, producing the asymmetric polyrhythmic structure characteristic of healthy cardiac rhythm (Bettermann et al., 1999).
[0005]Diagnostic phase. Ceryx/Cysoni: no diagnostic phase; the same variability pattern is applied to all patients without analysis of individual rhythmic identity. Present invention: a dedicated diagnostic phase recovers the patient's native Rhythmic Identity Profile from available cardiac data using rhythm classification methods derived from African musicological time-line theory and the Derler Rhythm Classification (Bettermann et al., 1999).
[0006]Therapeutic model. Ceryx/Cysoni: permanent imposition of a fixed variability pattern (prosthetic model). Present invention: progressive rehabilitation of the heart's own adaptive rhythmic capacity, with the therapeutic goal of increasing the range of rhythmic structures the heart can independently sustain (rehabilitative model). The Adaptive Rhythmic Capacity metric (Piskorski and Guzik, 2007) measures therapeutic progress.
[0007]Distal tissue diagnostics. Ceryx/Cysoni: not addressed. Present invention: introduces the Rockface Principle, a method of recovering the patient's native rhythmic identity from the morphological signatures left by decades of pulse wave interaction on terminal and surface tissues (retinal vasculature (Wong and Mitchell, 2004; McGeechan et al., 2009), gingival tissue (Lockhart et al., 2012), and terminal capillary beds of the hands and feet (Roustit and Cracowski, 2012; Anyfanti et al., 2018)), enabling rhythmic identity recovery even when the heart's current rhythm is too degraded for direct analysis.
[0008]No other known prior art addresses individual cardiac rhythmic identity, ethnomusicological rhythm classification applied to cardiac timing data, additive-meter pacing interval structures, the concept of Adaptive Rhythmic Capacity as a cardiac health metric, or the recovery of cardiac rhythmic history from distal tissue morphology.
§7. THEORETICAL RATIONALE
7.1 THE CATEGORY ERROR
The Western medical and engineering tradition inherited from the Enlightenment a fundamental assumption: regularity equals health, irregularity equals pathology. The metronome (1815), equal temperament, factory timekeeping, and eventually digital clock cycles all express the same epistemological project: imposing uniform grids on inherently non-uniform processes. The pacemaker is this project’s cardiac endpoint.
Contemporary HRV research has partially corrected this error by demonstrating that variability is healthy. The Ceryx bionic pacemaker represents a further correction by restoring one component of natural variability (RSA). The present invention proposes the complete correction: the heart is not merely variable, it is compositional. It has its own music. The therapeutic task is not to impose variability but to recover and restore the specific composition that belongs to the specific heart.
A note on the semantics of regularity: the healthy heart is not irregular. It is, in fact, perhaps the most regular thing in the body — it has beaten continuously since before birth. The error is semantic, not cardiac. The word 'regular' has been captured by a specific meaning — metronomic, uniform, grid-locked — that describes the Enlightenment's preferred temporal structure, not the heart's actual one. The heart is supremely regular in its own language: cyclically recurrent, state-responsive, asymmetrically structured, and individually consistent. To call this 'irregular' is to measure a coastline with a ruler and blame the coast. The clinical consequence of this semantic capture is two centuries of pacing technology built to enforce a regularity the heart never exhibited and never needed.
7.2 THE TUNING FORK VS. THE METRONOME
A metronome tells you what tempo to play. A tuning fork tells you what frequency you resonate at. Conventional pacing is metronomic: it imposes timing. RSA pacing is a variable metronome: it imposes timing that varies with breathing. The present invention is a tuning fork: it discovers the heart’s resonant rhythmic structure and provides that structure as a reference signal, enabling the heart to re-inhabit its own native pattern.
7.3 REHABILITATION VS. PROSTHESIS
Conventional pacing is prosthetic: it replaces a lost function with an artificial substitute, permanently. The present system is rehabilitative: it provides a scaffold that supports the heart’s native function while progressively restoring the heart’s own capacity. The ARC metric measures rehabilitation progress. The long-term therapeutic goal is increasing the heart’s independent rhythmic range, not maintaining dependence on externally imposed patterns.
§8. KEY REFERENCES
Core cardiac rhythm and pacing
Bettermann, H., Amponsah, D., Cysarz, D., and Van Leeuwen, P. (1999). Musical rhythms in heart period dynamics: A cross-cultural and interdisciplinary approach to cardiac rhythms. American Journal of Physiology -- Heart and Circulatory Physiology, 277(5), H1762-H1770.
Shanks, J., Paton, J. F. R., Ramchandra, R., et al. (2022). Reverse re-modelling chronic heart failure by reinstating heart rate variability. Basic Research in Cardiology, 117(1), 5.
Task Force of the European Society of Cardiology (1996). Heart rate variability: Standards of measurement, physiological interpretation and clinical use. Circulation, 93(5), 1043-1065.
Piskorski, J., and Guzik, P. (2007). Geometry of the Poincare plot of RR intervals and its asymmetry in healthy adults. Physiological Measurement, 28(3), 287-300.
Chew, E. (2018). Notating disfluencies and temporal deviations in music and arrhythmia. Music and Science, 1, 1-22.
Ceryx Medical (2022-2025). Cysoni bionic pacemaker: preclinical and clinical trial data. University of Auckland / Ceryx Medical Ltd.
Adaptive rhythmic capacity and cardiac-percussive research
Graves, M. (1941-2021). Research on cardiac rhythm, percussive entrainment, and adaptive rhythmic capacity. Body of work comprising: recordings of student and patient cardiac rhythms at Bennington College (1973-2012); development of software for analysing micro-rhythmic cardiac sounds; lecture-demonstrations on the relationship between drumming patterns and cardiac function; and the proposition that cardiac health is characterised by rhythmic adaptability rather than rhythmic regularity. Documented in: Meginsky, J. and Young, N. (dirs.) (2018), Milford Graves: Full Mantis, feature-length documentary film; Christman, M. (curator) (2020-2023), Milford Graves: A Mind-Body Deal, travelling retrospective exhibition (Institute of Contemporary Art Philadelphia; Artists Space New York; ICA Los Angeles; Bennington College); and Graves, M. (1998), Grand Unification, Tzadik Records (audio documentation of cardiac rhythm research). Guggenheim Fellow (2000). Doris Duke Foundation Impact Award (2015). Professor Emeritus, Black Music Division, Bennington College.
Retinal vasculature and cardiovascular diagnostics
Wong, T. Y., and Mitchell, P. (2004). Hypertensive retinopathy. New England Journal of Medicine, 351(22), 2310-2317.
McGeechan, K., Liew, G., Macaskill, P., Irwig, L., Klein, R., Klein, B. E. K., Wang, J. J., Mitchell, P., Vingerling, J. R., Dejong, P. T. V. M., Witteman, J. C. M., Breteler, M. M. B., Shaw, J., Zimmet, P., and Wong, T. Y. (2009). Meta-analysis: retinal vessel caliber and risk for coronary heart disease. Annals of Internal Medicine, 151(6), 404-413.
Liew, G., Wang, J. J., Mitchell, P., and Wong, T. Y. (2008). Retinal vascular imaging: a new tool in microvascular disease research. Circulation: Cardiovascular Imaging, 1(2), 156-161.
Kanbay, M., Guldan, M., Ozbek, L., Copur, S., Mallamaci, F., and Zoccali, C. (2024). Unveiling the intricacies of chronic kidney disease: from ocular manifestations to therapeutic frontiers. European Journal of Clinical Investigation, 55(1), e14324.
Liu, R., Jian, W., Zhao, Y., Lu, X., Wu, Y., and Duan, J. (2020). Retinal oxygen saturation and vessel diameter in patients with chronic kidney disease. Acta Ophthalmologica, 99(3), e352-e359.
Periodontal disease and cardiovascular correlation
Lockhart, P. B., Bolger, A. F., Papapanou, P. N., et al. (2012). Periodontal disease and atherosclerotic vascular disease: does the evidence support an independent association? A scientific statement from the American Heart Association. Circulation, 125(20), 2520-2544.
Tran, A. H., Zaidi, A. H., Bolger, A. F., et al. (2026). Periodontal disease and atherosclerotic cardiovascular disease: a scientific statement from the American Heart Association (updated). Circulation, 153, e73-e88.
Cardiac interoception and heartbeat-evoked potentials
Critchley, H. D., and Garfinkel, S. N. (2017). Interoception and emotion. Current Opinion in Psychology, 17, 7-14.
Garfinkel, S. N., Seth, A. K., Barrett, A. B., Suzuki, K., and Critchley, H. D. (2015). Knowing your own heart: distinguishing interoceptive accuracy from interoceptive awareness. Biological Psychology, 104, 65-74.
Garfinkel, S. N., and Critchley, H. D. (2016). Threat and the body: how the heart supports fear processing. Trends in Cognitive Sciences, 20(1), 34-46.
Edwards, L., Ring, C., McIntyre, D., Winer, J. B., and Martin, U. (2009). Sensory detection thresholds are modulated across the cardiac cycle: evidence that cutaneous sensibility is greatest for systolic stimulation. Psychophysiology, 46(2), 252-256.
Arterial stiffness, pulse wave velocity, and vascular remodelling
Laurent, S., Cockcroft, J., Van Bortel, L., Boutouyrie, P., Giannattasio, C., Hayoz, D., Pannier, B., Vlachopoulos, C., Wilkinson, I., and Struijker-Boudier, H. (2006). Expert consensus document on arterial stiffness: methodological issues and clinical applications. European Heart Journal, 27(21), 2588-2605.
Boutouyrie, P., Laurent, S., and Briet, M. (2008). Importance of arterial stiffness as cardiovascular risk factor for future development of new type of drugs. Fundamental and Clinical Pharmacology, 22(3), 241-246.
Microvascular assessment and capillaroscopy
Roustit, M., and Cracowski, J. (2012). Non-invasive assessment of skin microvascular function in humans: an insight into methods. Microcirculation, 19(1), 47-64.
Anyfanti, P., Gkaliagkousi, E., Triantafyllou, A., et al. (2018). Dermal capillary rarefaction as a marker of microvascular damage in patients with rheumatoid arthritis: association with inflammation and disorders of the macrocirculation. Microcirculation, 25(5), e12451.
Epilepsy, SUDEP, and brain-heart coupling
Nashef, L., So, E. L., Ryvlin, P., and Tomson, T. (2012). Unifying the definitions of sudden unexpected death in epilepsy. Epilepsia, 53(2), 227-233.
Ryvlin, P., Nashef, L., Lhatoo, S. D., et al. (2013). Incidence and mechanisms of cardiorespiratory arrests in epilepsy monitoring units (MORTEMUS): a retrospective study. Lancet Neurology, 12(10), 966-977.
Lotufo, P. A., Valiengo, L., Bensenor, I. M., and Brunoni, A. R. (2012). A systematic review and meta-analysis of heart rate variability in epilepsy and antiepileptic drugs. Epilepsia, 53(2), 272-282.
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The heart was beating before the word “regular” existed.
This patent proposes we stop correcting it and start listening.