Littérature scientifique sur le sujet « Cardiac contraction sensor »

From the origin of ancient Vedas or Shastras; there was an awareness of artificial intelligence but in different meanings. In present scenario, one has to perform a lot of research for the production of works relating with artificial intelligence. Basically, artificial intelligence is a huge group of skills from advanced machines used for finding the solutions of different fields i.e. in pharma fields or non-pharma fields. The problem of heart failure or heart attack is very big health issue which is assisted with more than 23 million peoples worldwide. Heart failure can be held due to the vasoconstriction or improper pumping mechanism of ventricles. Heart failure heart logic device is a new tsunami in the healthcare system for cardiac devices. This device is in two different forms which are as (ICD) implantable cardioverter defibrillator and other oneiscardiac resynchronization therapy defibrillator (CRT-D). Heart logic heart failure diagnostic device contains multiple sensors to track physiological functioning of the heart. There are Heart sound sensors which checks signs of elevated filling pressure and weakened ventricular contraction. There are also a sensor for checking pulmonary edema. Respiration sensor is used to monitor the rapid shallow breathing system which is associated with shortness of breath. Heart rate sensors check the heart rate and arrhythmia conditions. This device can predict heart failure events weeks before they happen. This artificial intelligence assisted device is showing the sensitivity in more than 70% of peoples to save the valuable lives of the human beings

Previous experimental studies demonstrated that in normal hearts, Peak Endocardial Acceleration (PEA), during isovolumic contraction phase, measured with an endocardial sensor (Best, Sorin) in the right ventricle (RV), tracks changes of left ventricular (LV) contractility. Aim of the study: To assess if PEA also tracks LV contractility changes in ischemic hearts resulting from coronary microembolizations (ME). Methods: Under general anaesthesia, six adult beagle dogs (12 ± 2 kg) were instrumented for chronic monitoring of LV pressure, ECG and PEA. Latex beads mixed with fluoroscopy dye were injected into the circumflex coronary artery to cause LV ischemia. Before and after ME, incremental dobutamine infusions were performed to evaluate the contractile response to adrenergic stimulation. Results: A significant correlation between PEA and LVdP /dt max was observed before and after ME. Such a strong correlation was maintained even during adrenergic stimulation (r = 0.83 to 0.99, p < 0.001). The sensor PEA appears to be an effective means for the chronic monitoring of the mechanical function of ischemic hearts.

The aortic media realized Windkessel vessel functions and maintain sustained ventricle ejection balance during cardiac circle. Wheatstone bridge circuit piezoresistive strain sensor had desirable sensing properties to investigate aortic cushion features. In this study, Wheatstone bridge sensor was used to evaluate quick stretching-induced aortic efficient cushions and spontaneous myogenic contractions. Mice aortic specimens were loosely hooked and stabilized to [Formula: see text][Formula: see text]mm stainless steel pin and strain sensor, whereas the other side was hooked and shows increasing specimen length. Specimen isometric tension and rhythmic spontaneous myogenic contraction were recorded. Isometric tension and spontaneous myogenic response at initial length ([Formula: see text] and ultimate length ([Formula: see text] were evaluated. Aortic specimen significantly eliminated mechanical rigid oscillations. The recovery to baseline time was significantly shortened at [Formula: see text] ([Formula: see text][Formula: see text]ms and [Formula: see text] ms at [Formula: see text] and [Formula: see text], respectively, but [Formula: see text][Formula: see text]ms and [Formula: see text][Formula: see text]ms in no-load test). High Ca[Formula: see text] incubation prolonged the recovery time to baseline at [Formula: see text] and [Formula: see text] ([Formula: see text][Formula: see text]ms and [Formula: see text][Formula: see text]ms, respectively) and suggested Ca[Formula: see text] decreased efficient cushion. Moreover, strain sensor successfully recorded the enhanced rhythmic spontaneous myogenic contractions in isometric specimen. Wheatstone bridge circuit sensor reflected the significance of efficient cushions under mechanical preload, which absolutely captured rhythmic myogenic contractions of mice aortic specimen.

A few simple polymeric microsystems, such as microcantilever sensors, have recently been developed for the preliminary screening of cardiac toxicity. The microcantilever deflection produced by a change in the cardiomyocyte (CM) contraction force is important for understanding the mechanism of heart failure. In this study, a new numerical model is proposed to analyze the contractile behavior of CMs cultured on a perforated microcantilever surface for improving the performance of the microcantilever sensor. First, the surface traction model is used to investigate the bending displacement of the plain microcantilever. In order to improve the bending effect, a new numerical model is developed to analyze the bending behavior of the perforated microcantilever covered with CMs. Compared with the designed molds, the latter yields better results. Finally, a simulation analysis is proposed based on a finite element method to verify the presence of a preformed mold. Moreover, the effects of various factors on the bending displacement, including microcantilever size, Young’s modulus, and porosity factor, are investigated. Both the simulation and numerical results have good consistency, and the maximum error between the numerical and simulation results is not more than 3.4%, even though the porosity factor reaches 0.147. The results show that the developed mold opens new avenues for CM microcantilever sensors to detect cardiac toxicity.

The functional separation between skeletal and cardiac muscles, which occurs at the threshold between vertebrates and invertebrates, involves the evolution of separate contractile and control proteins for the two types of striated muscles, as well as separate mechanisms of contractile activation. The functional link between electrical excitation of the surface membrane and activation of the contractile material (known as excitation–contraction [e–c] coupling) requires the interaction between a voltage sensor in the surface membrane, the dihydropyridine receptor (DHPR), and a calcium release channel in the sarcoplasmic reticulum, the ryanodine receptor (RyR). Skeletal and cardiac muscles have different isoforms of the two proteins and present two structurally and functionally distinct modes of interaction. We use structural clues to trace the evolution of the dichotomy from a single, generic type of e–c coupling to a diversified system involving a novel mechanism for skeletal muscle activation. Our results show that a significant structural transition marks the protochordate to the Craniate evolutionary step, with the appearance of skeletal muscle–specific RyR and DHPR isoforms.

Heart related ailments are some of the most common causes for death in the world, and some of the causes are cardiac toxicity due to drugs. Several platforms have been developed in this regard over the years that can measure electrical or mechanical behavior of cardiomyocytes. In this study, we have demonstrated a biomedical device that can simultaneously measure electrophysiology and contraction force of cardiomyocytes. This dual-function device is composed of a photosensitive polymer-based cantilever, with a pair of metal-based interdigitated electrodes on its surface, such that the cantilever can measure the contraction force of cardiomyocytes and the electrodes can measure the impedance between cells and substrate. The cantilever is patterned with microgrooves so that the cardiomyocytes can align to the cantilever in order to make a higher cantilever deflection in response to contraction force. Preliminary experimental results have identified the potential for use in the drug-induced cardiac toxicity tests, and further optimization is desirable to extend the technique to various bio-sensor areas.

This paper presents forcecardiography (FCG), a novel technique to measure local, cardiac-induced vibrations onto the chest wall. Since the 19th century, several techniques have been proposed to detect the mechanical vibrations caused by cardiovascular activity, the great part of which was abandoned due to the cumbersome instrumentation involved. The recent availability of unobtrusive sensors rejuvenated the research field with the most currently established technique being seismocardiography (SCG). SCG is performed by placing accelerometers onto the subject’s chest and provides information on major events of the cardiac cycle. The proposed FCG measures the cardiac-induced vibrations via force sensors placed onto the subject’s chest and provides signals with a richer informational content as compared to SCG. The two techniques were compared by analysing simultaneous recordings acquired by means of a force sensor, an accelerometer and an electrocardiograph (ECG). The force sensor and the accelerometer were rigidly fixed to each other and fastened onto the xiphoid process with a belt. The high-frequency (HF) components of FCG and SCG were highly comparable (r > 0.95) although lagged. The lag was estimated by cross-correlation and resulted in about tens of milliseconds. An additional, large, low-frequency (LF) component, associated with ventricular volume variations, was observed in FCG, while not being visible in SCG. The encouraging results of this feasibility study suggest that FCG is not only able to acquire similar information as SCG, but it also provides additional information on ventricular contraction. Further analyses are foreseen to confirm the advantages of FCG as a technique to improve the scope and significance of pervasive cardiac monitoring.

The ryanodine receptor (RyR) is a Ca2+ release channel in the sarcoplasmic reticulum of skeletal and cardiac muscles and plays a key role in excitation–contraction coupling. The activity of the RyR is regulated by the changes in the level of many intracellular factors, such as divalent cations (Ca2+ and Mg2+), nucleotides, associated proteins, and reactive oxygen species. Since these intracellular factors change depending on the condition of the muscle, e.g., exercise, fatigue, or disease states, the RyR channel activity will be altered accordingly. In this review, we describe how the RyR channel is regulated under various conditions and discuss the possibility that the RyR acts as a sensor for changes in the intracellular environments in muscles.

A novel transgenic rat strain has recently been generated that stably expresses the genetically engineered calcium sensor protein GCaMP2 in different cell types, including cardiomyocytes, to investigate calcium homeostasis. To investigate whether the expression of the GCaMP2 protein itself affects cardiac function, in the present work we aimed at characterizing in vivo hemodynamics in the GCaMP2 transgenic rat strain. GCaMP2 transgenic rats and age-matched Sprague-Dawley control animals were investigated. In vivo hemodynamic characterization was performed by left ventricular (LV) pressure-volume analysis. Postmortem heart weight data showed cardiac hypertrophy in the GCaMP2 group (heart-weight-to-tibial-length ratio: 0.26 ± 0.01 GCaMP2 vs. 0.23 ± 0.01 g/cm Co, P < 0.05). We detected elevated mean arterial pressure and increased total peripheral resistance in transgenic rats. GCaMP2 transgenesis was associated with prolonged contraction and relaxation. LV systolic function was not altered in transgenic rats, as indicated by conventional parameters and load-independent, sensitive indices. We found a marked deterioration of LV active relaxation in GCaMP2 animals (τ: 16.8 ± 0.7 GCaMP2 vs. 12.2 ± 0.3 ms Co, P < 0.001). Our data indicated myocardial hypertrophy, arterial hypertension, and impaired LV active relaxation along with unchanged systolic performance in the heart of transgenic rats expressing the GCaMP2 fluorescent calcium sensor protein. Special caution should be taken when using transgenic models in cardiovascular studies. NEW & NOTEWORTHY Genetically encoded Ca2+-sensors, like GCaMP2, are important tools to reveal molecular mechanisms for Ca2+-sensing. We provided left ventricular hemodynamic characterization of GCaMP2 transgenic rats and found increased afterload, cardiac hypertrophy, and prolonged left ventricular relaxation, along with unaltered systolic function and contractility. Special caution should be taken when using this rodent model in cardiovascular pharmacological and toxicological studies.

2009/2010
Therapy delivery in modern cardiac electrotherapy systems is based almost exclusively on the information about cardiac electrical depolarization. This kind of detection lacks any data about the myocardial contraction. An optimal heart rhythm control should integrate the assessment of the mechanical cardiac activity and related hemodynamic parameters to the already existing electrical signal analysis. A hemodynamic sensor integrated in pacing systems would be a valuable instrument for many applications. Only few hemodynamic sensors integrated in cardiac electrotherapy systems are currently available on the market. In order to fill the gap, I have explored the possibility of building a hemodynamic sensor for myocardial contraction detection that could be easily integrated in the existing cardiac pacing and defibrillator leads. In this thesis I propose two sensors. One is based on tribolectricity and the other one requires the measurement of high frequency lead parameters. The triboelectric sensor system measures the charge generated due to the triboelectric effect between one of the lead conductors and the inserted stylet as a result of the lead bending. The measurement system consists in sterile charge amplifiers for use in sterile operation field and a non-sterile enclosure containing isolation amplifiers and power supply. Atrial and right ventricular tensiometric signals were recorded during numerous ovine and human experiments and have shown good results under different measurement conditions. The main downside is the necessity of the additional hardware in terms of chronic stylet insertion in the pacing lead lumen. The sensor based on the measurement of high frequency (HF) pacing lead parameters has its origin in previous extensive in vitro experiments on the HF characteristics of the lead. These experiments have supported the idea of considering any bipolar lead to be a HF transmission line with its characteristic impedance and attenuation. An original study revaluing lead HF parameters after being soaked for more than a decade in the saline solution is presented. A parallel study on dry new leads was also carried out. The hemodynamic HF sensor is based on the variation of the pacing lead HF impedance and reflection coefficient due to its movement during cardiac contractions. The quality of the signal was proven in a series of ovine and human experiments and during dobutamine test in sheep. Both sensors would be feasible hemodynamic sensors for various applications: capture management, rate responsiveness, heart failure monitoring, CRT optimization, tachycardia hemodynamic stability assessment, AF therapy titration and vasovagal syncope prediction. These two sensors are unique for their simplicity and universality for all existing endovenous bipolar cardiac leads.
Nei moderni sistemi di stimolazione cardiaca, la terapia si basa quasi esclusivamente sull'informazione proveniente dalla depolarizzazione elettrica del miocardio. Questo metodo tuttavia, non prende in considerazione la componente meccanica della contrazione del muscolo cardiaco. Un sistema ottimale per il controllo dell'attività cardiaca dovrebbe valutare sia il segnale elettrico proveniente dal cuore sia i parametri emodinamici correlati alla contrazione del miocardio. Pertanto, un sensore emodinamico integrato nei sistemi di stimolazione cardiaca sarebbe uno strumento utile per varie applicazioni. Attualmente sul mercato sono disponibili pochi sensori emodinamici integrati nei sistemi di elettroterapia cardiaca. Nel mio progetto di ricerca ho investigato la possibilitŕ di realizzare un sensore emodinamico per la rivelazione delle contrazioni cardiache, che potesse essere facilmente integrato negli esistenti elettrocateteri per la stimolazione e defibrillazione. Ho proposto due sensori. Il primo si basa sull'effetto triboelettrico, il secondo misura le variazioni dei parametri degli elettrocateteri usati ad alta frequenza. Il primo sensore rileva la carica generata per effetto triboelettrico tra uno dei conduttori dell'elettrocatetere e il mandrino a forma di filo isolato, come conseguenza della piegatura dell'elettrocatetere durante le contrazioni del miocardio. Il sistema di rilevazione è composto da amplificatori sigillati e sterilizzati per l'utilizzo in campo operatorio sterile. Completa il sistema una scatola contenente l'alimentazione e amplificatori isolati, per l'uso al di fuori del campo sterile. Segnali elettrici sono stati registrati nell'atrio e ventricolo destro di ovini e umani, nel corso di numerosi esperimenti eseguiti in condizioni diverse. I risultati ottenuti confermano la fattibilitŕ di questo tipo di sensore, il cui maggiore svantaggio è rappresentato dalla necessità di tenere un supplementare mandrino isolato nell'elettrocatetere impiantato cronicamente. Il sensore basato sulla misurazione dei parametri in alta frequenza dell'elettrocatetere trova sue origini negli sperimenti sulle caratteristiche in alta frequenza dei cateteri considerati come una linea di trasmissione con un'impedenza caratteristica e l'attenuazione tipica della linea. Nella tesi viene descritto lo studio comparativo di questi parametri sugli stessi cateteri prima e dopo la loro immersione nella soluzione fisiologica per più di dieci anni. Inoltre, viene descritto lo stesso sperimento fatto con 15 nuovi cateteri. Il secondo sensore proposto si basa sulla misura della variazione dell'impedenza e del coefficiente di riflessione dell'elettrocatetere, considerato come una linea di trasmissione che viene piegata per effetto delle contrazioni del miocardio. La buona qualitŕ del segnale ottenuto è stata verificata con vari esperimenti condotti su ovini e umani. Il sensore è stato anche testato negli animali in ritmo artificialmente accelerato usando l'infusione di dobutamina. Entrambi i sensori proposti potrebbero venire impiegati in molteplici applicazioni nel campo dell'elettrostimolazione: adattamento automatico della corrente di stimolazione, stimolazione antibradicardica con frequenza adatta in pazienti cronotropicamente poco efficienti, monitoraggio dello scompenso cardiaco, ottimizzazione della CRT, valutazione della stabilitŕ emodinamica della tachicardia ventricolare, adattamento della terapia per la fibrillazione atriale e predizione della sincope neurocardiogenica. I due sensori descritti sono unici in termini di semplicità e versatilità, potendo venire integrati in tutti gli elettrocateteri bipolari attualmente presenti sul mercato.
XXII Ciclo
1980

Fetal magnetocardiography (fMCG) records the magnetic field generated by the electrical activity associated with the fetal cardiac muscle contraction and has emerged as an attractive tool for monitoring the fetal heart in-utero. The magnetic sensor array is placed above the maternal abdomen to receive the extremely weak magnetic signal of the fetal heart from 20 weeks of gestation onward. fMCG outperforms fetal electrocardiography (fECG) in its notably superior signal quality, as the magnetic field is considerably less affected by tissues with low electrical conductivity surrounding the fetal heart [1], which can drastically diminish the fECG signal amplitude.

Non invasive fractional flow reserve derived from CT coronary angiography (CT-FFR) has to date been typically performed using the principles of computational fluid analysis in which a lumped parameter coronary vascular bed model is assigned to represent the impedance of the downstream coronary vascular networks absent in the computational domain for each coronary outlet. This approach may have a number of limitations. It may not account for the impact of the myocardial contraction and relaxation during the cardiac cycle, patient-specific boundary conditions for coronary artery outlets and vessel stiffness. We have developed a novel approach based on 4D-CT image tracking (registration) and structural and fluid analysis based on one dimensional mechanical model, to address these issues. In our approach, we analyzed the deformation variation of vessels and the volume variation of vessels to better define boundary conditions and stiffness of vessels. We focused on the blood flow and vessel deformation of coronary arteries and aorta near coronary arteries in the diastolic cardiac phase from 70% to 100 %. The blood flow variation of coronary arteries relates to the deformation of vessels, such as expansion and contraction of the cross-sectional area, during this period where resistance is stable, pressure loss is approximately proportional to flow. We used a statistical estimation method based on a hierarchical Bayes model to integrate 4D-CT measurements and structural and fluid analysis data. Under these analysis conditions, we performed structural and fluid analysis to determine pressure, flow rate and CT-FFR. Furthermore, the reduced-order model based on fluid analysis was studied in order to shorten the computational time for 4D-CT-FFR analysis. The consistency of this method has been verified by a comparison of 4D-CT-FFR analysis results derived from five clinical 4D-CT datasets with invasive measurements of FFR. Additionally, phantom experiments of flexible tubes with and without stenosis using pulsating pumps, flow sensors and pressure sensors were performed. Our results show that the proposed 4D-CT-FFR analysis method has the potential to accurately estimate the effect of coronary artery stenosis on blood flow.