This project shows a design for a low power and low noise analog front end for a heart variability sensor. Chopper Stabilization is a well known technique for reducing noise of an amplifier and is used to reduce the noise in the Instrumentation Amplifier in this project. A d/dt peak detector is used to find the peaks of the heart beats. Low power, low noise heart variability sensors can look for patterns in a patient’s heart beat which can be correlated to known patterns for certain diseases. This can help doctors determine a patient’s susceptibility to these disease and prescribe preventitive treatment in advance / text

Abstract Neurogenic factors are known to be important in the development of hypertension. Our current knowledge of the role of autonomic nervous system in chronic hypertension is, however, limited. The purpose of the present study was to evaluate the possible abnormalities in heart rate variability (HRV) and baroreflex sensitivity (BRS) in patients with long standing systemic hypertension compared to subjects without evidence of cardiovascular disease. A particular aim was also to examine whether genetic variation in the renin-angiotensin-aldosterone system (RAS) genes have an influence on cardiovascular autonomic regulation. Case-control studies were carried out on a total of 280 normotensive and 214 hypertensive subjects drawn from a random middle-aged population originally recruited for an epidemiologic study of cardiovascular risk factors. The possible association of BRS with the genetic polymorphisms of renin-angiotensin-aldosterone system genes was studied in a cross-sectional study of 315 healthy controls. Genetic associations were also tested in a younger, independent population sample of 66 subjects. The effects of intensified antihypertensive treatment on autonomic cardiovascular control were evaluated in 33 hypertensive patients with poor blood pressure control. Wide interindividual variation in both HRV and BRS was observed in normotensive as well as hypertensive subjects. Overall HRV and autonomic responses to a change in body posture were blunted in long-standing hypertension. Decreased HRV was mainly related to elevated blood pressure and obesity. For the first time in a population-based study, it was confirmed that BRS is impaired in patients with long-standing hypertension despite adequate antihypertensive treatment. In contrast to HRV, BRS was reduced in hypertensive subjects also after adjustment for blood pressure and obesity. BRS also varied widely both between healthy and hypertensive individuals. The wide interindividual variation in the markers of autonomic cardiovascular regulation was not, however, completely explained by demographic variables, cardiovascular risk factors or lifestyle, suggesting a genetic component contributing to HRV and BRS. The polymorphism in the aldosterone synthase (CYP11B2) gene was found to strongly associate with BRS in two independent random populations of apparently healthy subjects. The association was even stronger in the younger population. On the basis of the observations made in the older population, it seems possible that women are protected against the effect of age and blood pressure on BRS and tend to maintain the genomic influence longer. Intensified antihypertensive combination therapy improved blood pressure control and caused regression of left ventricular hypertrophy, and resulted in significant improvements of HRV and BRS. The present study shows that HRV and BRS are altered in long-standing systemic hypertension. Together with age, blood pressure and obesity, genetic factors seem to be important determinants of BRS. However, abnormal autonomic cardiovascular regulation does not seem to be an irreversible phenomenon, but can be partly restored by modern combination antihypertensive therapy.

Made available in DSpace on 2016-08-17T14:52:55Z (GMT). No. of bitstreams: 1 Marcio de Oliveira Santos.pdf: 375867 bytes, checksum: 9316c23a45525634b808c0315c716985 (MD5) Previous issue date: 2003-12-12 / The patient diagnosis can be made through a analysis of the cardiac variability that, being formed of nervous interactions, give the status of the vagal and sympathetic systems. The main measure to do this analysis is HRV, obtained by RR temporal differences or spectral methods. A major disadvantage we can find in the latter methods is a high sampling tax that yields in lost of information and high storage cost. New methods has been developed to minimize these incovenients, like HIF. This method have two steps: a driver function and a wavelet filter. The proposed algorithm is based on HIF using a auto regressive method as driver function and otimized parameters to the wavelet filter. The obtained results are very promissor and the estimation error is smaller than traditional methods one. / O diagnóstico de um paciente pode ser feito através da análise da variabilidade cardíaca que, por ser resultado de interações nervosas, fornece o estado dos sistemas vagal e simpático. A principal medida utilizada para se fazer esta análise é a taxa de variabilidade cardíaca (HRV) que pode ser obtida por métodos de diferença temporal de ondas R e espectrais. A principal desvantagem que é encontrada nestes métodos é que a alta taxa de amostragem do ECG é herdada por estes métodos, ocasionando perda de informação e o aumento de custo para armazenamento dos dados se torna mais alto. Para que este problema fosse solucionado foram desenvolvidas novas medidas que não apresentassem esses inconvenientes, como o algoritmo HIF. Este algoritmo é composto de duas etapas: a construção de uma função driver e filtragem através de uma wavelet de Gabor. O algoritmo proposto neste trabalho foi baseado no HIF utilizando um novo método autoregressivo (EAR) para função driver e otimizando-se os parâmetros da wavelet de Gabor. Os resultados obtidos mostraram que o algoritmo desenvolvido é bastante promissor e o erro de estimação é bem menor em relação a HIF.

Le comportement empathique d’autrui peut avoir un effet positif sur le ressenti douloureux. Dans le milieu médical, cette stratégie est encouragée par les soignants pour interagir et soutenir les patients. A l’inverse, la non-empathie c’est-à-dire une attitude négative envers la personne qui souffre est proscrite par crainte d’effets délétères. Comment l’empathie et la non-empathie d’autrui influencent-elles la perception douloureuse ? Investiguer cette problématique est l’objectif de ce travail de thèse. Dans la première partie de ce travail, nous avons construit et validé une manipulation expérimentale nous permettant de délivrer des feedbacks empathiques à des sujets recevant des stimulations nociceptives. Les commentaires empathiques ont réduit significativement l’intensité douloureuse des sujets (-12%). En revanche, les commentaires non-empathiques n’ont pas changé la cotation douloureuse, comparativement à une situation neutre. Ils sont néanmoins suffisants pour influencer la réponse autonomique à la douleur. Les analyses d’imagerie cérébrale (IRMf) ont montré que la modulation de l’intensité douloureuse par l’empathie passerait par des interactions entre les structures du réseau par défaut (vmPFC et CCP/Prec), le DLPFC et l’insula postérieure. Seule l’activité du CCP/Prec est capable d’intégrer le contenu des feedbacks empathiques. Cette structure en changeant sa connectivité fonctionnelle engagerait des mécanismes de contrôle (vmPFC) capables d’interagir avec l’insula postérieure et antérieure pour réduire la perception douloureuse. L’étude d’un tel système de modulation à l’échelle du réseau fonctionnel de la douleur a apporté des résultats concordants. / Other’s empathetic behavior can have a positive effect on pain perception. In medical setting it is a known strategy from caregivers to support and interact with their patients. Conversely, unempathy, having a negative attitude towards the suffering person is outlawed out of fear of induce deleterious effects. How do empathy and unempathy from others influence pain perception? Investigating this issue is the aim of this thesis. First, we built and approved an experiment delivering different types of empathetic feedbacks to subjects who received nociceptive stimulations. The empathetic comments significantly alleviated subjects’ pain ratings (-12 %). The unempathetic comments did not influence the subjects’ pain ratings in comparison with neutral situation. However, they influenced autonomic response related to pain. Neuro-imaging studies shown that the pain intensity modulation related to empathetic feedbacks involved interactions between the core structures of the default network (vmPFC and PCC/Prec), the DLPFC and the posterior insula. Functional activations revealed that only the posterior cingulate cortex/precuneus activity was able to integrate the empathetic feedbacks’ content. Changing its functional connectivity, this structure would engage control mechanisms (vmPFC) able to interact with the posterior and anterior insula to reduce pain perception. The study of such modulation system at the level of the pain functional network provided consistent results.