pyPPG: A Python toolbox for comprehensive photoplethysmography signal analysis

Photoplethysmography is a non-invasive optical technique that measures changes in blood volume within tissues. It is commonly and increasingly used for in a variety of research and clinical application to assess vascular dynamics and physiological parameters. Yet, contrary to heart rate variability measures, a field which has seen the development of stable standards and advanced toolboxes and software, no such standards and open tools exist for continuous photoplethysmogram (PPG) analysis. Consequently, the primary objective of this research was to identify, standardize, implement and validate key digital PPG biomarkers. This work describes the creation of a standard Python toolbox, denoted pyPPG, for long-term continuous PPG time series analysis recorded using a standard finger-based transmission pulse oximeter. The improved PPG peak detector had an F1-score of 88.19% for the state-of-the-art benchmark when evaluated on 2,054 adult polysomnography recordings totaling over 91 million reference beats. This algorithm outperformed the open-source original Matlab implementation by ~5% when benchmarked on a subset of 100 randomly selected MESA recordings. More than 3,000 fiducial points were manually annotated by two annotators in order to validate the fiducial points detector. The detector consistently demonstrated high performance, with a mean absolute error of less than 10 ms for all fiducial points. Based on these fiducial points, pyPPG engineers a set of 74 PPG biomarkers. Studying the PPG time series variability using pyPPG can enhance our understanding of the manifestations and etiology of diseases. This toolbox can also be used for biomarker engineering in training data-driven models. pyPPG is available on physiozoo.orgComment: The manuscript was submitted to "Physiological Measurement" on September 5, 202

Electrocardiography versus photoplethysmography in assessment of maternal heart rate variability during labor

Evaluation of maternal heart rate (MHR) variability provides useful information on the maternal-fetal clinical state. Electrocardiography (ECG) is the most accurate method to monitor MHR but it may not always be available, and pulse oximetry using photoplethysmography (PPG) can be an alternative. In this study we compared ECG and PPG signals, obtained with conventional fetal monitors, to evaluate signal loss, MHR variability indices, and the ability of the latter to predict fetal acidemia and operative delivery.info:eu-repo/semantics/publishedVersio

Haemodynamic optimization of cardiac resynchronization therapy

Heart failure carries a very poor prognosis, unless treated with the appropriate pharmacological agents which, have been evaluated in large randomized clinical trials and have demonstrated improvements in morbidity and mortality of this cohort of patients. A significant proportion of these patients develop conduction abnormalities involving both the atrioventricular node and also the specialised conduction tissue (bundle of His and Purkinje fibers) of the ventricular myocardium which is most commonly evidenced by the presence of a wide QRS, typically left bundle branch block. The net effect of these conduction abnormalities is inefficient filling and contraction of the left ventricle. The presence of these conduction abnormalities is an additional strong marker of poor prognosis. Over the last 15 years pacing treatments have been developed aimed at mitigating the conduction disease. Large scale randomized multicentre trials have repeatedly demonstrated the effectiveness of cardiac pacing, officially recognized as cardiac resynchronization therapy (CRT). This mode of pacing therapy has undoubtedly had a positive impact on both the morbidity and mortality of these patients. Despite the large advancement in the management of heart failure patients by pacing therapies, a significant proportion of patients (30%) being offered CRT are classed as non-responders. Many explanations have been put forward for the lack of response. The presence of scar at the pacing site with failure to capture or delayed capture of myocardium, too much left ventricular scar therefore minimal contractile response, incorrect pacing site due to often limited anatomical options of lead placement and insufficient programming i.e optimization, of pacemaker settings such as the AV and VV delay are just some of the suggested areas perceived to be responsible for the lack of patients’ response to cardiac resynchronization therapy. The effect of optimization of pacemaker settings is a field that has been investigated extensively in the last decade. Disappointingly, current methods of assessing the effect of optimization of pacemaker settings on several haemodynamic parameters, such as cardiac output and blood pressure, are marred with very poor reproducibility, so measurement of any effect of optimization is close to being meaningless. Moreover, detailed understanding of the effects of CRT on coronary physiology and cardiac mechanoenergetics is equally, disappointingly, lacking. In this thesis, I investigated the acute effects of cardiac resynchronization therapy and AV optimization on coronary physiology and cardiac mechanoenergetics. This was accomplished using very detailed and demanding series of invasive catheterization studies. I used novel analytical mathematical techniques, such as wave intensity analysis, which have been developed locally and this provided a unique insight of the important physiological entities defining coronary physiology and cardiac mechanics. I explored in detail the application and reliability of photoplethysmography as a tool for non-invasive optimization of the AV delay. Photoplethysmography has the potential of miniaturization and therefore implantation alongside pacemaker devices. I compared current optimization techniques (Echocardiography and ECG) of VV delay against beat-to-beat blood pressure using the Finometer device and defined the criteria that a technique requires if such a technique can be used meaningfully for the optimization of pacemaker settings both in clinical practice and in clinical trials. Finally, I investigated the impact of atrial pacing and heart rate on the optimal AV delay and attempted to characterize the mechanisms underlying any changes of the optimal AV delay under these varying patient and pacing states. In this thesis I found that optimization of AV delay of cardiac resynchronization therapy not only improved cardiac contraction and external cardiac work, but also cardiac relaxation and coronary blood flow, when compared against LBBB. I found that most of the increase in coronary blood flow occurred during diastole and that the predominant drive for this was ventricular microcirculatory suction as evidenced by the increased intracoronary diastolic backward-travelling decompression wave. I showed that non-invasive haemodynamic optimization using the plethysmograph signal of an inexpensive pulse oximeter is as reliable as using the Finometer. Appropriate processing of the oximetric signal improved the reproducibility of the optimal AV delay. The advantage of this technology is that it might be miniaturized and implanted to provide automated optimization. In this thesis I found that other commonly used modalities of VV optimization such as echocardiography and ECG lack internal validity as opposed to non-invasive haemodynamic optimization using blood pressure. This finding will encourage avoidance of internally invalid modalities, which may cause more harm than good. In this thesis I found that the sensed and paced optimal AV delays have, on average, a bigger difference than the one assumed by the device manufacturers and clinicians. As a significant proportion of patients will be atrially paced, especially during exercise, optimization during this mode of pacing is equally crucial as it is during atrial sensing. Finally, I found that the optimal AV delay decreases with increasing heart rate, and the slope of this is within the range of existing pacemaker algorithms used for rate adaptation of AV delay, strengthening the argument for the rate adaptation to be programmed on.Imperial Users Onl

From Wearable Sensors to Smart Implants – Towards Pervasive and Personalised Healthcare

<p>Objective: This article discusses the evolution of pervasive healthcare from its inception for activity recognition using wearable sensors to the future of sensing implant deployment and data processing. Methods: We provide an overview of some of the past milestones and recent developments, categorised into different generations of pervasive sensing applications for health monitoring. This is followed by a review on recent technological advances that have allowed unobtrusive continuous sensing combined with diverse technologies to reshape the clinical workflow for both acute and chronic disease management. We discuss the opportunities of pervasive health monitoring through data linkages with other health informatics systems including the mining of health records, clinical trial databases, multi-omics data integration and social media. Conclusion: Technical advances have supported the evolution of the pervasive health paradigm towards preventative, predictive, personalised and participatory medicine. Significance: The sensing technologies discussed in this paper and their future evolution will play a key role in realising the goal of sustainable healthcare systems.</p> <p> </p

Pattern recognition applied to airflow recordings to help in sleep Apnea-Hypopnea Syndrome diagnosis

El Síndrome de la Apnea Hipopnea del Sueño (SAHS) es un trastorno caracterizado por pausas respiratorias durante el sueño. Se considera un grave problema de salud que afecta muy negativamente a la calidad de vida y está relacionada con las principales causas de mortalidad, como los accidentes cardiovasculares y cerebrovasculares. A pesar de su elevada prevalencia (2–7%) se considera una enfermedad infradiagnosticada. El diagnóstico estándar se realiza mediante polisomnografía (PSG) nocturna, que es un método complejo y de alto coste. Estas limitaciones han originado largas listas de espera. Esta Tesis Doctoral tiene como principal objetivo simplificar la metodología de diagnóstico del SAHS . Para ello, se propone el análisis exhaustivo de la señal de flujo aéreo monocanal. La metodología propuesta se basa en tres fases (i) extracción de características, (ii) selección de características, y (iii) procesado de la señal mediante métodos de reconocimiento de patrones. Los resultados obtenidos muestran un alto rendimiento diagnóstico de la propuesta tanto en la detección como en la determinación del grado de severidad del SAHS. Por ello, la principal conclusión de la Tesis Doctoral es que los métodos de reconocimiento automático de patrones aplicados sobre la señal de flujo aéreo monocanal resultan de utilidad para reducir la complejidad del proceso de diagnóstico del SAHS.Departamento de Teoría de la Señal y Comunicaciones e Ingeniería Telemátic

The heart of epilepsy: Cardiac comorbidity and sudden death

The research described in this thesis aims to increase understanding of cardiac comorbidities and sudden unexpected death in epilepsy (SUDEP). People with epilepsy have a three-fold increased risk of dying prematurely compared to the general population. Common contributors to this are cardiovascular comorbidities, of which I provide an overview. Cardiovascular conditions and epilepsy can both lead to transient loss of consciousness (TLOC) with overlapping semiology. Particularly, myoclonic jerks which are commonly observed during syncope can be mistaken for signs of epilepsy. A misdiagnosis with detrimental consequences. I provide evidence that a careful analysis of motor phenomena can distinguish the two conditions. SUDEP is the commonest direct epilepsy-related premature death (UK >500 people/year). It typically occurs following convulsive seizures (CS). Most victims are found prone and some suggested people should sleep supine. I assessed video-EEG recordings of 180 CS and demonstrated peri-ictal positions often change, and most ending prone turned during CS. Sleeping supine is thus unlikely to prevent a postictal prone position and reduce risk of SUDEP. Pathomechanisms underlying SUDEP are likely a combination of interacting cardiorespiratory and autonomic factors. People with Dravet syndrome (DS) have a particular high SUDEP risk. I show that 49% of reported deaths in DS are SUDEP cases, most <10 years (78%). In DS, SCN1A mutations are mostly found, encoding a sodium channel expressed in brain and heart. DS mouse models suggest a key role for peri-ictal cardiac arrhythmias in SUDEP. I conducted a multicentre observational study and recorded 547 seizures in 45 DS participants. No major peri-ictal arrhythmias were found. Peri-ictal QTc-lengthening was, however, more common in DS than controls. This may reflect unstable repolarisation and increased propensity for arrhythmias. Prospective data to determine whether these peri-ictal variables can predict SUDEP risk is warranted

Biomarkers of Sudden Unexpected Death in Epilepsy (SUDEP)

La SUDEP (Sudden Unexpected Death in Epilepsy) è una complicanza devastante dell’epilessia e rappresenta la più comune causa di mortalità prematura in epilessia. Studi volti alla definizione di fattori di rischio clinici hanno permesso di identificare gruppi ad alto rischio. Tuttavia al momento non esistono validati biomarkers genomici, elettrofisiologici o strutturali predittivi di aumentato rischio di SUDEP. Al fine di definire la base genetica della SUDEP, abbiamo condotto una analisi di sequenziamento esomico per esaminare la prevalenza di varianti con effetto deleterio in soggetti deceduti per SUDEP rispetto a pazienti epilettici non deceduti e controlli con altre patologie. Abbiamo riscontrato una prevalenza significativamente aumentata di varianti deleterie diffuse a livello dell’intero genoma nei soggetti deceduti per SUDEP in confronto agli altri gruppi. Un secondo studio di neuroimaging è stato dedicato alla valutazione di anomalie regionali del volume della sostanza grigia in soggetti deceduti per SUDEP, confrontati con soggetti epilettici viventi rispettivamente ad alto e basso rischio per SUDEP, e controlli sani. Abbiamo riscontrato un aumento del volume della sostanza grigia in emisfero destro a livello di amigdala, parte anteriore dell’ippocampo e paraippocampo nei soggetti deceduti per SUDEP e nei soggetti ad alto rischio, rispetto ai soggetti a basso rischio ed ai controlli. Sia il sequenziamento esomico sia il neuroimaging strutturale hanno fornito dati significativi per il profilo di rischio di SUDEP. La definizione dei meccanismi eziologici della SUDEP è fondamentale. La traslazione di tali dati in algoritmi predittivi di rischio individuale consente di promuovere la ‘medicina personalizzata’, allo scopo di adottare strategie preventive e ridurre il rischio individuale di SUDEP in pazienti con epilessia.SUDEP (Sudden Unexpected Death in Epilepsy) is the most devastating outcome in epilepsy and the commonest cause of epilepsy-related premature mortality. Studies of clinical risk factors have allowed identifying high-risk populations. However no genomic, electrophysiological or structural features have emerged as established biomarkers of an increased SUDEP risk. To elucidate the genetic architecture of SUDEP, we used an unbiased whole-exome sequencing approach to examine overall burden and over-representation of deleterious variants in people who died of SUDEP compared to living people with epilepsy and non-epilepsy disease controls. We found significantly increased genome-wide polygenic burden per individual in the SUDEP cohort when compared to epilepsy and non-epilepsy disease controls. The polygenic burden was driven both by the number of variants per individual, and overrepresentation of variants likely to be deleterious in the SUDEP cohort. To elucidate which brain regions may be implicated in SUDEP, we investigated whether regional abnormalities in grey matter volume appear in those who died of SUDEP, compared to subjects at high and low risk for SUDEP, and healthy controls. We identified increased grey matter volume in the right anterior hippocampus/amygdala and parahippocampus in SUDEP cases and people at high risk, when compared to those at low risk and controls. Compared to controls, posterior thalamic grey matter volume, an area mediating oxygen regulation, was reduced in SUDEP cases and subjects at high risk. It is fundamental to understand the range of SUDEP aetiological mechanisms. Our results suggest that both exome sequencing data and structural imaging features may contribute to generate SUDEP risk estimates. Translation of this knowledge into predictive algorithms of individual risk and preventive strategies would promote stratified medicine in epilepsy, with the aim of reducing an individual patient's risk of SUDEP

SCMR Position Paper (2020) on clinical indications for cardiovascular magnetic resonance

The Society for Cardiovascular Magnetic Resonance (SCMR) last published its comprehensive expert panel report of clinical indications for CMR in 2004. This new Consensus Panel report brings those indications up to date for 2020 and includes the very substantial increase in scanning techniques, clinical applicability and adoption of CMR worldwide. We have used a nearly identical grading system for indications as in 2004 to ensure comparability with the previous report but have added the presence of randomized controlled trials as evidence for level 1 indications. In addition to the text, tables of the consensus indication levels are included for rapid assimilation and illustrative figures of some key techniques are provided