De nombreux événements cardiovasculaires se déroulent au cours du sommeil(13).Divers auteurs ont étudié la variabilité du rythme cardiaque durant les différentes phases du sommeil chez le sujet sain (2) ou souffrant de diverses pathologies (3,5). Seules quelques publications décrivent le lien entre le sommeil et la variabilité du rythme cardiaque (4). L’interaction entre la variabilité du rythme cardiaque et les spectres de puissance du signal EEG de sommeil peut être étudiée par une analyse de cohérence (12). Cette méthode donne les fonctions de cohérence, de gain et de décalage de phases entre deux signaux à une fréquence déterminée. Les signaux principaux utilisés pour cette analyse de cohérence sont la bande de puissance de haute fréquence (HF) de la variabilité de l’intervalle RR, reflet de l’activité cardiaque vagale (14), et la bande de puissance de fréquence delta du signal EEG, associée au sommeil lent profond (1), à la fréquence du maximum de cross-spectrum entre ces bandes de puissances. Dans le but de mieux comprendre cette interaction, diverses questions se posent : • Existe-t-il, chez l’homme jeune en bonne santé, une interaction entre les spectres de puissance de l’intervalle RR et du signal EEG ? • Quelle bande de fréquence des puissances du signal EEG est la plus liée à la bande de puissance de haute fréquence de la variabilité de l’intervalle RR au cours du sommeil ? • Quel est l’impact du vieillissement sur ce lien ? • Existe-t-il une altération complète (cohérence, gain, décalage de phase) de l’interaction entre la bande de puissance de HF de l’intervalle RR et la bande de puissance de fréquence delta de sommeil chez l’individu souffrant d’un syndrome d’apnées-hypopnées de sommeil (SAHS) modéré ou sévère ? • Y a-t-il une diminution des valeurs de la cohérence et une modification du décalage de phase entre les signaux de puissance des bandes de HF du signal ECG et de la fréquence delta de l’EEG au cours du sommeil de la personne souffrant d’insomnie chronique primaire? • Les valeurs du gain pourraient-elles être les seules à être altérées chez le patient souffrant d’un trouble dépressif majeur (TDM)? Pour répondre à ces questions, plusieurs groupes ont été constitués : 8 adultes jeunes (18-23 ans)(11), 19 hommes d’âge moyen (36-54 ans) vs. 16 adultes jeunes (16-28 ans)(10), 12 patients souffrant d’un SAHS sévère vs. 12 patients souffrant d’un SAHS modéré à sévère vs. 12 hommes contrôles (9), 14 hommes souffrant d’insomnie chronique primaire vs. 12 adultes contrôles (8), 10 hommes souffrant de TDM vs. 10 hommes contrôles(7). Aucun patient ne présente une autre pathologie que celle décrite et tous ont été sevrés d’éventuelles médications psychotropes. De ces analyses, il apparaît que, chez l’homme jeune en bonne santé, de toutes les bandes de puissance du signal EEG de sommeil, les modifications de la bande de puissance delta est la plus liée aux modifications de la bande de puissance de haute fréquence de la variabilité du rythme cardiaque (11); et que le lien entre les modifications observées entre les bandes de puissance delta et HF est stable malgré l’effet du vieillissement observé dans l’architecture du sommeil et le contrôle de l’activité cardiaque (10). Les patients souffrant de SAHS présentent une perte du contrôle du lien entre le sommeil et la variabilité du rythme cardiaque, avant même l’apparition des symptômes cliniques cardiaques (9). Les personnes souffrant d’insomnie chronique primaire montrent une diminution de la force, voire une instabilité, du lien dynamique entre l’activité cérébrale de sommeil et la variabilité du rythme cardiaque(8). Les patients souffrant de trouble dépressif majeur démontrent une diminution de l’efficacité du lien entre les structures impliquées dans le contrôle du sommeil et les centres cardiovasculaires, mais pas de la force de ce lien (7), comme suggéré par les observations d’une neuroplasticité altérée chez les personnes dépressives (6). L’étude de la relation entre l’activité cérébrale et la variabilité du rythme cardiaque au cours du sommeil pourrait donc permettre une meilleure compréhension des processus neuro-cérébraux impliqués dans le développement des maladies cardiovasculaires mais également des pathologies de sommeil et des maladies psychiatriques. Elle pourrait peut-être, à l’aide d’une technique simple comprenant des enregistrements ECG et EEG au cours du sommeil, anticiper l’apparition de maladies graves cardiovasculaires, bien avant les premiers signes de la pathologie et permettre ainsi l’application de mesures préventives plutôt que curatives. Références. 1. Aeschbach D, Borbély AA. All-night dynamics of the human sleep EEG. J Sleep Res 1993; 2:70-81. 2. Bonnet MH, Arand DL. Heart rate variability: sleep stage, time of night, and arousal influences. Electroencephalogr Clin Neurophysiol 1997; 102(5):390-396. 3. Bonnet MH, Arand DL. Heart rate variability in insomniacs and matched normal sleepers. Psychosom Med. 1998 Sep-Oct;60(5):610-5. 4. Brandenberger G, Viola AU, Ehrhart J, Charloux A, Geny B, Piquard F, Simon C. Age-related changes in cardiac autonomic control during sleep. J Sleep Res. 2003; 12(3):173-80. 5. Dingli K, Assimakopoulos T, Wraith PK, Fietze I, Witt C, Douglas NJ. Spectral oscillations of RR intervals in sleep apnoea/hypopnoea syndrome patients. Eur Respir J. 2003; 22: 943-50. 6. Fossati P, Radtchenko A, Boyer P. Neuroplasticity: from MRI to depressive symptoms. Eur Neuropsychopharmacol. 2004; 14 Suppl 5:S503-10. 7. Jurysta F, Kempenaers C; Lancini J; Lanquart JP; van de Borne P; Linkowski P. Altered interaction between cardiac vagal influence and delta sleep EEG suggests an altered neuroplasticity in patients suffering from major depressive disorder. Acta Psych Scand (in press) 8. Jurysta F, Lanquart J, Sputaels V, Dumont M, Migeotte PF, Leistedt S, Linkowski P, van de Borne P. The Impact of Chronic Primary Insomnia on the Heart Rate - EEG Variability Link. Clin. Neurophysiol. 2009; 120(6):1054-60. 9. Jurysta F, Lanquart JP, van de Borne P, Migeotte PF, Dumont M, Degaute JP, Linkowski P. The link between cardiac autonomic activity and sleep delta power is altered in men with sleep apnea-hypopnea syndrome. Am J Physiol Regul Integr Comp Physiol. 2006; 291(4):R1165-71. 10. Jurysta F, van de Borne P, Lanquart JP, Migeotte PF, Degaute JP, Dumont M, Linkowski P. Progressive aging does not alter the interaction between autonomic cardiac activity and delta EEG power. Clin Neurophysiol. 2005; 116(4):871-7. 11. Jurysta F, van de Borne P, Migeotte PF, Dumont M, Lanquart JP, Degaute JP, Linkowski P. A study of the dynamic interactions between sleep EEG and heart rate variability in healthy young men. Clin. Neurophysiol. 2003; 114(11):2146-55. 12. Koopmans LH. The Spectral Analysis of Time Series. Academic Press. New York and London, 1974. 13. Lavery CE, Mittleman MA, Cohen MC, Muller JE, Verrier RL. Nonuniform nighttime distribution of acute cardiac events: a possible effect of sleep states. Circulation. 1997; 96(10):3321-7. 14. Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. Heart rate variability. Standards of measurement, physiological interpretation, and clinical use. Eur Heart J 1996; 17: 354-381.

Doctorat en Sciences médicales / info:eu-repo/semantics/nonPublished

Made available in DSpace on 2016-06-02T20:18:12Z (GMT). No. of bitstreams: 1 2946.pdf: 2432239 bytes, checksum: 38088e144c053efcf31c8e90a089b74f (MD5) Previous issue date: 2010-04-07 / Universidade Federal de Sao Carlos / Patients with chronic heart failure (CHF) and chronic obstructive pulmonary disease (COPD) present significant exertional dyspnea. The peripheral muscle dysfunction appears to be the greatest impact on the inability to perform physical exercise. Additionally, there is respiratory muscle weakness caused by a limited supply of O2 and alteration of mechanical ventilation. In this context, in order to better understand the manifestations of these disorders and to establish management strategies, we have proposed the development of three studies. The first study was entitled Deep breathing heart rate variability is associated with respiratory muscle weakness in patients with chronic obstructive pulmonary disease . The purpose of the present investigation was to evaluate the influence of respiratory muscle strength on autonomic control of heart rate variability (HRV) in these patients. Ten COPD patients (69±9 years; forced expiratory volume in the first second (FEV1)/forced vital capacity (FVC) 59±12% and FEV1 41±11% predicted) and nine age-matched healthy male volunteers (64±5 years) participated in this study. The maximal inspiratory pressure was obtained in the sitting position. Then, electrocardiography signal was obtained in three conditions: 1) lying position for 15 min; 2) lying position during the respiratory sinusal arrhythmia maneuver (RSA-M) for 4 min; and 3) sitting position for 15 min. Data was analyzed by the time (RMSSD and SDNN indexes) and the frequency domains, in total power, low frequency (LF), high frequency (HF) absolute (ab) and normalized (nu) units and LF/HF ratio. Regarding the RSA-M indexes, the expiratory/inspiratory ratio (E/I) and the inspiratory/expiratory difference (&#916;IE) were calculated. The patients with COPD demonstrated significantly impaired cardiac autonomic modulation at rest and during RSA-M when compared with healthy subjects (ratio E/I: 1.1±0.06 vs. 1.2±0.1 e &#916;IE: 7.0±3.5 vs 12.7±4.2, respectively). Moreover, significant and positive correlations between maximal inspiratory pressure (MIP) and the inspiratory-expiratory difference (&#916;IE) (r = 0.60, p<0.01) were found. In conclusion, patients with COPD presented impaired sympathetic-vagal balance at rest and during RSA-M. In addition, cardiac autonomic control of heart rate was associated with inspiratory muscle weakness in chronic obstructive pulmonary disease. Based on this evidence, future research applications of respiratory muscle training may bring to light a potentially valuable target for rehabilitation. The second study was entitled to Deep breathing heart rate variability xviii is able to reflect the respiratory muscle weakness in chronic heart failure . The purpose of the present investigation was to evaluate the influence of respiratory muscle strength on autonomic control in these patients. Ten CHF (62 ± 7 years left ventricle eject fraction of 40 ± 5% and NYHA class I-III) and nine matched-age healthy volunteers (64±5 years) participated in this study. Heart rate variability (HRV) was obtained at rest and during RSA-M by electrocardiograph (as previously described). CHF patients demonstrated impaired cardiac autonomic modulation at rest and during RSA-M when compared with healthy subjects (p<0.05). Moreover, significant and positive correlations between MIP and IE-differences (r: 0.79), E/I ratio (r: 0.83), RMSSD (r: 0.77), SDNN (r: 0.77), LFab (r: 0.77), HFab (r: 0.70) were found during RSA-M. At rest, significant correlations were also found. Patients with CHF presented impaired sympathetic-vagal balance at rest. In addition, cardiac autonomic control of heart rate was associated with inspiratory muscle weakness in CHF. Based on this evidence, recommendations for future research applications of respiratory muscle training can bring to light a potentially valuable target for rehabilitation. Finally, the third study: "Behavior of heart rate on determination of anaerobic threshold in healthy men: comparison with cardiopulmonary exercise testing and near-infrared spectroscopy" aimed to identify the anaerobic threshold (AT) obtained from the V-slope method , visual method on oxihemoglobin (O2Hb) and deoxihemoglobin (HHb) and compare the method with heteroscedastic (HS) applied to VCO2, HR and HHb data. Secondly, to assess the degree of agreement between the methods for determination of AT. Fourteen healthy men were subjected to incremental cardiopulmonary test (CPT) in the electromagnetic cycle-ergometer until physical exhaustion. At the same time they obtained the following biological signals: (i) ventilatory and metabolic variables - a breath to breath - measured by the Cardio2 System (Medical Graphics Corporation, St. Paul, MO, USAI), (ii) spectroscopy, quasiinfrared rays - NIRS (NIRO 300 - Hamamatsu Photonics, Japan), and (iii) heart rate through cardiofrequencymeter (Polar S810i). We observed temporal equivalence and similar values of power (W), absolute O2 consumption (mL/min) and relative O2 consumption (mL/kg/min) and HR (bpm) on determination of AT by the methods performed. In addition, by the Bland-Altman plot, HR (bpm) confirmed the good agreement between the methods with biases between -1.3 and 3.5. In conclusion: (i) all methods were sensitive in identifying the AT1, including the HS applied to FC, and (ii) the methods showed a good correlation in the identification of AT1. Thus the xix results support the FC, a methodology that is simple and economically feasible, seems to be a valid parameter in determining the AT of the individuals in our study. Therefore it remains to be clarified if these results can be replicated in patients with chronic cardiopulmonary disorders, contributing in safe, individualized and adequate prescribing physical exercise in rehabilitation programs. / Pacientes com insuficiência cardíaca crônica (ICC) e doença pulmonar obstrutiva crônica (DPOC) apresentam significativa dispnéia exercional. A disfunção muscular periférica parece ser a causa de maior impacto na incapacidade de realização de exercício físico. Adicionalmente, pode coexistir a fraqueza muscular respiratória provocada pela limitada oferta de O2 e a alteração da mecânica ventilatória. Neste contexto, com intenção de compreender melhor as manifestações dessas disfunções e estabelecer estratégias de manejo, foi proposto o desenvolvimento de três estudos. O primeiro intitulado por Deep breathing heart rate variability is associated with respiratory muscle weakness in patients with chronic obstructive pulmonary disease teve como objetivo, avaliar a influência da fraqueza muscular inspiratória sobre a o controle autonômico da frequência cardíaca (FC) de homens com DPOC. Foram estudados 10 pacientes (69±9 anos; FEV1/FVC 59±12% and FEV1 41±11% do predito) e 9 homens saudáveis (64±5 anos). Na posição sentada, foi medida a pressão inspiratória máxima (PIMax) dos voluntários. Na sequência, em repouso, o sinal eletrocardiográfico foi obtido em três situações: 1) 15 min na posição supina; 2) quatro min durante a manobra de acentuação da arritmia sinusal respiratória (MASR) na posição supina; e 3) 15 min na posição sentada. Os dados foram analisados no domínio do tempo (índices RMSSD e SDNN) e da freqüência, pela densidade espectral total (DET), bandas de baixa (BF) e alta freqüências (AF) - absolutas (ab) e normalizadas (un), e a razão BF/AF. Durante M-ASR foram calculadas a razão expiração/inspiração (E/I) e a diferença inspiração/expiração (&#916;IE). Os pacientes com DPOC apresentaram valores significativamente menores da variabilidade da frequência cardíaca (VFC) quando comparados ao grupo controle em repouso e durante a M-ASR (razão E/I: 1,1±0,06 vs. 1,2±0,1 e &#916;IE: 7,0±3,5 vs 12,7±4,2, respectivamente). Adicionalmente, foi observado correlação positiva entre PIMax e &#916;IE (r = 0.60, p<0.01). Em conclusão: (i) pacientes com DPOC apresentam prejuízos da modulação autonômica da FC em repouso e durante a M-ASR; e (ii) a fraqueza muscular inspiratória parece influenciar no desbalanço simpato-vagal desses pacientes. Em similaridade, no segundo estudo, intitulado com Deep breathing heart rate variability is able to reflect the respiratory muscle weakness in chronic heart failure o objetivo foi avaliar a influência da PIMax no controle autonômico da FC de pacientes com ICC. Foram estudados 10 pacientes com ICC xv (62±7 anos Fração de Ejeção do ventrículo esquerdo de 40 ± 5% e classificação IIII da NYHA). Seguindo a metodologia descrita no estudo anterior, os resultados mostraram que os pacientes com ICC também apresentaram menores valores da VFC em repouso e durante a M-ASR e correlações positivas e significativas entre PIMax e diferença expiração-inspiração (r: 0,79), razão expiração/inspiração (r: 0,83), RMSSD (r: 0,77), SDNN (r: 0,77), BF (r: 0,77), AF (r: 0,70). Em conclusão: (i) pacientes com ICC apresentam prejuízos da modulação autonômica da FC em repouso e durante a M-ASR; e (ii) a fraqueza muscular inspiratória parece influenciar no desbalanço simpato-vagal desses pacientes. Por fim, o terceiro estudo: Comportamento da frequência cardíaca na determinação do limiar de anaerobiose em homens saudáveis: análise comparativa com o teste cardiopulmonar e a espectroscopia por raios quasi-infravermelhos objetivou identificar do limiar de anaerobiose (LA) obtido pelo método padrão-ouro, método visual pelo comportamento da oxihemoglobina (O2Hb) e deoxihemoglobina (HHb) e comparar com o método heteroscedástico (HS) aplicado aos dados de VCO2, HHb e da FC. Secundariamente, avaliar o grau de concordância entre os métodos de determinação do limiar de LA. Quatorze homens saudáveis foram submetidos ao teste cardiopulmonar (TCP) incremental em cicloergômetro de frenagem eletromagnética até a exaustão física. Concomitantemente foram obtidos os seguintes sinais biológicos: (i) variáveis ventilatórias e metabólicas respiração a respiração - medida pelo sistema CardiO2 System (Medical Graphics Corporation, St. Paul, MO, USAi); (ii) espectroscopia por raios quasi-infravermelhos - NIRS (NIRO 300 Hamamatsu Photonics, Japan); e (iii) frequência cardíaca por meio do cardiofreqüencímetro (Polar S810i). Foram observadas equivalências temporais e das variáveis potência (W), consumo de O2 absoluto (mL/min) e relativo (mL/kg/min) e FC (bpm) na determinação do LA pelos métodos empregados. Em adição, pela análise de Bland-Altman, a FC (bpm) confirmou a boa concordância entre os médotos com viéses entre -1,3 e 3,5. Em conclusão: (i) todos os métodos mostraram-se sensíveis na identificação do LA1, inclusive o HS aplicado a FC; e (ii) os médotos apresentaram boa correlação na identificação do LA1. Assim os resultados suportam que a FC, uma metodologia mais simples e economicamente viável, parece ser um parâmetro válido na determinação do LA dos indivíduos do nosso estudo. Agora, basta saber se estes resultados podem ser replicados em pacientes com disfunções cardiorrespiratórias crônicas, contribuíndo na prescrição xvi segura, individualizada e adequada de exercício físico em programas de reabilitação.