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Cardiac Autonomic Control Buffers Blood Pressure Variability Responses to Challenge

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Abstract

This article presents a model that identifies effects of blood pressure variability (BPV) as a possible mechanism by which psychological/psychiatric factors and health behaviors confer increased risk of coronary artery disease (CAD) and acute coronary syndromes. Recent research in vascular biology and dynamics of coronary artery blood flow suggests that BPV may have pathogenic effects on the coronary endothelium, plaque formation, and plaque stability. Thus, BPV may be a risk factor for cardiovascular disease independent of mean arterial pressure. The model proposes that autonomic control of the heart exerts a buffering or inhibitory influence on oscillations in blood pressure. Established psychological/behavioral risk factors for CAD, such as depression, hostility, and anxiety, as well as physical deconditioning and aging, are associated with diminished autonomic control of the heart, which may disinhibit pathogenic BPV. Together, these data suggest a coherent, testable psychophysiological model of CAD. In this article, we review these data and make recommendations for research to examine the model.

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... In studies of 7-11year-old boys and in aggressive adolescents, heart rate variability was found to be inversely related to hostility and aggression, consistent with reduced parasympathetic (vagal) antagonism to increases in heart rate [121,122]. It has long been known that the same relationship exists between behavior and autonomic control of heart rate and of blood pressure in hostile/aggressive adults (so-called "Type A" personalities): this mode of reduced vagal control of heart rate and blood pressure is a significant predictor of cardiovascular disease [141,142]. In summary, developmental studies have established that early aggression and reduced parasympathetic autonomic control of heart rate are markers for adult antisocial behavior and cardiovascular disease. ...
... Post hoc tests demonstrated that high-frequency variability in Lows was lower than both Highs and Random males, consistent with a lack parasympathetic restraint on heart rate in Low line rats. At the same time, blood pressure variability was greater in Low line adult males, a condition that predicts later elevated blood pressure [142]. ...
... Thus, it is possible that High line adults will exhibit either the same sympathetic over-activity that characterizes High line juveniles, or lower parasympathetic activity, or both, in line with their anxious/depressed lifetime profile. Conversely, Low line cardiovascular functioning is expected to be characterized primarily by parasympathetic under-activity, consistent with their low anxiety profile, and paralleling human populations exhibiting lifelong aggression/ hostility [141,142]. ...
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Since its origin more than 30 years ago, developmental psychobiology has had as its central focus the role of early experience in the development of behavior and physiology. Genetically heterogeneous strains have generally been used in order to assure that any effects of experimentally altered early environments would not be likely to depend upon a unique genetic contribution. There were early interests in genetic effects, however, and in some instances, specific inbred strains were used in order to study environmental effects on a particular vulnerability or predisposition. It did not take researchers long to realize that the early environment of most mammals and birds consists of a complex and changing interaction with its parents and siblings. To better understand the mysteries of the prenatal and preweaning environments, an array of novel methods and approaches have been created that continue to be effectively used by researchers in developmental psychobiology. Yet this focus has come at a cost. There have been few cross-disciplinary efforts with the field of behavior genetics. This emphasis on environmental over genetic contributions to development over the last decades could perhaps have been justified on the grounds that the early genetic contribution could not be as readily described mechanistically or varied experimentally. In the past few years this picture has changed radically and so has the biological orientation toward genetic determinism. Development can now be studied by manipulating identified genes with known cellular effects at specific stages of development
... It buffers the body's fluctuations in blood pressure that occur in response to challenge via the baroreflexes. 51 Diastolic and systolic BP variability can carry different diagnostic associations. 52 Low beat-to-beat diastolic BP variability has been associated with high heart rate variability, potentially through a healthy, dampening baroreflex response to high systolic BP. 51 Nonetheless, participants in BPV studies exploring its diagnostic value are often cardiovascular patients or otherwise unwell. ...
... 51 Diastolic and systolic BP variability can carry different diagnostic associations. 52 Low beat-to-beat diastolic BP variability has been associated with high heart rate variability, potentially through a healthy, dampening baroreflex response to high systolic BP. 51 Nonetheless, participants in BPV studies exploring its diagnostic value are often cardiovascular patients or otherwise unwell. Hence, these studies may be skewed towards diseased individuals. ...
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Music lowers hypertensive patients’ blood pressure (BP) in the long-term, but the dynamics of BP during music-listening are not well understood. This study aims to determine: (1) whether individuals with high and normal BP respond to music differently; and, (2) whether music’s loudness or tempo drives these differences. Music with computer-altered tempo and loudness is rendered on a reproducing piano to 40 middle-aged participants, 20 with baseline BP above 140/90 mmHg (H-bBP) and 20 below (N-bBP) but above 90/60 mmHg, paired by playlist. Continuous BP was recorded whilst they listened to playlists of 9 tempo-and loudness-transposed versions of 8 distinct pieces of Western classical music (40 min) after a 5-minute baseline silence. Both participant groups’ mean systolic and diastolic BP rose significantly higher than baseline during music, with normotensives’ mean systolic and diastolic BP rising significantly more than hypertensives’. Both groups’ BP variability (indexed by range and standard deviation of continuous BP measurements) reduced during faster tempi, but not during increased loudness. BP variability is significantly higher for both groups during the slowest pieces, which maintain the originally performed tempi. These findings suggest that music’s long-term benefit, like exercise, may come from its power to temporarily physiologically activate listeners.
... The cardiac control system responds to mental and physical challenges. It buffers the body's fluctuations in blood pressure that occur in response to challenge via the baroreflexes 57 . Diastolic and systolic BP variability can carry different diagnostic associations 58 . ...
... Diastolic and systolic BP variability can carry different diagnostic associations 58 . Low beat-to-beat diastolic BP variability has been associated with high heart rate variability, potentially through a healthy, dampening baroreflex response to high systolic BP 57 . Nonetheless, participants in BPV studies exploring its diagnostic value are often cardiovascular patients or otherwise unwell. ...
Article
Full-text available
Music lowers hypertensive patients’ blood pressure (BP) in the long-term, but the dynamics of BP during music-listening are not well understood. This study aims to determine: (1) whether individuals with high and normal BP respond to music differently; and, (2) whether music’s loudness or tempo drives these differences. Music with computer-altered tempo and loudness is rendered on a reproducing piano to 40 middle-aged participants, 20 with baseline BP above 140/90 mmHg (H-bBP) and 20 below (N-bBP) but above 90/60 mmHg, paired by playlist. Continuous BP was recorded whilst they listened to playlists of 9 tempo- and loudness-transposed versions of 8 distinct pieces of Western classical music (40 min) after a 5-minute baseline silence. Both participant groups’ mean systolic and diastolic BP rose significantly higher than baseline during music listening, with normotensives’ mean systolic and diastolic BP rising significantly more than hypertensives’. Both groups’ BP variability (indexed by range and standard deviation of continuous BP measurements) reduced during faster tempi, but not during increased loudness. BP variability is significantly higher for both groups during the slowest pieces, which maintain the originally performed tempi. These findings suggest that music’s long-term benefit, like exercise, may come from its power to temporarily physiologically activate listeners.
... Subsequently, SAP oscillations are related to the changes in the systolic volume and/or strength of the systolic contraction via the Frank-Starling mechanism [8,37]. Short-term blood pressure oscillations are buffered by the high pressure baroreflex mechanism involving parasympathetic control of the heart rate [38]. In this context, the higher information transfer from RESP to SAP observed during HUT can be ascribed to the decreased ability of the baroreflex to buffer respiratory-related SAP oscillations during the orthostatic challenge, where parasympathetic nervous system influences are decreased [39]. ...
... Previous data show that detailed analyses of HRV and BPV together with baroreflex characteristics substantially improve our understanding of the autonomic dysregulation as an important pathogenetic mechanism of cardiovascular diseases [38]. An improved ability to disentangle the mechanisms underlying cardiovascular oscillations during various physiological conditions can improve our interpretation of the changes observed in their dynamics at the occurrence of pathological states. ...
Article
Cardiovascular complexity is a feature of healthy physiological regulation, which stems from the simultaneous activity of several cardiovascular reflexes and other non-reflex physiological mechanisms. It is manifested in the rich dynamics characterizing the spontaneous heart rate and blood pressure variability (HRV and BPV). The present study faces the challenge of disclosing the origin of short-term HRV and BPV from the statistical perspective offered by information theory. To dissect the physiological mechanisms giving rise to cardiovascular complexity in different conditions, measures of predictive information, information storage, information transfer and information modification were applied to the beat-to-beat variability of heart period (HP), systolic arterial pressure (SAP) and respiratory volume signal recorded non-invasively in 61 healthy young subjects at supine rest and during head-up tilt (HUT) and mental arithmetics (MA). Information decomposition enabled to assess simultaneously several expected and newly inferred physiological phenomena, including: (i) the decreased complexity of HP during HUT and the increased complexity of SAP during MA; (ii) the suppressed cardiorespiratory information transfer, related to weakened respiratory sinus arrhythmia, under both challenges; (iii) the altered balance of the information transferred along the two arms of the cardiovascular loop during HUT, with larger baroreflex involvement and smaller feedforward mechanical effects; and (iv) an increased importance of direct respiratory effects on SAP during HUT, and on both HP and SAP during MA. We demonstrate that a decomposition of the information contained in cardiovascular oscillations can reveal subtle changes in system dynamics and improve our understanding of the complexity changes during physiological challenges.
... CVR leads to the development of CVD by accelerating heart rate and blood pressure, causing increases in blood flow with enough force to damage the coronary endothelium and initiate coronary lesions (Knox, 2001). The specific processes by which CVR leads to CHD are thoroughly described (Knox, 2001;Sloan, Shapiro, Bagiella, Myers, & Gorman, 1999;Spence, Barnett, Manuck, & Jennings, 1996). ...
... As researchers attempt to understand the physiological processes mediating the effects of psychological variables on CVD, it may be useful to expand beyond the simple hyperreactivity model. The focus of research has shifted from measures of acute reactivity to measures of recovery (Glynn et al., 2002;Mayne, 2001) and variability (Roman, Pickering, Schwartz, Pini & Devereux, 2001;Sloan et al., 1999). Research should consider the influence of psychological variables on other cardiovascular responses not necessarily associated with hyperreactivity, such as increased vascular resistance. ...
... A cute stress has long been connected to cardiovascular risk (1). For individuals with posttraumatic stress disorder (PTSD), a disorder characterized by hyperarousal and frequent physiological symptoms related to anxiety and stress, dysregulation of the autonomic nervous system has been identified as an important precursor to cardiovascular disease, diabetes, and other health risks (2,3). Indeed, a key indicator of autonomic functioning and cardiovascular health, heart rate variability (HRV), is often depressed among individuals with PTSD (4). ...
... Lower HRV is a risk factor for arrhythmia and in turn is predictive of heart disease and cardiac arrest (12Y14). Reduced HRV may also accelerate atherosclerosis (2) and result in increased variability in blood pressure, which is itself an independent risk factor for coronary artery disease (15). ...
Article
Objective: Posttraumatic stress disorder (PTSD) has been linked to reduced heart rate variability (HRV), which is in turn a risk factor for cardiovascular disease and death. Although hyperarousal and anxiety are thought to underlie this association, behavioral health risks, including smoking, alcohol dependence, obesity, and sleep disturbance, represent potential mechanisms linking PTSD and HRV. Methods: To test this hypothesis, short-term laboratory-based and 24-hour ambulatory measures of HRV were collected from 227 young adults (18-39 years), 107 of whom were diagnosed as having PTSD. Latent variable modeling was used to assess the relationship of PTSD symptoms with HRV along with potential behavioral health mediators. Results: PTSD symptoms were associated with reduced HRV (β = -0.21, p = .002). However, this association was reduced in models that adjusted for cigarette consumption and history of alcohol dependence and was rendered nonsignificant in a model adjusting for sleep disturbance. Independent mediation effects were deemed significant via bootstrapping analysis. Together, the three behavioral health factors (cigarette consumption, history of alcohol dependence, and sleep disturbance) accounted for 94% of the shared variance between PTSD symptoms and HRV. Abdominal obesity was not a significant mediator. Conclusions: These results indicate that behavioral factors-specifically smoking, alcohol overuse, and sleep disturbance-mediate the association between PTSD and HRV-based indices of autonomic nervous system dysregulation. Benefits from psychiatric and psychological interventions in PTSD may therefore be enhanced by including modification of health behaviors.
... Nonlinear indices of heart rate variability can provide additional information to traditional measures, which have been shown to be independently relevant to cardiovascular morbidity (Lahiri et al. 2008;Stein et al. 2005). Increased blood pressure variability in response to challenge has been linked to an unfavorable reduction in cardiac autonomic control (Sloan et al. 1999;Taylor and Eckberg 1996). ...
... Higher levels of beat-tobeat blood pressure variability characterize a more activated state. Low-frequency blood pressure variability is mediated by vascular sympathetic activity (Sloan et al. 1999). ...
Article
Since there are several popular beliefs about putative health benefits of amusement which are empirically substantiated poorly about putative health benefits of amusement, the immediate cardiovascular effects of amusement were studied in detail. Cardiovascular activity was studied while participants were viewing humorous films, relative to a control condition involving no amusement. High-resolution measures of heart rate, heart rate variability, continuous blood pressure, and respiration were recorded, and the phase synchronization among the variables was analyzed, which provides information on the coordinated behavior of response systems. Viewing humorous films had cardiovascular effects indicating heightened sympathetic arousal, if they elicited intense amusement. No effects were observed for variables indicating parasympathetic input to the heart. The observed effects associated with amusement were not driven by changes in the respiration. The suppression of positive affect expressions did not produce any additional activation. The transient cardiovascular effects of amusement do not correspond to beneficial correlates of a habitual positive affect disposition reported in the literature, demonstrating that it would be erroneous to argue from the long-term effects of a positive affect disposition to the effects of a single amusing event.
... There are several potential mechanisms through which autonomic nervous system and vagal regulation may be associated with cognitive function, although the observational nature of our study means that we could not determine causality. Besides the above mentioned antiinflammatory reflex of vagus nerve, vascular conditions may be involved; sympathetic and parasympathetic activity interact to maintain blood pressure within a normal range and optimise brain blood perfusion (Sloan, Shapiro, Bagiella, Myers & Gorman, 1999). Disturbance of this regulation, leading to increased blood pressure variability, has been associated with cognitive problems (De Heus et al., 2021) and structural brain changes. ...
Article
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Background Autonomic dysfunction is common in dementia, yet its contribution to neurocognitive changes remains unknown. We investigated whether midlife cardiac vagal modulation, indexed by heart rate variability, associates with subsequent cognitive decline in adults without prior coronary heart disease or stroke. Methods The sample comprised 2702 (1924 men) individuals initially aged 44–69 years from the UK Whitehall II cohort. Data from the fifth (1997–1999), seventh (2002–2004) and ninth (2007–2009) phases were analysed. Global cognitive function was ascertained from tests assessing memory, reasoning, vocabulary, and fluency. We used 12-lead-ECG-based heart rate variability measures, that primarily reflect vagal modulation (i.e. RMSSD and HF-HRV). Linear mixed-effects models and logistic regression were employed. Results Results showed consistent associations between both vagally-mediated HRV measures and faster decline in global cognitive function. Specifically, low RMSSD and HF-HRV (lowest versus upper four quintiles) were associated with 0.07 SD (95% CI: -0.13, -0.01) and 0.06 SD (95% CI: -0.12, -0.004) accelerated 10-year cognitive decline after sociodemographic adjustments and faster decline in older ages. Further adjustments for lifestyle factors, medication use and other cardiometabolic conditions did not change the findings. Cognitive decline in individuals with low RMSSD and HF-HRV was estimated to progress 3 and 3.5 years faster per decade, respectively, compared to their counterparts. Additionally, participants with low RMSSD had 37% higher odds of low cognitive function (lowest quintile) at follow-up (OR 1.37: 95% CI,1.03, 1.80). Conclusion Our findings support the aetiological significance of the autonomic nervous system, specifically vagal modulation, in the processes of cognitive decline and neurodegeneration. Low heart rate variability emerges as a potential biomarker indicative of acclerated cognitive decline that may extend over decades.
... Psychological stress decreases the high-frequency component of heart rate variability (HRV) and increases the low-frequency component of HRV [8]. HRV decreases in patients with depression, manifestations of high hostility and anxiety [9]. Stress lowers the body's resistance to negative health effects [10]. ...
Article
Surgical trauma provokes body's stress response with activation of inflammatory, endo-crine, metabolic, and immunological factors, which is believed to be necessary and beneficial response. Aim of the study was to compare the effectiveness of local anesthetics lidocaine and articaine in septoplasty and tonsillectomy in terms of assessing the severity of stress reactions. Patients and Methods: 125 patients with nasal septum deviation (NSD) and chronic tonsillitis (CT) were observed. Patients with NSD were divided into 2 groups: 1A – 32 patients treated by 2% lidocaine local infiltration analgesia (LIA); 1B – 30 patients treated by 2% articaine LIA. Corresponding groups of patients with CT were 2A (32 patients) and 2B (31 patients). For all patients, heart rate variability (HRV), high, low and very low frequency components were measured. Results: Estimation of group variances of HRV showed there were some disadaptation in groups 1B and 2A. High dispersion of SDANN, SDNN index and rMSSD in 1B group, SDANN values in 2A group indicate the sympathetic/parasympathetic imbalance. High frequency component were augmented in 2B group which pointed out prevailing parasympathetic tone but its high dispersion was indicative of disadaptation as well. Conclusion: Thus, with the local infiltration application of an articaine solution during septoplasty, the autonomic nervous system dystonia is observed in the early postoperative period. When anesthesia with lidocaine solution during tonsillectomy, there is also a breakdown of adaptive responses against the background of surgical stress. Based on the above data, of the presented local anesthetics, lidocaine is more effective in septoplasty, and articaine in tonsillectomy.
... hRV is quantified primarily using respiratory sinus arrhythmia (Rsa), a measure of hRV in synchrony with respiration (shaffer et al., 2014;Yasuma & hayano, 2004). trauma and PtsD are both associated with lower hRV, which is linked with increased risk for cardiovascular disease (Dennis et al., 2017;sloan et al., 1999). similarly, a meta-analysis (k = 8) compared hRV between PlWh on aRt and individuals without hiV and found evidence for a shift toward sympathetic dominance in PlWh on aRt, with lower hRV (Mcintosh, 2016). ...
Article
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Objective People living with HIV (PLWH) experience high rates of childhood maltreatment, which increases risk for posttraumatic stress disorder (PTSD). Thus, it is important to understand how HIV status interacts with childhood maltreatment to influence PTSD symptom severity and underlying psychophysiology. Methods The current study assessed whether HIV status interacts with childhood maltreatment to influence PTSD symptom severity and heart rate variability during a dark-enhanced startle (DES) task in 88 Black women with (n=30) and without HIV (n=58). Results HIV was associated with greater PTSD symptom severity only in women with low levels of childhood maltreatment (p=.024). Startle potentiation during DES was highest in women living without HIV and with high childhood maltreatment (p=.018). In women who had experienced low levels of childhood maltreatment, respiratory sinus arrhythmia (RSA) was lower during the dark phase of DES in women living without HIV than women living with HIV (WLWH), (p=.046). RSA during the light phase of DES was lower in WLWH than in women living without HIV (p=.042). Conclusion In the current sample of Black women, HIV status was associated with PTSD symptom severity in a manner dependent on level of childhood maltreatment, suggesting that HIV status may be an important factor to consider for behavioral and pharmacological treatment strategies for PTSD. Additionally, HIV status is associated with lower percent potentiation to darkness and lower RSA during the light phase of DES, suggesting physiological mechanisms by which HIV may contribute to PTSD symptoms in individuals exposed to low levels of childhood maltreatment.
... Anxiety is associated with sympathetic activation. The effect of this activation could be the influence and possibly alteration of endothelial integrity [31][32][33][34][35][36], a strong indicator of progression of atherosclerosis. The relationship with anxiety reflects in the condition of anxious patients: they have sympathetic nervous system hyper reactivity [34].As such, diminished autonomic control of the heart and may induce higher blood pressure variability, with effects on the coronary endothelium and plaque formation [35]. ...
... La estimulación de los receptores b 2 produce vasodilatación en los vasos sanguíneos esqueléticos y coronarios, mientras que la estimulación de los receptores a produce vasoconstricción generalizada, aumentando la resistencia vascular periférica y la presión sanguínea. La estimulación del SNP reduce la tasa cardiaca y tiene una función protectora sobre el corazón (Sloan, Shapiro, Bagiella, Myers y Gorman, 1999), previniendo la aparición de arritmias e infartos. Un indicador no invasivo muy usado de la actividad vagal es la variabilidad de la tasa cardiaca (Reyes del Paso, Langewitz, Mulder, Van Roon y Duschek, 2013). ...
... Электрофизиологические данные указывают на то, что патологическая тревога нарушает вегетативную регуляцию сердечного ритма. Для тревожных состояний характерны активация симпатической нервной системы и изменение вагусного контроля с возможным увеличением вариабельности сердечного ритма при физической нагрузке, а затем и вне ее [16,17]. В этиологии СДВНС играют роль наследственно-конституциональные особенности деятельности вегетативной нервной системы, неблагоприятное течение беременности и родов; из приобретенных факторов имеют значение повреждения центральной нервной системы, психоэмоциональное напряжение, особенности личности, умственное и физическое перенапряжение, гормональный дисбаланс, инфекции, соматические заболевания, дегенеративно-дистрофические заболевания позвоночника, перенесенные операции, регулярное употребление алкоголя, курение, избыточная масса тела, гиподинамия, длительная работа за компьютером, длительный просмотр телевизионных программ и др. ...
Article
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This article is devoted to the analysis of hypertesive crises in patients with adrenal incidentalomas. Such patients, as a rule, have no symptoms of primary hyperaldosteronism or Cushing’s syndrome. In the meanwhile, sudden elevation of blood pressure suggests an idea of a pheochromocytoma. However this diagnosis is confirmed further not always. According to the conducted research authors came to a conclusion that crises of arterial hypertension in these patients could be most often caused by idiopathic hypertensia, somatoform disorder and, much more rare, sudden emission of catecholamins in a blood stream by a pheochromocytoma. The results of the analysis show the fact that a diagnostic opinion has been reached correctly doesn’t exclude need of undergoing the complete evaluation of patients.
... A esto hay que sumarle el hecho de que niveles elevados de noradrenalina, neurotransmisor implicado en la ansiedad y el estrés, se asocian con mayores niveles de colesterol total y LDLc [107]. Hay evidencias de que factores psicológicos y comportamentales (estrés, ansiedad, depresión…) se asocian con una disminución en el control autonómico del corazón, lo que induce una mayor variabilidad en la presión arterial debida a efectos en el endotelio y formación de placas de ateroma [137]. Estos factores también pueden afectar al estilo de vida, predominando un patrón más perjudicial caracterizado por menor actividad física, mayor consumo de tabaco y hábitos dietéticos menos saludables, lo que se traduce en un perfil lipídico más aterogénico [138][139][140]. ...
Thesis
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Las enfermedades cardiovasculares son la principal causa de muerte a nivel mundial. Aproximadamente entre el 30 y el 40 % de los infartos de miocardio suceden en situaciones con niveles normales de colesterol total y LDLc, por lo que no se pueden explicar por los factores de riesgo tradicionales. Esta situación crea la necesidad de buscar nuevos factores de riesgo a través de análisis más exhaustivos. Los factores analizados son el diámetro y número de partículas lipoproteicas, la carga eléctrica neta, el contenido y los componentes del LPS y las glicoformas de Apo CIII. Las poblaciones utilizadas son pacientes diagnosticados de LES, participantes controles y mujeres y hombres jóvenes y sanos. Los resultados obtenidos demuestran la importancia de análisis exhaustivos en la búsqueda de nuevos factores de riesgo, ya que favorecen el diagnóstico de perfiles lipídicos aterogénicos. El diámetro y número de partículas ayudan a identificar un perfil lipídico aterogénico en situaciones de estrés y ansiedad. La carga eléctrica se ve influenciada en casos de estrés y ansiedad, y en los pacientes con lupus tiene un efecto sobre el grosor de la íntima-media carotídea independiente a las características antropométricas, tabaquismo y perfil lipídico. Las glicoformas de Apo CIII se distribuyen de la misma forma en plasma y en las lipoproteínas; en cambio, el LPS y sus componentes no. Además, se obtienen una gran variedad de correlaciones con distintos comportamientos entre dichos parámetros y el perfil lipídico, en función del parámetro y de la lipoproteína en la que se encuentre. Por último, las glicoformas de Apo CIII afectan sobre la cantidad de LPS y de sus componentes que se encuentran unidos a las lipoproteínas. Todo esto lleva a la conclusión de la importancia de realizar análisis exhaustivos de las propiedades fisicoquímicas de las lipoproteínas, además del estudio de las interacciones entre ellas. Cardiovascular diseases are the main cause of death worldwide. Approximately, 30 - 40% of myocardial infarctions occur in situations with normal levels of total cholesterol and LDLc, so they cannot be explained by traditional risk factors. This situation creates the need to look for new risk factors through more exhaustive analysis. The factors analyzed are the diameter and particles number of lipoproteins, the net electric charge, the content and the components of LPS and the glycoforms of Apo CIII. The populations used are patients diagnosed with SLE, control participants and young, healthy women and men. The results obtained demonstrate the importance of exhaustive analysis in the search for new risk factors, since they favor the diagnosis of atherogenic lipid profiles. The diameter and particles number of lipoproteins help to identify an atherogenic lipid profile in situations of stress and anxiety. The net electric charge is influenced by stress and anxiety and, in patients with lupus, the net electric charge has an effect on the thickness of the carotid intima-media independent of the anthropometric characteristics, smoking and lipid profile. The Apo CIII glycoforms are also distributed in plasma and in lipoproteins; however, the LPS and its components do not. In addition, a great variety of correlations are obtained with different behaviors between these parameters and the lipid profile, as a function of the parameter and the lipoprotein where it is focated. Finally, Apo CIII glycoforms affect the amount of LPS and its components that are bound to lipoproteins. All this leads to the conclusion of the importance of carrying out exhaustive analyzes of the physical-chemical properties of lipoproteins, and the study of the interactions between them.
... The sympathetic and parasympathetic activity interact to maintain blood pressure within a normal range and regulate proper perfusion to the brain. 7,8,27 Failure to do so, resulting in higher blood pressure variability, has been associated with cognitive impairment, 28,29 and with structural brain changes related to hypertension, including cerebral white matter lesions, 30 and to stroke, including lacunar infarctions. 31 Furthermore, depressive symptoms 12,32 and cardiovascular disease risk factors 33 such as type-2 diabetes 10,11 and hypertension 7-9,34 have been associated with both lower HRV and worse cognitive function. ...
Article
Background: Low heart rate variability (HRV), a marker of cardiac autonomic dysfunction, has been associated with major risk factors of cognitive impairment. Yet, the direct association of HRV with cognitive function remains relatively unexplored, particularly in midlife. Methods: In 2005, 2 measures of short-term HRV, the SD of normal-to-normal intervals (SDNN) and the root mean square of successive differences (RMSSD), were calculated for participants of the Coronary Artery Risk Development in Young Adults study, and then categorized into quartiles. Five years later, 3 cognitive tests were administered for verbal memory ("Rey Auditory-Verbal Learning Test", RAVLT, range 0-15), processing speed ("Digit Symbol Substitution Test", DSST, range 0-133), and executive function ("Stroop interference"). Results: Two thousand one hundred and eighteen participants (57.7% female, 42.2% Black) with a mean baseline age of 45.3 years were included in this analysis. In demographic-adjusted models, compared to participants with quartile 1 SDNN (lowest quartile), participants in the upper quartiles of SDNN scored better on the DSST (quartile 4: β = 1.83 points better, P = 0.03; and quartile 3: β = 1.95 points better, P = 0.03) and on the stroop (quartile 3: β = 1.19 points better, P < 0.05; and quartile2: β = 1.44 points better, P = 0.02). After adjusting for behavioral and cardiovascular risk factors, higher quartile SDNN remained significantly associated with better stroop score (quartile 3: β = 1.21 points better, P = 0.04; and quartile 2: β = 1.72 points better, P < 0.01) but not with DSST. There was no association between quartile of RMSSD and cognitive function, from fully adjusted models. Conclusions: Our findings suggest that higher quartile SDDN is associated with better executive function in midlife, above, and beyond cardiovascular risk factors.
... 4,25 On the other hand, a lack of flexibility can lead to physical and psychological pathologies. 24,26 The sympathetic hyperactivity accompanying parasympathetic hypoactivity could characterize potential pathological mechanism causing the heightened risk of not only a cardiovascular pathology but also depression and anxiety disorders. 21,[27][28][29][30] Reduced HRV reflects amplified sympathetic activity and decreased parasympathetic activity in depressive patients. ...
Article
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Objective The aim of the study was to determine psychological, psychophysiological, and anthropometric factors connected with life events, level of depression, and quality of life in people at risk for cardiovascular disease and healthy controls. Methods This is a cross-sectional study involving arterial hypertension patients and healthy controls. There were several measurements including physical, anthropological, cardiovascular, and psychophysiological measurements and administration of questionnaires. Results A total of 99 participants were recruited for this study, 54 healthy controls (mean age: 35.59±13.39 years) and 45 patients with cardiovascular disease (CVD) (mean age: 46.33±12.39 years). The healthy controls and the patients with CVD significantly differed in the mean total score of life events, level of depression, quality of life score, temperature, blood pressure (BP), pulse transit time, heart rate, high-frequency total power, heart rate variability total power, waist-to-height ratio (WHtR), body fat percentage, fat control, pulse wave velocity, and augmentation index. In healthy subjects, the total score of the life events was not correlated with any cardiovascular or anthropometric factor. A score of depression significantly correlated with the WHtR, augmentation index, body fat percentage, and fat control. The quality of life – visual scale correlated with the body temperature, BP, and percentage of body fat. In the group of the patients with CVD, the score of the life events did not correlate with any measured cardiovascular or anthropometric factor. The level of depression correlated with the augmentation index. The quality of life – visual scale significantly correlated with body temperature, WHtR, and fat control. Conclusion The patients with CVD reported higher scores of life events, worse quality of life, and a greater level of depressive symptoms than healthy controls. In healthy controls, a higher mean total score of life events significantly negatively correlated with high-frequency total power, and the degree of depression correlated with being overweight. In patients with CVD, a score of depression was linked to being overweight.
... 4,25 On the other hand, a lack of flexibility can lead to physical and psychological pathologies. 24,26 The sympathetic hyperactivity accompanying parasympathetic hypoactivity could characterize potential pathological mechanism causing the heightened risk of not only a cardiovascular pathology but also depression and anxiety disorders. 21,[27][28][29][30] Reduced HRV reflects amplified sympathetic activity and decreased parasympathetic activity in depressive patients. ...
Article
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Background Psychological distress is considered as a component of the cardiovascular risk. The present study aims to determine which psychophysiological, electrocardiographic and anthropometric factors are correlated with life events, depression and quality of life in healthy adults. Method A total of 114 adults were examined using the Social Readjustment Rating Scale, the EuroQol Group 5-Dimension Self-Report Questionnaire, Beck Depression Inventory – Second Edition, Zung Self-Rating Depression Scale. Physiological measures included heart rate variability, skin conductance level and skin temperature. Anthropometric characteristics included weight, height, hip size, waistline, blood pressure, heart rate at rest and after mental activity, muscle mass, fat stock, percentage of the body fat, segmental distribution of muscle and fat mass, fat-free mass and the water content in the body. Finally, data from electrocardiographic examination included aortic pulse wave velocity, central aortic pressure and augmentation index. Results Life events in last two years correlate with worse quality of life and a higher level of depression. Life events in last two years also correlate with the increase of the risk factors for cardiovascular problems in terms of several anthropometric and physiological measures. Finally, life events in last two years was also related with the overweight. Conclusions Results suggest some possible mechanisms by which stress may exert adverse effects on cardiovascular morbidity and mortality in healthy persons. Primary preventive strategies with the stress management training may prove beneficial.
... This is also evidenced in reduced heart rate variability in psychological disorders including MDD [77][78][79]. Such autonomic dysfunction has been linked to increased risk of heart disease [80] and heart disease mortality and morbidity in MDD [35,81]. At a cellular level chronic sympathetic activation can increase oxidative stress and dysregulate apoptotic pathways to worsen myocardial injury [82] Sustained release or sudden spikes in catecholamine levels also increase risk of cardiac complications such as arrhythmias and sudden cardiac death. ...
Article
Ample evidence identifies strong links between major depressive disorder (MDD) and both risk of ischemic or coronary heart disease (CHD) and resultant morbidity and mortality. The molecular mechanistic bases of these linkages are poorly defined. Systemic factors linked to MDD, including vascular dysfunction, atherosclerosis, obesity and diabetes, together with associated behavioral changes, all elevate CHD risk. Nonetheless, experimental evidence indicates the myocardium is also directly modified in depression, independently of these factors, impairing infarct tolerance and cardioprotection. It may be that MDD effectively breaks the heart's intrinsic defense mechanisms. Four extrinsic processes are implicated in this psycho-cardiac coupling, presenting potential targets for therapeutic intervention if causally involved: sympathetic over-activity vs. vagal under-activity, together with hypothalamic-pituitary-adrenal (HPA) axis and immuno-inflammatory dysfunctions. However, direct evidence of their involvement remains limited, and whether targeting these upstream mediators is effective (or practical) in limiting the cardiac consequences of MDD is unknown. Detailing myocardial phenotype in MDD can also inform approaches to cardioprotection, yet cardiac molecular changes are similarly ill defined. Studies support myocardial sensitization to ischemic insult in models of MDD, including worsened oxidative and nitrosative damage, apoptosis (with altered Bcl-2 family expression) and infarction. Moreover, depression may de-sensitize hearts to protective conditioning stimuli. The mechanistic underpinnings of these changes await delineation. Such information not only advances our fundamental understanding of psychological determinants of health, but also better informs management of the cardiac consequences of MDD and implementing cardioprotection in this cohort.
... progress to chronic conditions, such as cardiovascular and metabolic diseases. PTSD has been linked to physiological reactivity indices (i.e., basal heart rate, blood pressure, heart rate variability, cortisol secretion, epinephrine, and norepinephrine; Buckley, Holohan, Greif, Bedard, & Suvak, 2004;Buckley & Kaloupek, 2001;Sloan, Shapiro, Bagiella, Myers, & Gorman, 1999), psychological states (i.e., trait hostility), and health risk behaviors (i.e., alcohol/substance use, higher body mass index [BMI], cigarette smoking, physical inactivity, poor diet, poor selfcare; Schnurr & Green, 2003) that elevate risk for chronic medical conditions. The majority of researchers have implicated the likely role of the autonomic nervous system dysregulation and abnormalities across stress-response systems in the onset and progression of chronic diseases among individuals with PTSD (Dedert et al., 2010;Lohr et al., 2015). ...
Article
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Nuestro estudio profundiza la literatura respecto de la asociación entre el trastorno de estrés postraumático (TEPT) y distintas condiciones médicas evaluando la magnitud de las diferencias en estas asociaciones según grupo étnico. El estudio examinó las diferencias entre grupos en la magnitud de la relación entre el TEPT y condiciones médicas crónicas (enfermedad cardiovascular, obesidad, diabetes, e hipertensión). Los datos obtenidos fueron de participantes Latinos (n = 3,224) y blancos no-Latinos (n = 4,180) de las Encuestas Psiquiátricas Epidemiológicas Colaborativas (Collaborative Psychiatric Epidemiology Surveys). Mediante la construcción de modelos de regresión logística se examinó la modificación del efecto del TEPT en condiciones médicas crónicas según grupo étnico, y después según lugar de nacimiento. Modelos no ajustados resultaron con interacciones significativas entre participantes Latinos y el TEPT teniendo mayores probabilidades de enfermar con diabetes (OR = 2.18 [Latinos] v. 0.81 [blancos no-Latinos), con enfermedad cardiovascular (OR = 3.23 [Latino] v. 1.28 [blancos no-Latinos]), y con hipertensión (OR = 1.61 [Latino] v 0.98 [blancos no-Latinos]). Aquellos participantes Latinos, que nacieron en los EE.UU. obtuvieron una interacción significativa según grupo étnico y el TEPT teniendo mayores probabilidades de tener enfermedad cardiovascular (OR = 4.18 [Latino] v. 1.28 [blancos no-Latinos]) y diabetes (OR = 2.27 [Latino] v. 0.81 [blancos no-Latinos]). Los hallazgos obtenidos fueron atenuados tras la utilización de modelos ajustados excepto en las diferencias entre el TEPT y las probabilidades de diabetes entre Latinos (incluso grupos agregados y nacidos en los EE.UU.) comparados con participantes blancos no-Latinos. Nuestros hallazgos sostienen la importancia de nuevas investigaciones para entender las compleja relación entre el TEPT y condiciones médicas crónicas, particularmente la investigación del riesgo condicional para subgrupos de origen Latino.
... Что касается спектрального профиля ВРС, то однозначной модели изменений в настоящее время нет. Существуют данные [123,130,131], что у пациентов с депрессией снижена преимущественно мощность спектра высокочастотного диапазона. В то же время в исследовании R.M.Carney и соавт. ...
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A review is devoted to a comorbidity of myocardial infarction and anxious and depressive disorders. In the first part data concerning prevalence of depression in myocardial infarction, pathophysiological mechanisms connecting depression and ischemic heart disease (IHD) are given. Influence of concomitant depressive disorders on clinical state and forecast of patients after myocardial infarction is discussed. The second part of the review (Rational Pharmacother. Cardiol. 2007, 4) will be devoted to the anxious disorders in myocardial infarction as well as to influence of anxious and depressive disorders on life quality of patients with myocardial infarction. Besides, contemporary approaches to the therapy of anxious and depressive disorders in patients with IHD will be discussed.
... As such, the baroreflex mechanism has an important role in maintaining perfusion through modulation of the heart rate and contractility via the cardiac autonomic nervous system. 24,25 Therefore, individuals with cardiac autonomic dysfunction, indicated by reduced HRV, are more prone to increased BPV. Studies also have shown that an increase in short-term BPV is associated with cognitive dysfunction 26,27 and hypertensive brain damage, such as silent cerebral white matter lesions 28 and lacunar infarction. ...
... By some, this term is used more or less synonymously with "autoregulation" for the stabilization of organ blood flow [30,31]. By others, "blood pressure buffering" is employed in the sense of "blood pressure variability buffering" in the face of external or internal disturbances; this has become a popular paradigm in cardiovascular physiology [31][32][33][34][35][36][37]. ...
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Current Usage of the "Buffering" Paradigm Outside Acid-Base Chemistry
... Moreover, given the influence of hormones and autonomic outflow from the brain upon activity of the immune system, the direct and indirect feedback actions of circulating cytokines on the brain (Maier and Watkins, 1998) must also be considered in a broader definition of neuroendocrinology. Furthermore., the autonomic nervous system itself, both parasympathetic and sympathetic arms, is a partner of neuroendocrine regulation as more broadly defined (Sloan et al., 1999;Tracey, 2002). ...
Article
The discovery of steroid hormone receptors in brain regions that mediate virtually every aspect of brain function has broadened the definition of 'neuroendocrinology' to include the reciprocal communication between the brain and the body via hormonal and neural pathways. The brain is the central organ of stress and adaptation to stress because it perceives and determines what is threatening, as well as determining the behavioral and physiological responses to the stressor. The adult and developing brain possess remarkable structural and functional plasticity in response to stress, including neurogenesis leading to neuronal replacement, dendritic remodeling, and synapse turnover. Stress causes an imbalance of neural circuitry subserving cognition, decision-making, anxiety and mood that can alter expression of those behaviors and behavioral states. The two Brain Research papers noted in this review played an important role in triggering these advances.
... Alternatively, reduced cerebral perfusion is related to both cognitive dysfunction (Vogels et al., 2008) and depression (Navarro et al., 2002), and may also be linked to low HRV. Reduced HRV is related to increased blood pressure variability (Sloan et al., 1999), which adversely impacts cerebral perfusion as consistent blood pressure is necessary to maintain adequate blood flow. As a result, reduced cerebral perfusion associated with increased blood pressure variability and autonomic dysregulation may contribute to cognitive dysfunction and depression. ...
Article
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Heart failure (HF) is associated with high rates of depression. In turn, depression is associated with reduced heart rate variability (HRV), a marker of parasympathetic dysfunction and poorer cardiac outcomes. Cognitive impairment-especially executive dysfunction-is also highly prevalent in HF, but it is unknown whether executive function (EF) impacts the depression-HRV relationship. The primary objective of this paper is to examine whether EF moderates the relationship between depression and HRV in HF. Participants were 109 HF patients. Depressive symptoms were measured using the Beck Depression Inventory-II. EF was assessed using a composite of age-adjusted T scores on the Frontal Assessment Battery, Trail Making Test B, and Stroop Color Word subtest. Parasympathetic function was assessed using resting high frequency HRV (HF-HRV). Multiple hierarchical regression was used to conduct BDI × EF moderation analyses. BDI scores were associated with reduced resting HF-HRV (p < .05). No main effects were detected between EF and resting HF-HRV (p > .05). However, EF moderated the relationship between BDI scores and resting HF-HRV (β = 0.59, p < .01). Simple slope analyses revealed that among participants with poorer EF, higher BDI scores were associated with lower resting HF-HRV (p < .001). Structural brain changes common in HF may contribute to lower EF, increased depression, and poorer autonomic functioning. Alternatively, the results may indicate that individuals with intact EF engage in self-care strategies that negate the detrimental impact of depression on autonomic function. Additional work is needed to clarify these possibilities and the potential benefits of treating depression in HF patients with different cognitive abilities.
... Of importance, indices of vagal cardiac control in the laboratory were inversely related to 24 h BPV. These results suggest that cardiac vagal influences serve to buffer BPV [15], and explicate the possible underlying mechanisms responsible for both the negative effects of BPV and the cardioprotective effects of vagally mediated HRV. BPV is associated with time-varying shear stress. ...
Article
The study explored the relationship between time- and frequency-domain indices of cardiac autonomic control and 24 h blood pressure variability (BPV) in a sample of healthy men and women. Vagally mediated cardiac control was inversely related to 24 h BPV, and measures of cardiac autonomic control were better predictors of systolic BPV in men and better predictors of diastolic BPV in women. These findings may help researchers to understand the disparity in cardiovascular disease morbidity and mortality between men and women.
... 12,13 Finally, this increased blood pressure is harmful to the coronary arteries, contributing to arterial stiffness, plaque formation, plaque rupture, and acute coronary events. 14 Hypertension is the strongest predictor of cardiovascular risk, and anxiety has been associated with hypertension both cross-sectionally and prospectively. 13,15 A number of theories of self-esteem converge on its potential to buffer the effects of stress and anxiety, and potentially reduce blood pressure reactivity to stressful or anxietyprovoking experiences. ...
Article
Recent research suggests that self-esteem may be associated with improved parasympathetic nervous system functioning. This study tested whether high self-esteem is associated with decreased ambulatory systolic blood pressure (ASBP) reactivity to anxiety in healthy adults during the waking hours of a normal day. Each of 858 participants completed a short version of the Rosenberg Self-Esteem Scale and then wore an ABP monitor that took two blood pressure readings per hour for 24 hours. Immediately after each blood pressure reading, participants completed an electronic diary report that included an anxiety rating on a 100-point visual analog scale. Using multilevel models, we assessed the association of momentary anxiety, high trait self-esteem, and their interaction on momentary ASBP, with adjustment for age, sex, race, ethnicity, and body mass index. Sensitivity analyses were conducted examining psychological factors associated with self-esteem: sense of mastery, optimism, social support, and depressive symptoms. On average, a 1-point increase in cube root-transformed anxiety was associated with a 0.80-mm Hg (standard error = 0.09, p < .001) increase in ASBP, and the interaction of high self-esteem and momentary anxiety was significant, such that this effect was 0.48 (standard error = 0.20, p = .015) less in individuals with high self-esteem compared with all others. Results for self-esteem remained significant when adjusting for sex and psychological factors. Momentary increases in anxiety are associated with acute increases in ASBP, and high self-esteem buffers the effect of momentary anxiety on blood pressure. Thus, high self-esteem may confer cardiovascular benefit by reducing the acute effects of anxiety on systolic blood pressure.
... Low heart-rate variability is a risk factor for arrhythmia, heart disease, and cardiac arrest (Bigger et al., 1992;Dekker et al., 2000). It can also accelerate artherosclerosis (Gorman & Sloan, 2000), resulting in increased variability in blood pressure, which is itself an independent risk factor for coronary artery disease (Sloan, Shapiro, Bagiella, Myers, & Gorman, 1999). ...
Article
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The purpose of this research is (a) to evaluate differences in orthostatic hypotension (OH) among young adults with and without posttraumatic stress disorder (PTSD) and (b) to examine whether group differences may be attributable to behavioral risk factors frequently associated with PTSD. Volunteers and U.S. veterans 18 to 39 years old (N = 222) completed a semistructured interview assessment of PTSD status. Direct measurements were obtained for supine and standing systolic and diastolic blood pressure at study visits, as well as height and weight, from which body mass index (BMI) was calculated. After controlling for use of psychotropic medications, a logistic regression model revealed that PTSD status was positively associated with OH, such that participants with PTSD were at 4.51 greater odds of having OH than control participants. Moreover, this effect was partially mediated by lifetime alcohol dependence (bootstrapped 95% confidence interval [-0.83, -0.20]). Overall, PTSD may pose a significant risk for OH among younger adults. In the present sample, this relationship was primarily driven by the disproportionately high history of alcohol dependence among individuals with PTSD. These results suggest that traditional therapy for PTSD should be coupled with treatment for alcohol dependency, when applicable, to reap both psychological and physiological benefits. (PsycINFO Database Record (c) 2015 APA, all rights reserved).
... hormones and autonomic outflow from the brain upon activity of the immune system, the direct and indirect feedback actions of circulating cytokines on the brain must also be considered in a broader definition of neuroendocrinology (Maier & Watkins 1998). Furthermore, the autonomic nervous system itself, both parasympathetic and sympathetic arms, is a partner of neuroendocrine regulation as is here more broadly defined (Sloan et al. 1999, Tracey 2002. ...
Article
The discovery of steroid hormone receptors in brain regions that mediate every aspect of brain function has broadened the definition of "neuroendocrinology" to include the reciprocal communication between the brain and the body via hormonal and neural pathways. The brain is the central organ of stress and adaptation to stress because it perceives and determines what is threatening, as well as the behavioral and physiological responses to the stressor. The adult and developing brain possess remarkable structural and functional plasticity in response to stress, including neuronal replacement, dendritic remodeling, and synapse turnover. Stress causes an imbalance of neural circuitry subserving cognition, decision-making, anxiety and mood that can alter expression of those behaviors and behavioral states. This imbalance, in turn, affects systemic physiology via neuroendocrine, autonomic, immune and metabolic mediators. In the short term, as for increased fearful vigilance and anxiety in a threatening environment, these changes may be adaptive. But, if the danger passes and the behavioral state persists along with the changes in neural circuitry, such maladaptation may need intervention with a combination of pharmacological and behavioral therapies, as is the case for chronic anxiety and depression. There are important sex differences in the brain responses to stressors that are in urgent need of further exploration. Moreover, adverse early-life experience, interacting with alleles of certain genes, produce lasting effects on brain and body over the life-course via epigenetic mechanisms. While prevention is most important, the plasticity of the brain gives hope for therapies that take into consideration brain-body interactions.
... 12 Worldwide, adults exposed to the disaster at Chernobyl experienced increased rates of CHD up to 10 years after the event, 13 and studies of stressors resulting from the civil war in Lebanon found elevated CHD mortality. 14,15 Although the exact biological mechanism by which PTSD contributes to CHD remains unclear, several hypotheses have been suggested, including autonomic nervous system dysfunction, 16 inflammation, 17 hypercoagulability, 18 cardiac hyperreactivity, 19 altered neurochemistry, 20 and co-occurring metabolic syndrome. 16 One of the hallmark symptoms of PTSD is hyperarousal, 21 and the neurobiological changes brought on from sustained sympathetic nervous system activation affect the release of neurotransmitters and endocrine function. ...
Article
Objectives: We investigated the association between posttraumatic stress disorder (PTSD) and incident heart failure in a community-based sample of veterans. Methods: We examined Veterans Affairs Pacific Islands Health Care System outpatient medical records for 8248 veterans between 2005 and 2012. We used multivariable Cox regression to estimate hazard ratios and 95% confidence intervals for the development of heart failure by PTSD status. Results: Over a mean follow-up of 7.2 years, veterans with PTSD were at increased risk for developing heart failure (hazard ratio [HR] = 1.47; 95% confidence interval [CI] = 1.13, 1.92) compared with veterans without PTSD after adjustment for age, gender, diabetes, hyperlipidemia, hypertension, body mass index, combat service, and military service period. Additional predictors for heart failure included age (HR = 1.05; 95% CI = 1.03, 1.07), diabetes (HR = 2.54; 95% CI = 2.02, 3.20), hypertension (HR = 1.87; 95% CI = 1.42, 2.46), overweight (HR = 1.72; 95% CI = 1.25, 2.36), obesity (HR = 3.43; 95% CI = 2.50, 4.70), and combat service (HR = 4.99; 95% CI = 1.29, 19.38). Conclusions: Ours is the first large-scale longitudinal study to report an association between PTSD and incident heart failure in an outpatient sample of US veterans. Prevention and treatment efforts for heart failure and its associated risk factors should be expanded among US veterans with PTSD.
... Studies examining the relationship between parasympathetic cardiovascular control and disregulation of anger states (inhibition of hostility, under-expression of anger, etc.), support that the lack of heart rate and blood pressure variability is a prime contributor to CVD (Sloan, Shapiro, Bagiella, Myers & Gorman, 1999). In one such study, Brosshot and Thayer (1988) found that anger inhibition and slow cardiovascular recovery were associated with persistently low vagal tone. ...
... For example, the baroflex mechanism regulates blood flow and maintains proper perfusion to vital organs, including the brain, by modulation of the heart rate and contractibility. 7,8,35 In other words, cardiac autonomic function and the sympathetic and parasympathetic activity interact to maintain blood pressure within a normal range. HRV and blood pressure variability have been shown to be inversely associated. ...
Article
Reduced heart rate variability is a strong predictor of cardiovascular risk factors, cardiovascular events, and mortality and thus may be associated with cognitive neurodegeneration. Yet, this has been relatively unexplored, particularly in minority populations with high cardiovascular burden. We used data from the Sacramento Area Latino Study on Aging to examine the cross-sectional association of reduced heart rate variability with cognitive function among elderly Mexican Americans. A total of 869 participants (mean age, 75 years; 59% women) had their 6-minute heart rate variability measured using an ECG monitor and respiration pacer in response to deep breathing. We used the mean circular resultant, known as R bar, as a measure of heart rate variability and categorized it into quartiles (Q1 to Q4 of R bar: reduced to high heart rate variability). Cognitive function was assessed using the modified Mini-Mental State Examination, a 100-point test of global cognitive function, and the Spanish and English verbal learning test, a 15-point test of verbal memory recall. In fully adjusted linear regression models, participants in quartile 1 had a 4-point lower modified Mini-Mental State Examination score (P<0.01), those in quartile 2 had a 2-point lower score (P=0.04), and those in quartile 3 had a 1-point lower score (P=0.35) compared with those in the highest quartile of R bar. Reduced R bar was not associated with verbal memory. Our results suggest that reduced heart rate variability is associated with worse performance on the test of global cognitive function, above and beyond traditional cardiovascular risk factors.
Chapter
Psychological and psychiatric issues that arise in the setting of major surgery for the elderly patient are both challenging and complex. The psychological implications of cardiothoracic surgery, the meaning of the operation in the context of the patient’s life, will vary from person to person. There are numerous potential complications caused by normal age-related changes in physiology that may affect the patient’s mental status and cause or exacerbate psychiatric conditions. The patient’s social environment, including how he or she affects and is affected by interpersonal exchanges with family and staff, will also impact on the preoperative and postoperative phases. This chapter will focus on common influences on geriatric patients’ mental health, including social relations, character structure and coping methods, vulnerability to the emotional and cognitive sequelae of surgery, underlying psychiatric conditions, and adverse responses to medication. In addition to the discussion of diagnoses, therapeutic interventions will be suggested, including psychotherapeutic, systems-oriented, and pharmacological treatments.
Chapter
This chapter reviews the emerging area of research after summarizing the key concepts and describing the systems that are involved. In order to understand the role of injury-immune-healing responses (IIHR) to trauma in the central nervous system (CNS), one must have a clear understanding of the mechanisms underlying regional regulation of IIHR, and the relationship between adaptive responses of the body to challenge and exacerbation of the IIHR that leads to pathophysiology. The central nervous system is not isolated from the immune system. Rather, it should be viewed as a tertiary immune tissue, and the elements of immune-system function in the CNS play an important role in the IIHR, as well as in normal adaptation and plasticity. The neuropeptide CGRP appears to be a particularly potent local-tissue mediator of the IIHR in the central nervous system. Immune-cell trafficking into brain may be one mechanism to respond to damage, and even, perhaps, to normal physiological processes.
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The aim of this article is to describe the protocol of a trial focusing on the psychological, anthropometric, cardiac, and psychophysiological factors contributing to increased risk of cardiovascular diseases (CVDs). As background, the article provides a short overview of research literature linking personal traits, maladaptive schemas, and coping styles with CVDs through reactivity of the autonomic nervous system.
Chapter
In this chapter, we investigate smart maintenance for human capacity management from the physiology viewpoint. We describe the general knowledge of physiology in Sect. 10.1. Then, in order to demonstrate how smart maintenance strategy can be better implemented in such hybrid asset management, in particular, internal aspect, two representative research avenues are introduced in Sects. 10.2 and 10.3, respectively. Section 10.4 summarises this chapter.
Article
Introduction According indicators from the OECD in 2015, cardiovascular diseases remain the main cause of mortality in most OECD countries. But main risk factor, as smoking, obesity, hypertension or physical activity do not explain that Slovak republic was the worst from OECD countries with number 404 age-standardized rates per 100,000 population. Objectives Determine which psychological, psycho-physiological and anthropometrics factors are at risk of cardiovascular diseases: Aim The aim is to determine, which risk psychological, psycho-physiological and anthropometrics markers are remarkable in time, when individual subjectively perceives himself as health. Based on the analysis of these correlates will be identified predictors, mediators and moderators of the cardiovascular diseases from the area of psychological variables, which accentuates the clinical picture of a patient with cardiovascular disease. Another aim is to identify specific risk factors for target advice on a lifestyle modification and creation of an interdisciplinary methodology for the prevention of cardiovascular diseases. Methods Project is aimed to clarify the relation between psychological factors (measuring by personal inventories as temperament predispositions, maladaptive schemes, coping, personality characteristics), balance of autonomic nervous system (by measuring HRV, skin conductance, muscle tension, respiration, and surface temperature), anthropometrics characteristics (BMI, weight, height) with potential symptoms of cardiovascular diseases confirmed in cardiac evaluation (12-lead ECG), blood pressure, examination of pulse wave, and data of arteriographic examination. Conclusions The results of the study can help to the better understanding of the interface between psychological factors and cardiovascular problems, which help to find new diagnostic, preventive and treatment approaches.
Chapter
Humans have developed “clock” genes of the circadian, and probably many other components in the spectral element of chronomes, beyond about-yearly (circannual) and about-weekly (circaseptan) features, as a product of adaptation to, or rather integration with, cycles in the cosmos. While life originally integrated itself into the cycles of an anthropogenically unpolluted environment, the environmental cycles are now being changed in keeping with the schedules of societal life as in the case of global temperature. Hence, a variety of cognitive, neurobehavioral and neuropsychological as well as cardiovascular functions will need to be investigated to more precisely map their chronomes in space and time, in order to understand chronoastrobiology, based on both the system times and time horizons yielded by chronomes. We have started a project (chronoecological health-watch) on stroke prevention, based on community-based comprehensive medical assessment, including 7-day/24-hour monitoring of blood pressure (BP) as a public service, in Uraus, a town in Hokkaido, Japan (latitude: 43.45° N, longitude: 141.85° E), according to plans originally made in the city of Roseville, a suburb of St. Paul, Minnesota. In Uraus, Mayor Kaname Yamamoto has extended to all residents of his city an offer of 7-day/24-hour blood pressure monitoring and has started a historic first chronome mapping for stroke prevention. Chronoecological health-watch was started in 2000 and consultations were repeated every 3 months. Several results of the follow-up on adverse cardiovascular outcomes, or cancer death, are presented here, especially focusing on the relations of depressive mood, 7-day/24-hour BP monitoring, and heart rate variability.
Article
Objective: Posttraumatic stress disorder (PTSD) has been linked to elevated heart rate (HR) and reduced heart-rate variability (HRV) in cross-sectional research. Recent evidence suggests that this link may be driven by individual differences in autonomic arousal associated with momentary negative affect (NA). Using ecological momentary assessment (EMA) of NA and minute-to-minute HR/HRV monitoring, we examined whether NA-related HR/HRV mediated the association of PTSD symptom severity with 24-hour HRV and endothelial functioning. Methods: One hundred ninety-seven young adults (18-39 years old), 93 with PTSD, underwent one day of Holter monitoring while concurrently reporting NA levels via EMA. Two non-invasive measures of endothelial functioning—flow-mediated dilation (FMD) and hyperemic flow—were also collected. Multilevel modeling was used to assess the associations of momentary NA with HR and low- (LF) and high-frequency (HF) HRV during the 5-minute intervals following each EMA reading. Latent variable modeling was then used to determine whether individual differences in these associations mediated the association of PTSD symptom severity with 24-hour HRV, FMD, and hyperemic flow Results: PTSD symptom severity was positively associated with NA-related autonomic arousal (β = .21, p < .001), which significantly mediated the association of PTSD symptom severity with 24-hour HRV and hyperemic flow, accounting for 62% and 34% of their associations, respectively, while overshadowing the influence of smoking, lifetime alcohol dependence, sleep duration, mean NA, and episodes of acute NA. Conclusions: Results suggest that NA-related autonomic arousal is both a primary factor driving cardiovascular risk in PTSD and a potential point of intervention.
Article
Intra-individual reaction time variability (IIV), defined as the variability in trial-to-trial response times, is thought to serve as an index of central nervous system function. As such, greater IIV reflects both poorer executive brain function and cognitive control, in addition to lapses in attention. Resting-state vagally mediated heart rate variability (vmHRV), a psychophysiological index of self-regulatory abilities, has been linked with executive brain function and cognitive control such that those with greater resting-state vmHRV often perform better on cognitive tasks. However, research has yet to investigate the direct relationship between resting vmHRV and task IIV. The present study sought to examine this relationship in a sample of 104 young and healthy participants who first completed a 5-minute resting-baseline period during which resting-state vmHRV was assessed. Participants then completed an attentional (target detection) task, where reaction time, accuracy, and trial-to-trial IIV were obtained. Results showed resting vmHRV to be significantly related to IIV, such that lower resting vmHRV predicted higher IIV on the task, even when controlling for several covariates (including mean reaction time and accuracy). Overall, our results provide further evidence for the link between resting vmHRV and cognitive control, and extend these notions to the domain of lapses in attention, as indexed by IIV. Implications and recommendations for future research on resting vmHRV and cognition are discussed.
Chapter
The connection between the mind and body is a concept that is increasingly being accepted in mainstream Western culture. Technological advances have made it possible to understand and map the connection among emotion, mood, and biology. As a result, we now have a mounting body of evidence that supports the link between psychological state, autonomic activity, and the development of coronary heart disease (CHD) (1–6). This basic mind—brain—body paradigm has been diagrammatically represented by Sloan et al. (7), as seen in Fig. 1 below. In this model, the autonomic nervous system is seen as a factor linking psychology and chronic stress to CHD development and outcome.
Article
Depressive disorders and cardiovascular disease are inter-connected by a whole range of pathophysiological mechanisms. Three biological mechanisms are fundamental: activation of the hypothalamus-hypophysis-adrenal axis with a subsequent increase in sympathetic-adrenal system activity, decrease in vagal tone with a decrease in heart rate variability, and alterations of thrombogenesis with increased platelet aggregability. Behavioral mechanisms and psycho-social factors are also integral to this common pathophysiology. Recently, research has focused mainly on studying various forms of stress, as well as changes and possibilities of influencing the autonomous vegetative system. Temporal aspects of the incidence and development of depressive episodes in relation to cardiovascular disease and subsequent cardiovascular morbidity and mortality are being studied, as well as general mortality risk factors. These findings are important for clinical practice. It is evident that in patients with untreated depressive disorder, the risk of developing cardiovascular disease is significantly higher than in patients suffering from a depressive disorder being treated with anti-depressants. From the data published so far, it may be summarised that depressive disorders in patients with cardiovascular disease may be reliably and safely treated with antidepressants that act as inhibitors of serotonin re-uptake.
Article
Objectives : Psychological coronary-proncncss is most probably one of the first recognised risk factors for coronary heart disease (CHD). The mechanisms by which psychological risk factors might exert their influence on the cardiovascular system arc less clear than those for the more standard biological risk factors. The aim of this review was to classify all possible mechanisms of potentiation of CHD by psychological factors. Method : A MEDLINE search was conducted by selecting literature on both standard biological risk factors (eg. dyslipidaemia, hypertension, smoking) and psychological risk factors (eg. personality traits, behavioural characteristics, coping with stress) for CHD. Results : It was suggested that six biological mechanisms could mediate psychological influences specifically for CHD, of course, together with the seventh mechanism of general alterations in health-related behaviours. These are: increased oxygen demand of the heart muscle, decreased blood supply to the heart muscle, increased concentration of blood, enhanced blood clotting, increase in cholesterol and other plasma lipids, disturbances of blood sugar level, and alterations in health-related behaviours. Conclusions : If more studies of CHD were conducted with both physical and psychological risk factors simultaneously, it would be possible to investigate which of the above suggested mechanisms are important, which could in turn substantially improve both primary and secondary preventive measures.
Article
Aims: (1) To confirm that head‐up tilting causes sustained increases in the heart rate (HR) of newborn infants but not during the period of maximum vulnerability to SIDS at 2–4 mo of age, and (2) to determine whether electrocortical activation (changes in high‐frequency EEG power) also shows topographic and age‐dependent effects of tilting. Methods: HR and electrocortical activity were recorded in 15 newborn and 12 2‐ to 4‐mo‐old infants during head‐up tilting. Infants were tilted, three times, to a 30° head‐up position. Electrocortical activity was acquired using a 128‐lead EEG system. Changes in HR and high‐frequency (12–50 Hz) power in the electrocortical signal were computed from the flat to the head‐up position. Results: Newborn infants had significant increases in HR and robust increases in high‐frequency power in the left frontal, right frontal‐temporal, and occipital regions following head‐up tilt. At 2 to 4 mo of age, HR did not change significantly and tilt‐related increases in high‐frequency power were smaller. Conclusion: The patterns of HR change and electrocortical activation with tilting of newborn infants are different from infants at the age of highest risk for SIDS.
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In 57 normal subjects (age 20-60 years), we analyzed the spontaneous beat-to-beat oscillation in R-R interval during control recumbent position, 90° upright tilt, controlled respiration (n = 16) and acute (n = 10) and chronic (n = 12) β-adrenergic receptor blockade. Automatic computer analysis provided the autoregressive power spectral density, as well as the number and relative power of the individual components. The power spectral density of R-R interval variability contained two major components in power, a high frequency at ~ 0.25 Hz and a low frequency at ~ 0.1 Hz, with a normalized low frequency: high frequency ratio of 3.6 ± 0.7. With tilt, the low-frequency component became largely predominant (90 ± 1%) with a low frequency: high frequency ratio of 21 ± 4. Acute β-adrenergic receptor blockade (0.2 mg/kg IV propranolol) increased variance at rest and markedly blunted the increase in low frequency and low frequency: high frequency ratio induced by tilt. Chronic β-adrenergic receptor blockade (0.6 mg/kg p.o. propranolol, t.i.d.), in addition, reduced low frequency and increased high frequency at rest, while limiting the low frequency: high frequency ratio increase produced by tilt. Controlled respiration produced at rest a marked increase in the high-frequency component, with a reduction of the low-frequency component and of the low frequency: high frequency ratio (0.7 ± 0.1); during tilt, the increase in the low frequency: high frequency ratio (8.3 ± 1.6) was significantly smaller. In seven additional subjects in whom direct high-fidelity arterial pressure was recorded, simultaneous R-R interval and arterial pressure variabilities were examined at rest and during tilt. Also, the power spectral density of arterial pressure variability contained two major components, with a relative low frequency: high frequency ratio at rest of 2.8 ± 0.7, which became 17 ± 5 with tilt. These power spectral density components were numerically similar to those observed in R-R variability. Thus, invasive and noninvasive studies provided similar results. More direct information on the role of cardiac sympathetic nerves on R-R and arterial pressure variabilities was derived from a group of experiments in conscious dogs before and after bilateral stellectomy. Under control conditions, high frequency was predominant and low frequency was very small or absent, owing to a predominant vagal tone. During a 9% decrease in arterial pressure obtained with IV nitroglycerin, there was a marked increase in low frequency, as a result of reflex sympathetic activation. Bilateral stellectomy prevented this low-frequency increase in R-R but not in arterial pressure autospectra, indicating that sympathetic nerves to the heart are instrumental in the genesis of low-frequency oscillations in R-R interval.
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Two experiments examined the relationship between Type A behavior and cardiovascular and plasma catecholamine responses to experimental competition and harassment. Experiment I showed that, in 44 male adults, the presence of a hostile opponent caused no significant differences in the responses of Type B's. In A's, by contrast, hostility elicited greater increases in systolic blood pressure, heart rate and plasma epinephrine during competition. Behavior pattern A appears selectively predisposed to enhanced reaction to hostile interactions, but competition alone does not distinguish between individuals with A and B behavior patterns. Experiment II, with 20 cases, was carried out to determine whether or not the absence of A-B differences in the presence of a nonhostile competitor could be explained by Type B's reactivity to the challenge of competition alone. The results were consistent with this interpretation. A's showed greater blood pressure and plasma epinephrine evaluations than B's when both types were confronted by the challenge of task performance. Consideration was given to the role of sympathetic activation in mediating the tendency of Type A individuals to develop coronary heart disease.
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Cardiac autonomic activity, as assessed by heart rate variability, has been found to be associated with postmyocardial infarction mortality, sudden death, and all-cause mortality. However, the association of heart rate variability and the incidence of coronary heart disease (CHD) is not well described. The authors report on the association of baseline cardiac autonomic activity (1987–1989) with incident CHD after 3 years (1990–1992) of follow-up of the Atherosclerosis Risk in Communities Study cohort selected from four study centers in the United States by using a case-cohort design. The authors examined 137 incident cases of CHD and a stratified random sample of 2, 252 examinees free of CHD at baseline. Baseline, supine, resting beat-to-beat heart rate data were collected. High- (0.16–0.35 Hz) and low- (0.025–0.15 Hz) frequency spectral powers and high-/low-frequency power ratio, estimated from spectral analysis, and standard deviation of all normal R-R intervals, calculated from time domain analysis, were used as the conventional indices of cardiac parasym-pathetic, sympatho-parasympathetic, and their balance, respectively. Incident CHD was defined sis hospitalized myocardial infarction, fatal CHD, or cardiac revascularization procedures during 3 years of follow-up. The age, race, gender, and other CHD risk factor-adjusted relative risks (and 95% confidence intervals) of incident CHD comparing the lowest quartile with the upper three quartiles of high-frequency power, low-frequency power, high-/low-frequency power ratio, and standard deviation of R-R intervals were 1.72 (95% confidence interval (CI) 1.17–2.51), 1.09 (95% CI 0.72–1.64), 1.25 (95% CI 0.84–1.86), and 1.39 (95% CI 0.94–2.04), respectively. The findings from this population-based, prospective study suggest that altered cardiac autonomic activity, especially lower parasympathetic activity, is associated with the risk of developing CHD. Am J Epidemiol 1997; 145: 696–706.
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The purpose of this study was to assess whether hypertensive target organ damage is related to average nighttime blood pressure (BP) and to BP variability. Sixty-seven normotensive subjects and 171 borderline, 309 mild, 140 moderate, and 41 severe hypertensive patients were studied with noninvasive ambulatory BP monitoring. Each subject was assigned a target organ damage score of 0 to 5 on the basis of funduscopic changes and degree of left ventricular hypertrophy calculated from electrocardiogram and chest roentgenogram. When the 728 subjects were subdivided into five classes of increasing daytime BP, in each class a significantly higher degree of target organ damage was present in the subjects with higher nighttime diastolic BP. A similar, although nonsignificant, trend was observed in the subjects with higher nighttime systolic BP. In particular, higher nighttime BP levels were accompanied by a more severe degree of left ventricular hypertrophy. As for variability, subjects with higher daytime systolic BP SD, but not with higher daytime diastolic SD, displayed a more severe degree of target organ damage; this was accounted for by a higher degree of retinal abnormalities. The association between target organ damage and systolic BP SD was present both in men and women, while that with nighttime BP was present only in men. No relationship was found between degree of cardiovascular complications and peaks of pressure. These results suggest that a reduced day-night BP difference and an increased daytime BP variability, evaluated as the SD, are associated with a higher degree of hypertensive cardiovascular complications. Whether this BP profile is the cause or the consequence of target organ damage remains to be established.
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Recent research has renewed interest in the potential influence of hostility on physical health. This review indicates that the evidence available from prospective studies, although not entirely consistent, suggests that hostile persons may be at increased risk for subsequent coronary heart disease and other life-threatening illnesses. Further, several plausible mechanisms possibly linking hostility and health have been articulated and subjected to initial evaluation. Hostile individuals display heightened physiological reactivity in some situations, report greater degrees of interpersonal conflict and less social support, and may have more unhealthy daily habits. Additional research is needed, and it must address a variety of past conceptual and methodological limitations. Perhaps the most central of these concerns are the assessment of individual differences in hostility and the role of social contexts in the psychosomatic process. Key words: hostility, coronary heart disease (CHD), personality, physiological reactivity, psychosomatics
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To test the prognostic value of plasma renin activity prospectively, we determined the pretreatment renin-sodium profile of 1717 subjects with mild-to-moderate hypertension (mean age, 53 years; 36 percent white; 67 percent men) in a systematic work-site treatment program. Renin profiles, obtained by plotting plasma renin activity against the urinary excretion of sodium, were classified as high (12 percent of the subjects), normal (56 percent), and low (32 percent), and there were expected variations according to age, sex, and race. Modified stepped-care treatment for hypertension, prescribed without reference to the renin profile, was similar in the three renin groups. Mean (+/- SD) blood pressure at entry was 151 +/- 19/100 +/- 10 mm Hg in the subjects with a high renin profile, 151 +/- 19/97 +/- 10 mm Hg in those with a normal profile, and 151 +/- 20/96 +/- 11 mm Hg in those with a low profile. During 8.3 years of follow-up, there were 27 myocardial infarctions. As adjusted for age, sex, and race, the incidence of myocardial infarction per 1000 person-years was 14.7 among the subjects with a high renin profile, 5.6 among those with a normal profile, and 2.8 among those with a low profile (rate ratio for high vs. low, 5.3; 95 percent confidence interval, 3.4 to 8.3). The rate of mortality from all causes was 9.3 in the high-profile group, 5.3 in the normal-profile group, and 3.9 in the low-profile group. The independent association of a high renin profile with myocardial infarction (but not with stroke or noncardiovascular events) was affirmed by Cox analyses (rate ratio for high vs. normal plus low, 3.2; 95 percent confidence interval, 1.2 to 8.4) after adjustment for race, sex, age at entry, serum cholesterol level, smoking status, electrocardiographic evidence of left ventricular hypertrophy, blood glucose level, body-mass index, history of cardiovascular disease or treatment, blood pressure, and use of beta-blockers. In the study population, whose blood pressure before and during treatment was in a narrow range, and after other cardiovascular risk factors had been considered, the renin profile before treatment remained independently associated with the subsequent risk of myocardial infarction.
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We have demonstrated previously that transfer function analysis can be used to precisely characterize the respiratory sinus arrhythmia (RSA) in normal humans. To further investigate the role of the autonomic nervous system in RSA and to understand the complex links between respiratory activity and arterial pressure, we determined the transfer functions between respiration, heart rate (HR), and phasic, systolic, diastolic, and pulse arterial pressures in 14 healthy subjects during 6-min periods in which the respiratory rate was controlled in a predetermined but erratic fashion. Pharmacological autonomic blockade with atropine, propranolol, and both, in combination with changes in posture, was used to characterize the sympathetic and vagal contributions to these relationships, as well as to dissect the direct mechanical links between respiration and arterial pressure from the effects of the RSA on arterial pressure. We found that 1) the pure sympathetic (standing + atropine) HR response is characterized by markedly reduced magnitude at frequencies greater than 0.1 Hz and a phase delay, whereas pure vagal (supine + propranolol) modulation of HR is characterized by higher magnitude at all frequencies and no phase delay; 2) both the mechanical links between respiration and arterial pressure and the RSA contribute significantly to the effects of respiration on arterial pressure; 3) the RSA contribution to arterial pressure fluctuations is significant for vagal but not for sympathetic modulation of HR; 4) the mechanical effects of respiration on arterial pressure are related to the negative rate of change of instantaneous lung volume; 5) the mechanical effects have a higher magnitude during systole than during diastole; and 6) the mechanical effects are larger in teh standing than the supine position. Most of these findings can be explained by a simple model of circulatory control based on previously published experimental transfer functions from our laboratory.
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Studies have shown that the circadian blood pressure profile is similar in normotensive and hypertensive subjects, and that the observed increase in blood pressure variability in hypertensive patients is proportional to the increase over the normotensive baseline blood pressure, suggesting that transient blood pressure oscillations on a percentage basis are not altered by hypertension. It has also been found that although antihypertensive therapy tends to reduce mean arterial blood pressure (MAP), the tendency to oscillate around a mean pressure is modified to a lesser extent.
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Recent research has renewed interest in the potential influence of hostility on physical health. This review indicates that the evidence available from prospective studies, although not entirely consistent, suggests that hostile persons may be at increased risk for subsequent coronary heart disease and other life-threatening illnesses. Further, several plausible mechanisms possibly linking hostility and health have been articulated and subjected to initial evaluation. Hostile individuals display heightened physiological reactivity in some situations, report greater degrees of interpersonal conflict and less social support, and may have more unhealthy daily habits. Additional research is needed, and it must address a variety of past conceptual and methodological limitations. Perhaps the most central of these concerns are the assessment of individual differences in hostility and the role of social contexts in the psychosomatic process.
Article
Background.— The purpose of this study was to assess whether hypertensive target organ damage is related to average nighttime blood pressure (BP) and to BP variability. Methods.— Sixty-seven normotensive subjects and 171 borderline, 309 mild, 140 moderate, and 41 severe hypertensive patients were studied with noninvasive ambulatory BP monitoring. Each subject was assigned a target organ damage score of 0 to 5 on the basis of funduscopic changes and degree of left ventricular hypertrophy calculated from electrocardiogram and chest roentgenogram. Results.— When the 728 subjects were subdivided into five classes of increasing daytime BP, in each class a significantly higher degree of target organ damage was present in the subjects with higher nighttime diastolic BP. A similar, although nonsignificant, trend was observed in the subjects with higher nighttime systolic BP. In particular, higher night-time BP levels were accompanied by a more severe degree of left ventricular hypertrophy. As for variability, subjects with higher daytime systolic BP SD, but not with higher day-time diastolic SD, displayed a more severe degree of target organ damage; this was accounted for by a higher degree of retinal abnormalities. The association between target organ damage and systolic BP SD was present both in men and women, while that with nighttime BP was present only in men. No relationship was found between degree of cardiovascular complications and peaks of pressure. Conclusions.— These results suggest that a reduced day-night BP difference and an increased daytime BP variability, evaluated as the SD, are associated with a higher degree of hypertensive cardiovascular complications. Whether this BP profile is the cause or the consequence of target organ damage remains to be established.(Arch Intern Med. 1992;152:1855-1860)
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• Heart transplant recipients provide a useful model for study of the autonomic control of the cardiovascular response to mental stress. Utilizing the innervated native atrial tissue of heart transplant recipients as an internal control exposed to the same circulatory milieu as the denervated graft heart was exposed to, the effect of innervation on the heart rate response to a mentally stressful arithmetic task was examined in eight subjects. Compared with the graft, the innervated atrial tissue manifested a larger heart rate increase during the task, larger heart rate decrease after the task, and more rapid rate of change in heart rate during the task and recovery periods. Thus, cardiac denervation results in a chronotropic response to mental arithmetic-induced stress that is blunted and more gradual than that of the innervated heart but not completely eliminated. The cardiac chronotropic response to mental arithmetic stress is dependent on both humoral factors and, predominantly, its direct autonomic innervation.
Article
Objective. —To determine if the diagnosis of major depression in patients hospitalized following myocardial infarction (Ml) would have an independent impact on cardiac mortality over the first 6 months after discharge.Design. —Prospective evaluation of the impact of depression assessed using a modified version of the National Institute of Mental Health Diagnostic Interview Schedule for major depressive episode. Cox proportional hazards regression was used to evaluate the independent impact of depression after control for significant clinical predictors in the data set.Setting. —A large, university-affiliated hospital specializing in cardiac care, located in Montreal, Quebec.Patients. —All consenting patients (N=222) who met established criteria for Ml between August 1991 and July 1992 and who survived to be discharged from the hospital. Patients were interviewed between 5 and 15 days following the MI and were followed up for 6 months. There were no age limits (range, 24 to 88 years; mean, 60 years). The sample was 78% male.Primary Outcome Measure. —Survival status at 6 months.Results. —By 6 months, 12 patients had died. All deaths were due to cardiac causes. Depression was a significant predictor of mortality (hazard ratio, 5.74; 95% confidence interval, 4.61 to 6.87; P=.0006). The impact of depression remained after control for left ventricular dysfunction (Killip class) and previous Ml, the multivariate significant predictors of mortality in the data set (adjusted hazard ratio, 4.29; 95% confidence interval, 3.14 to 5.44; P=.013).Conclusion. —Major depression in patients hospitalized following an Ml is an independent risk factor for mortality at 6 months. Its impact is at least equivalent to that of left ventricular dysfunction (Killip class) and history of previous Ml. Additional study is needed to determine whether treatment of depression can influence post-MI survival and to assess possible underlying mechanisms.(JAMA. 1993;270:1819-1825)
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• The relationship between casual BPs and measures of cardiac hypertrophy, derived from the ECG, has been described as fairly weak. In this study, ECG and echocardiographic measurements of left ventricular muscle mass were related to various measures of BP obtained during circadian ambulatory BP monitoring in 12 patients with hypertension. Casual BP did not correlate substantially with ECG voltages or with echocardiographic measurements of muscle mass. The correlations between whole-day, daytime, or nighttime BP averages and ECG voltages were not significant. However, echocardiographic left ventricular muscle mass correlated significantly with the averages of whole-day, daytime, and nighttime, and two-hour morning systolic pressures. The correlations between diastolic BP and left ventricular muscle mass were not significant. Therefore, serial BP measurements are required to evaluate the relationship between BP and left ventricular muscle mass as measured by the M-mode echocardiogram. The ECG is of little value in this relationship. (Arch Intern Med 1983;143:90-92)
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Myocardial infarction is the most frequent cause of mortality in the United States as well as in most western countries. In this review, the processes leading to myocardial infarction are described based on the most recent studies of vascular biology; in addition, evolving strategies for prevention are outlined. The following was specifically discussed. (1) Five phases of the progression of coronary atherosclerosis (phases 1 to 5) and eight morphologically different lesions (types I, II, III, IV, Va, Vb, Vc, and VI) in the various phases are defined. (2) The present understanding of the pathogenesis of each of the phases of progression and of the various lesion types preceding myocardial infarction is described; particular emphasis is placed on the physical, structural, cellular, and chemical characteristics of the "vulnerable or unstable plaques" prone to disruption (types IV and Va lesions). (3) The fate of plaque disruption (type VI lesion) in the genesis of the various coronary syndromes and especially acute myocardial infarction is defined; particular emphasis is placed on the combination of plaque disruption and a high thrombogenic risk profile--local factors (ie, degree of plaque disruption, exposure of lipid-macrophage-rich plaque, etc) and systemic factors (ie, catecholamines, RAS, fibrinogen, etc)--in the genesis of myocardial infarction. (4) Strategies of regression or stabilization of "vulnerable or unstable plaques" for prevention of myocardial infarction are presented within the context of recent favorable experience with risk factor modification and lipid-modifying angiographic trials, beta-blockade and angiotensin-converting enzyme inhibition, antithrombotic strategies, and the possible role of estrogens. The recent past has been very fruitful in yielding a better understanding of the processes leading to myocardial infarction, and the near future appears very promising in terms of preventing the number 1 killer in the western world.
Article
To determine the reproducibility of frequency domain measures of heart period variability in patients with previous myocardial infarction, 2 random samples of 40 patients each (1 from the Cardiac Arrhythmia Pilot Study [CAPS] [unsustained ventricular arrhythmias], and 1 from the Electrophysiologic Studies Versus Electrocardiographic Monitoring [ESVEM] [sustained ventricular arrhythmias] trial) were studied. For each patient, two 24-hour continuous electrocardiographic recordings were analyzed, and the average normal RR interval, total power and 4 components of total power were calculated. Group means and standard deviations for each sample were virtually identical for the pairs of 24-hour recordings. Furthermore, measurements for individual patients were stable from day to day, as measured by the intraclass correlation coefficients and the standard errors of measurement. Reproducibility of heart period variability measurements is excellent in patients with previous myocardial infarction and ventricular arrhythmias, and is comparable to the high stability previously found in a small group of normal subjects. The stability of measures of heart period variability facilitates distinguishing real changes due to progression or regression of cardiac disease or to drug effects from apparent changes due to random variation.
Article
Clinical coronary heart disease (CHD) occurred in 257 subjects during eight to nine years of follow-up (average, 8 1/2 years) in a prospective study of 39- to 59-year-old employed men. Incidence of CHD was significantly associated with parental CHD history, reported diabetes, schooling, smoking habits, overt behavior pattern, blood pressure, and serum levels of cholesterol, triglyceride, and β-lipoproteins. The type A behavior pattern was strongly related to the CHD incidence, and this association could not be explained by association of behavior pattern with any single predictive risk factor or with any combination of them.(JAMA 233:872-877, 1975)
Article
To examine associations between heart period variability (HPV) and psychopathology in young urban boys at risk for delinquency, a series of 69 7–11-year-old younger brothers of adjudicated delinquents received a standardized psychiatric evaluation and an assessment of heart period variability (HPV). Psychiatric symptoms were rated in two domains: externalizing and internalizing psychopathology. Continuous measures of both externalizing and internalizing psychopathology were associated with reductions in HPV components related to parasympathetic activity. These associations could not be explained by a number of potentially confounding variables, such as age, ethnicity, social class, body size, or family history of hypertension. Although familial hypertension predicted reduced HPV and externalizing psychopathology, associations between externalizing psychopathology and HPV were independent of familial hypertension. Psychiatric symptoms are associated with reduced HPV in young urban boys at risk for delinquency.
Article
Objectives: This study compares 24-h parasympathetic activity in aerobically trained and untrained healthy young men. Background: Higher values of parasympathetic nervous system activity are associated with a low mortality rate in patients after myocardial infarction, but it remains uncertain what therapeutic interventions can be used to increase parasympathetic activity. Although it is thought that exercise training can increase parasympathetic activity, studies have reported conflicting results, perhaps because this variable was measured for only brief intervals and usually inferred from changes in reflex responses induced by pharmacologic blockade. Methods: Parasympathetic activity was assessed noninvasively from 24-h ECG recordings by calculating high frequency (0.15 to 0.40 Hz) beat to beat heart period variability in eight endurance-trained men (maximal oxygen consumption greater than or equal to 55 ml/kg per min) and eight age-matched (mean = 29 yr) untrained men (maximal oxygen consumption less than or equal to 40 ml/kg per min). The data were analyzed separately for sleeping hours when parasympathetic activity is dominant and also for waking hours. Results: The geometric mean of high frequency power was greater in the trained than in the untrained men during the day (852 vs. 177 ms2, p less than 0.005), during the night (1,874 vs. 427 ms2, p less than 0.005) and over the entire 24 h (1,165 vs. 276 ms2, p less than 0.001). Conclusions: Parasympathetic activity is substantially greater in trained than in untrained men, and this effect is present during both waking and sleeping hours. These data suggest that exercise training may increase parasympathetic activity over the entire day and may therefore prove to be a useful adjunct or alternative to drug therapy in lessening the derangements of autonomic balance found in many cardiovascular diseases.
Article
A relationship exists between blood pressure and cardiovascular morbidity and mortality. Recent data suggest that the variability of blood pressure is also related to hypertensive target organ damage. We studied the relationship of ambulatory daytime and night-time and supine beat-to-beat Finapres blood pressure variability to left ventricular mass index (LVMI) and urinary albumin excretion (albumin/creatinine ratio: ACR) in 33 hypertensive patients, untreated for more than 3 months. In a multiple stepwise regression model the strongest relationship with the LVMI existed for night-time systolic pressure (R = 0.46, multiple regression coefficient: 0.90± 0.26 P < .01) and daytime diastolic blood pressure variability (multiple R increased to 0.60, multiple regression coefficient 3.16 ± 1.18, P < .05). Log ACR had the strongest relationship to ambulatory systolic daytime pressure (R = 0.40, multiple regression coefficient 0.0093 ± 0.0040, P < .05) and the variability of diastolic Finapres blood pressure (multiple R increased to 0.52, multiple regression coefficient 0.081 ± 0.0036, P < .05). Both ambulatory and steady state blood pressure variability are related to early hypertensive target organ damage. This relationship exists independent of the height of blood pressure.
Article
Objectives: To determine whether spectral measures of heart period (RR) variability predict death when measured late after infarction, we studied patients in the Cardiac Arrhythmia Pilot Study (CAPS) who survived for 1 year and had a 24-h electrocardiographic (ECG) recording made after the CAPS drug was washed out. Background: Four components of the heart period power spectrum--ultra low frequency (< 0.0033 Hz), very low frequency (0.0033 to < 0.04 Hz), low frequency (0.04 to < 0.15 Hz) and high frequency power (0.15 to < 0.40 Hz)--plus total power (1.157 x 10(-5) to < 0.40 Hz) and the ratio of low to high frequency power predict mortality when measured < 30 days after myocardial infarction. However, these variables increase to steady state values by 3 months after infarction and the prognostic significance of recovery values is unknown. Methods: The 24-h power spectral density was computed from ECG recordings made 1 year after infarction using fast Fourier transforms and the six measures listed were calculated. The values were dichotomized at cut points that maximized the association with mortality. Results: Each measure of RR variability had a strong and significant univariate association with mortality; the relative risks for these variables ranged from 2.5 to 5.6. After adjustment for age, New York Heart Association functional class, rales in the coronary care unit, left ventricular ejection fraction and ventricular arrhythmias, some measures of heart period variability still had a strong and significant independent association with all-cause mortality. Conclusions: Spectral measures of heart period variability, measured late after infarction, predict death.
Article
We developed an isolated rabbit atrial preparation which responds consistently and reproducibly to brief, submaximal stimulation of the autonomic nerves contained in it. In 6 of 11 preparations in the presence of propranolol (1 mg/liter), the time course of changes in the atrial rate following 120 msec vagal stimulation was bimodal. The maximal slowing occurred at 0.64 +/- 0.16 second, and the peak secondary slowing occurred at 2.3 +/- 1.0 seconds. An acceleratory component occurred between the first and second peaks between 0.8 and 1.6 seconds. The total time course of vagal effect lasted for 5.0 +/- 2.0 seconds. These changes in rate could not be explained by shifts in the location of the primary pacemaker. The acceleratory component was due to a 4.7 +/- 2.0 (SD) mV depolarization of the maximum diastolic membrane potential of the primary pacemaker of the sinus node which lasted for 1.8 +/- 0.3 seconds. Following vagal stimulation, there was an increase of 0.2 mM in the activity of potassium in the extracellular space recorded with a potassium-sensitive electrode; this peaked between 1.4 and 2.5 seconds and cleared with an exponential time course. The halftimes for recovery ranged between 2.8 and 4.6 seconds. The initial peak slowing of the bimodal time course and the acceleratory component therefore appear to be direct effects of acetylcholine. The secondary slowing occurs after acetylcholine presumably has been inactivated and occurs coincidently with the accumulation of potassium in the extracellular space.
Article
Clinical coronary heart disease (CHD) occurred in 257 subjects during eight to nine years of follow-up (average, 8 1/2 years) in a prospective study of 39- to 59-year-old employed men. Incidence of CHD was significantly associated with parental CHD history, reported diabetes, schooling, smoking habits, overt behavior pattern, blood pressure, and serum levels of cholesterol, triglyceride, and beta-lipoproteins. The type A behavior pattern was strongly related to the CHD incidence, and this association could not be explained by association of behavior pattern with any single predictive risk factor or with any combination of them.
Article
Prior research has suggested a weaker parasympathetic antagonism of sympathetic effects on the heart in type A (coronary-prone) men. To confirm this phenomenon and extend our understanding of it, we investigated the effects of prior muscarinic blockade on the electrocardiogram T wave and other cardiovascular and neuroendocrine responses to isoproterenol in type A and type B (non-coronary-prone) men. Responses to two 5-minute intravenous isoproterenol infusions (0.01 micrograms/kg/min and 0.02 micrograms/kg/min) were evaluated in six type A and six type B men after pretreatment with either dextrose placebo or atropine (1.2 mg). Atropine significantly potentiated T wave attenuation in the recovery period after isoproterenol infusion (0.30 +/- 0.07 mV) compared with placebo (0.54 +/- 0.09 mV, p less than 0.001). Atropine also potentiated the heart rate increase to isoproterenol (39 +/- 3 beats per minute versus 20 +/- 2 beats per minute after placebo). Atropine enhanced decreases in systolic, diastolic, and mean arterial pressures as well as pulse pressure to isoproterenol. Atropine enhancement of many of these responses was increased among subjects with high scores on various hostility/anger scales. Isoproterenol alone produced greater T wave attenuation in type A than in type B men. However, atropine enhancement of T wave attenuation and blood pressure falls by isoproterenol was present only in type B men. These findings indicate that there is accentuated parasympathetic antagonism of T wave attenuation and blood pressure responses induced by beta-adrenergic stimulation. Relative weakness of this antagonism of sympathetic effects on the heart in hostile type A individuals may contribute to their higher coronary disease risk.
Article
To determine the reproducibility of frequency domain measures of heart period variability in patients with previous myocardial infarction, 2 random samples of 40 patients each (1 from the Cardiac Arrhythmia Pilot Study [CAPS] [unsustained ventricular arrhythmias], and 1 from the Electrophysiologic Studies Versus Electrocardiographic Monitoring [ESVEM] [sustained ventricular arrhythmias] trial) were studied. For each patient, two 24-hour continuous electrocardiographic recordings were analyzed, and the average normal RR interval, total power and 4 components of total power were calculated. Group means and standard deviations for each sample were virtually identical for the pairs of 24-hour recordings. Furthermore, measurements for individual patients were stable from day to day, as measured by the intraclass correlation coefficients and the standard errors of measurement. Reproducibility of heart period variability measurements is excellent in patients with previous myocardial infarction and ventricular arrhythmias, and is comparable to the high stability previously found in a small group of normal subjects. The stability of measures of heart period variability facilitates distinguishing real changes due to progression or regression of cardiac disease or to drug effects from apparent changes due to random variation.
Article
It has been shown that in hypertensive patients the degree of target organ damage correlates more closely with average blood pressure as recorded by ambulatory monitoring (ABPM) throughout 24 h than with clinic blood pressure. We examined a group of 91 clinically healthy subjects, 23 normotensives and 68 hypertensives according to clinic blood pressure. Cardiac anatomy was investigated by echocardiography. As an index of arterial structural changes forearm minimal vascular resistance was calculated from mean arterial pressure and maximal postischemic blood flow, as assessed by venous occlusion plethysmography. The results were correlated to clinic blood pressure or ABPM values (measured by noninvasive ABPM ICR 5200, Spacelabs, Bellevue, CA). Left ventricular mass was correlated more closely with the average blood pressure recorded during 24 h, or during daytime or nighttime periods, than with clinic blood pressure. Minimal vascular resistance was also significantly correlated to ABPM values, but the correlation was similar to that observed with clinic blood pressure. Minimal vascular resistance was significantly correlated to blood pressure variability, as evaluated by the standard deviation of the mean. Minimal vascular resistance and left ventricular mass were higher in a subgroup of patients in whom blood pressure was not significantly reduced during the night. The results of this study confirm that elevated average ABPM values are associated to higher left ventricular mass; in addition, they suggest that increased blood pressure variability may be associated with vascular structural changes, as evaluated by minimal vascular resistance. It remains to be clarified whether cardiac hypertrophy and/or vascular structural changes are a cause or consequence of increased blood pressure values and variability.
Article
Significant increases in maximum oxygen consumption (VO2max) were noted in nine young track athletes following an 8-week high-intensity running period (P less than 0.05). VO2max was measured, prior to and following the training program, using an on-line, open-circuit spirometry system. Parasympathetic activity was assessed using heart period variation (R-R interval in milliseconds) during carefully controlled breathing activity (R sinus arrhythmia). Following the training program, a 7.3% increase in aerobic capacity was associated with a 23.1% augmentation of efferent parasympathetic activity (P less than 0.01). These data suggest that enhanced aerobic capacity increases efferent parasympathetic tone.
Article
Studies have shown that the circadian blood pressure profile is similar in normotensive and hypertensive subjects, and that the observed increase in blood pressure variability in hypertensive patients is proportional to the increase over the normotensive baseline blood pressure, suggesting that transient blood pressure oscillations on a percentage basis are not altered by hypertension. It has also been found that although antihypertensive therapy tends to reduce mean arterial blood pressure (MAP), the tendency to oscillate around a mean pressure is modified to a lesser extent. The significance of this observation is unknown; however, this effect should possibly be considered and studied in view of the incomplete protection against cardiovascular complications that is afforded by the current management of hypertension.
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IN the 19th century there were two major hypotheses to explain the pathogenesis of atherosclerosis: the "incrustation" hypothesis and the "lipid" hypothesis. The incrustation hypothesis of von Rokitansky,1 proposed in 1852 and modified by Duguid,2 suggested that intimal thickening resulted from fibrin deposition, with subsequent organization by fibroblasts and secondary lipid accumulation. The lipid hypothesis, proposed by Virchow3 in 1856, suggested that lipid in the arterial wall represented a transduction of blood lipid, which subsequently formed complexes with acid mucopolysaccharides; lipid accumulated in arterial walls because mechanisms of lipid deposition predominated over those of removal. The two hypotheses are now . . .
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The purpose of this study was to examine the relationship between the variability of awake ambulatory blood pressure and the level of plasma renin activity (PRA) in age-matched samples of untreated hypertensive white men. The ambulatory pressures of 376 men (145 under 45 years of age, 231 over 45) were compared across three levels of PRA: less than 1.0 ng/mL/h, 1.0 to 4.0 ng/mL/h and 4.0 ng/mL/h or greater. The results showed that the average diastolic pressure declined with PRA, particularly in men under 45 (95 to 89; P less than .05), but that among the men 45 and older there was a strong, positive relationship between awake diastolic pressure variability and the level of PRA (p less than .001). These results may have important clinical implications since both higher PRA and greater blood pressure variability have been associated with a greater cardiovascular disease risk.
Article
We have demonstrated previously that transfer function analysis can be used to precisely characterize the respiratory sinus arrhythmia (RSA) in normal humans. To further investigate the role of the autonomic nervous system in RSA and to understand the complex links between respiratory activity and arterial pressure, we determined the transfer functions between respiration, heart rate (HR), and phasic, systolic, diastolic, and pulse arterial pressures in 14 healthy subjects during 6-min periods in which the respiratory rate was controlled in a predetermined but erratic fashion. Pharmacological autonomic blockade with atropine, propranolol, and both, in combination with changes in posture, was used to characterize the sympathetic and vagal contributions to these relationships, as well as to dissect the direct mechanical links between respiration and arterial pressure from the effects of the RSA on arterial pressure. We found that 1) the pure sympathetic (standing + atropine) HR response is characterized by markedly reduced magnitude at frequencies greater than 0.1 Hz and a phase delay, whereas pure vagal (supine + propranolol) modulation of HR is characterized by higher magnitude at all frequencies and no phase delay; 2) both the mechanical links between respiration and arterial pressure and the RSA contribute significantly to the effects of respiration on arterial pressure; 3) the RSA contribution to arterial pressure fluctuations is significant for vagal but not for sympathetic modulation of HR; 4) the mechanical effects of respiration on arterial pressure are related to the negative rate of change of instantaneous lung volume; 5) the mechanical effects have a higher magnitude during systole than during diastole; and 6) the mechanical effects are larger in teh standing than the supine position. Most of these findings can be explained by a simple model of circulatory control based on previously published experimental transfer functions from our laboratory.
Article
Psychological data from 560 male survivors of acute myocardial infarction (AMI) were documented in the third week after onset of AMI. The psychodiagnostic assessment was designed to detect different forms of depression as well as hyperactive behaviour. A complete follow-up of these patients, which covers a period of 6 months, is available. Our findings indicate that affective disorders play an important role in the post-acute phase after AMI although the extent of myocardial infarction (as defined by an ECG score) and behaviour responses are not significantly related to one another. Different subforms of depression are not influenced by a history of angina pectoris, the degree and location of myocardial infarction, the occurrence of late potentials and age, whereas dyspnoea (P < 0·001) and the recurrence of myocardial infarction (P < 0·001) favour depressive mood states. Twelve cardiac deaths and 17 arrhythmic events occurred during the study period; they were significantly predicted by severe forms of post-AMI depression as revealed by univariate analysis. The evidence was stronger for predicting cardiac death (P < 0·001) than for arrhythmic events (P = < 0·035). The effect remains of borderline significance for cardiac death if all risk factors with a significant univariate influence are included in a multiple logistic regression model. The effect of depression is illustrated by Kaplan—Meier survival curves separated for patient groups with high as compared to low degrees of depression. Hyperactivity showed no impact on patient survival.
Article
Studies of the association between type A behavior and coronary heart disease have yielded inconsistent findings. A possible explanation for these inconsistent findings is that type A behavior is simply a marker for other behaviors that are truly related to coronary heart disease. Hostility is one such behavior that has been found in several recent studies to predict coronary heart disease and coronary atherosclerosis; however, several other studies have found null results. In the present study, the predictive power of hostility was tested in a study population of hospitalized men (n = 118) and women (n = 40) scheduled for coronary angiography. Potential coronary risk behaviors were assessed in the angiography patients and they were given the type A Structured Interview. Hostility was measured with the Cook-Medley Hostility Inventory and the Behavior Pattern Hostility Index, a measure of hostility derived from the type A Structured Interview. No significant positive associations were found for either Cook-Medley hostility or behavior pattern hostility and coronary occlusion. This was true whether hostility or coronary occlusion was treated as a dichotomous variable or as a continuous variable. In fact, most of the observed associations were opposite to the predicted direction, although none was statistically significant. Replicating cutpoints of the Cook-Medley Hostility Inventory used in other studies that have reported positive associations with coronary heart disease also yielded null findings. The association between hostility and coronary occlusion was slightly modified by age and sex, but the interaction coefficients were not significant. The sample size yielded adequate statistical power to detect the hypothesized associations, and there was no evidence that selection bias, measurement error, or unexamined confounding accounted for the null findings. These results failed to confirm some earlier reports showing a positive association between hostility and coronary artery disease.
Article
Decreased vagal activity is frequently observed in coronary artery disease, but the mechanism of this association is unknown. We investigated cardiac autonomic function by relating heart rate spectral components to clinical and angiographic findings in 80 patients who were undergoing coronary angiography. The age- and sex-adjusted magnitude of the respiratory spectral component, which is an index of cardiac vagal tone, showed a significant negative correlation with the extent of coronary atheromatosis (r = -0.43, p less than 0.0001) and a less significant negative correlation with the severity of coronary stenosis (r = -0.30, p = 0.0070). These relationships were independent of previous myocardial infarction and of left ventricular function. Stepwise regression analysis showed that the respiratory spectral component contributed to atheromatosis independently of established coronary risk factors (partial R2 = 9.4%, p = 0.002), but not to stenosis. Our results support the hypothesis that decreased cardiac vagal activity is associated with an increased risk of coronary atherosclerosis.
Article
Although thrombosis associated with a fissured atherosclerotic plaque is believed to be the most common cause of acute coronary syndromes, the underlying factors that trigger plaque rupture are currently unknown. However, the mechanical behavior of the plaque is probably of critical importance. To test the hypothesis that the mechanical properties of a plaque are dependent on its composition and, in particular, that the stiffness of fibrous caps changes within the range of frequencies carried by a physiological pressure wave, the stress-strain relation was studied in 27 fibrous caps and related to the underlying histological structure of the fibrous cap. Fibrous caps were obtained during 14 autopsies from the abdominal aorta and were classified by histological examination as cellular (n = 7), hypocellular (n = 9), or calcified (n = 11). Hypocellular fibrous caps were 1-2 times stiffer than cellular caps (p less than 0.005), and calcified caps were 4-5 times stiffer than cellular caps (p less than 0.005). All 27 fibrous caps demonstrated an increase in stiffness with increasing frequencies of stress ranging from 0.05 to 10 Hz; the increase in stiffness was similar in all three histological classes. We conclude that the stiffness of fibrous caps from human atherosclerotic plaques is related to the underlying histological structure and that the stiffness increases with frequency in the range of physiological heart rates. The protective benefit of beta-adrenergic receptor blocking agents in coronary artery disease may, in part, be related to the frequency dependence of atherosclerotic plaque stiffness.
Article
This study correlates variables derived from blood pressure (BP) and heart rate (HR) monitoring with the degree of left ventricular structural changes in essential hypertension. Forty patients with mild-to-moderate hypertension according to World Health Organization criteria underwent 24-hour ambulatory monitoring. Echocardiographic (posterior wall and interventricular septum thickness, left ventricular mass) or ECG (SV1 + RV5) indices of hypertrophy were significantly (p less than 0.01) correlated (positive correlations) with derivatives of BP monitoring (mean systolic and diastolic BP values) but not with HR derivatives. Echocardiographic indices of dilatation (left ventricular end-diastolic volume and diameter) were significantly (p less than 0.01 to less than 0.001) correlated (negative correlations) with derivatives of HR monitoring (mean HR values, mainly during the night) but not with BP derivatives. It is concluded that in essential hypertension, left ventricular hypertrophy depends on mean 24-hour systolic and diastolic BP values, whereas left ventricular dilatation appears to be more prominent in patients with bradycardia mainly during the night.
Article
The frequency of ventricular premature complexes and the degree of impairment of left ventricular ejection fraction are major predictors of cardiac mortality and sudden death in the year after acute myocardial infarction. Recent studies have implicated psychosocial factors, including depression, the interaction of social isolation and life stress, and type A-B behavior pattern, as predictors of cardiac events, controlling for known parameters of disease severity. However, results tend not to be consistent and are sometimes contradictory. The present investigation was designed to test the predictive association between biobehavioral factors and clinical cardiac events. This evaluation occurred in the context of a prospective clinical trial, the Cardiac Arrhythmia Pilot Study (CAPS). Five-hundred two patients were recruited with greater than or equal to 10 ventricular premature complexes/hour or greater than or equal to 5 episodes of nonsustained ventricular tachycardia, recorded 6 to 60 days after a myocardial infarction. Baseline behavioral studies, conducted in approximately 66% of patients, included psychosocial questionnaires of anxiety, depression, social desirability and support, and type A-B behavior pattern. In addition, blood pressure and pulse rate reactivity to a portable videogame was assessed. The primary outcome was scored on the basis of mortality or cardiac arrest. Results indicated that the type B behavior pattern, higher levels of depression and lower pulse rate reactivity to challenge were significant risk factors for death or cardiac arrest, after adjusting statistically for a set of known clinical predictors of disease severity. The implication of these results for future research relating behavioral factors to cardiac endpoints is discussed.
Article
The relationship of major depression and cardiovascular disease has been the subject of much study. In this paper, the authors review the literature concerning the clinical importance of this relationship in four areas including the diagnosis and treatment of major depression in the setting of cardiovascular disease, the effect of concurrent major depression on the prognosis of cardiovascular disease, and the higher-than-expected rate of cardiovascular death in depressed patients. In addition, they present preliminary data which may suggest a mechanism to explain, in part, this increased rate of cardiovascular death in depression.
Article
We studied in seven conscious dogs the dynamic rearrangements in neural control of heart rate and left ventricular pressure during treadmill exercise as assessed by spectral analysis. The presence, at rest, of a major high-frequency component (HF), an indicator of vagal tone, was reverted during exercise to a major low-frequency component (LF), an indicator of sympathetic activation. These changes were blunted by chronic beta and alpha 1 adrenergic receptor blockade.
Article
Follow-up studies of psychiatric patients with panic disorder have shown an abnormally high mortality rate in men due to cardiovascular and cerebrovascular events. The authors report that in the New Haven portion of the Epidemiologic Catchment Area program the risk for stroke in persons with lifetime diagnoses of panic disorder was over twice that in persons with other psychiatric disorders or no psychiatric disorder. After adjustments for demographic differences between groups, the risk was even higher. While the results should be interpreted cautiously because of the small sample and absence of medical examinations, these findings are consistent with clinical studies showing an association between panic disorder and cardiovascular/cerebrovascular events.
Article
To assess the contribution of the heart's autonomic innervation to reactivity to psychological stressors, hemodynamic responsiveness of the denervated human heart was examined in two studies. In Study 1, cardiac output measured by thermodilution. heart rate, and systolic and diastolic blood pressure responses to a 4‐min mental arithmetic task were studied in 7 cardiac transplant patients during routine post‐transplant cardiac catheterization. In Study II, 6 cardiac transplant patients, 5 normal controls, and 5 renal transplant patients participated in a 78‐min psychophysiological stress protocol during which heart rate, systolic and diastolic pressure, and cardiac output (measured noninvasively by impedance cardiography) as well as serum epinephrine and norepinephrine were measured at baseline and while subjects performed mental arithmetic and reaction time tasks. In Study I, transplant patients showed significant increases, relative to baseline, in heart rate, systolic blood pressure, and cardiac output in response to mental arithmetic. The diastolic blood pressure response was marginally significant. In Study II, mental arithmetic produced significant reactivity in systolic blood pressure and marginally significant increases in heart rate and diastolic blood pressure in cardiac transplant patients. Reaction time produced only marginally significant diastolic blood pressure reactivity. Hemodynamic reactivity of the cardiac transplant group generally was lower than that of the two innervated groups, which generally were similar to each other. Although the small number of subjects makes conclusions tentative, these data suggest that: 1) Cardiac transplant patients are capable of significant reactivity to psychological stressors despite the absence of innervation of the heart, and 2) reactivity to these stressors is diminished relative to innervated control subjects. In the absence of cardiac innervation, reactivity is due to the vascular system and cardiac effects mediated by humoral factors.
Article
In this study, we tested the hypothesis that the neural control of circulation in humans undergoes continuous but in part predictable changes throughout the day and night. Dynamic 24-hour recordings were obtained in two groups of ambulant subjects. In 18 hospitalized patients free to move, direct high-fidelity arterial pressures and electrocardiograms were recorded, and in an additional 28 nonhospitalized subjects, only electrocardiograms were obtained. Spectral analysis of systolic arterial pressure and of RR interval variabilities provided quantitative markers of sympathetic and vagal control of the sinus node and of sympathetic modulation of vasomotor tone. With this approach, the low-frequency (approximately 0.1 Hz) component of RR interval and systolic arterial pressure variabilities is considered a marker primarily of sympathetic activity, whereas the high-frequency (approximately 0.25 Hz) component of RR interval variability, related to respiration, seems to be a marker primarily of vagal activity. We observed a pronounced and consistent reduction in the markers of sympathetic activity and an increase in those of vagal activity during the night. In the invasive studies, while the subjects were still lying in bed after waking up, the markers of sympathetic activity rose rapidly and concomitantly with a simultaneous vagal withdrawal. Noninvasive studies confirmed the early morning rise of the markers of sympathetic activity and the circadian pattern of sympathovagal balance. These data indicate that the ominously increased rate of cardiovascular events in the morning hours may reflect the sudden rise of sympathetic activity and the reduction of vagal tone.
Article
We analyzed the spectral components of RR interval variability under controlled respiration (15 breaths/min) in 56 patients (age range, 35-73 years) referred for coronary angiography; 14 patients had multivessel disease (group M), 21 had one-vessel disease (group S), and 21 had nonsignificant disease or normal coronary artery (group N). There were 43 healthy controls (age range, 36-71 years) (group C). The patients had no clinical evidence of heart failure, hypertension, diabetes mellitus, or acute stage of infarction and had taken no medication for 3 days. The autoregressive power spectral density of RR interval variability contains two major components, respiratory sinus arrhythmia (RSA) (0.25 Hz) and Mayer wave-like sinus arrhythmia (MWSA) (0.04-0.15 Hz), which have magnitudes that are quantitative markers of cardiac vagal activity and sympathetic activity with vagal modulation, respectively. We represented the magnitudes by the coefficient of component variance (CCV), which provided the amplitude relative to the mean RR interval. The age- and sex-adjusted mean of CCVRSA significantly decreased with advancing angiographic severity (1.64 +/- 0.09%, 1.66 +/- 0.12%, 1.22 +/- 0.13%, and 0.81 +/- 0.16% for groups C, N, S, and M, respectively) (p = 0.0001). The CCVRSA was unrelated to left ventricular function, previous myocardial infarction, or stenosis of any specific artery including the sinoatrial and atrioventricular node arteries. The CCVMWSA decreased only in group M (p = 0.0462). These results indicate that coronary artery disease is associated with vagal dominant impairment in autonomic cardiac function and that reduction in the vagal cardiac function correlates with the angiographic severity.
Article
To investigate autonomic function in panic disorder patients (n = 30), we compared postural changes in heart rate and the R-R interval variance in patients and normal controls (n = 20). There was no significant difference in the immediate changes in heart rate upon standing between the groups. R-R variance was significantly decreased during resting supine condition in patients as indicated by the corrected standard deviation of the R-R intervals. The standing R-R variance was significantly lower than that of normal controls as indicated by the corrected standard deviations, the corrected mean consecutive difference and the corrected standard deviation of the mean consecutive difference of the R-R intervals, suggesting an increase in vagal withdrawal in patients, especially upon standing. If this finding is specific to panic disorder patients, it may be a useful peripheral marker for this condition.