PubMed · 8617408
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I A Macdonald. 1995. How do we study autonomic function in humans?. https://doi.org/10.1111/j.1472-8206.1995.tb00519.x
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Starting from the observation of the relationships of the biological system with its environments and of the genetically determined neuronal properties of plasticity and rhythmicity, it is possible to propose a new hypothesis about the functional role and organization of the visceral nervous system based on the physical model of the Dissipative Structure by I. Prigogine. The similarily between the visceral nervous system function and this model is supported by the following observations: (1) The visceral nervous system is a complex system, composed of many interacting units, which works away from thermodynamic equilibrium; (2) the functional organization of the nervous system is strongly dependent on internal and external environmental stimuli; (3) it is characterized by the presence of rhythms and periodic behaviors and (4) the internal order of the system is maintained in the continuous interplay between function, structure and fluctuations. On the basis of the present hypothesis, a few general principles can be formulated: (1) the higher brain centers, the fluid matrix and the external world, are the visceral nervous system natural environments; (2) with which it is plastically interfaced as a thermodynamic dissipative structure; (3) its main functional role is to regulate, distribute and maintain ordered exchanges of matter, energy and information between these environments. The present is a general interpretation of the operations of the visceral nervous system as a whole. In the frame of this interpretation the hypotheses so far formulated, including the homeostatic theory, can be viewed as the description of discrete and complementary aspects of the visceral nervous system functions.
A previous report on heart rate (HR) turbulence showed its value in postinfarction risk stratification. The present study determines the predictive value of HR turbulence in a low-risk population after acute myocardial infarction and provides insight into its pathophysiologic correlates. With use of the database of the The Autonomic Tone and Reflexes After Myocardial Infarction (ATRAMI) study, data were obtained from 1,212 survivors with a mean duration of follow-up of 20.3 months. The a priori end point was defined as the combination of fatal cardiac arrest and nonfatal cardiac arrest. HR turbulence characterized by turbulence onset (TO) and turbulence slope (TS) was calculated and correlated with baroreflex sensitivity (BRS) and the SD of the normal-to-normal RR intervals (SDNN). A composite index of cardiac autonomic function was assessed by combining HR turbulence (TO and TS), BRS, and SDNN. Both TO and TS correlated moderately but significantly with BRS and SDNN (r = 0.26 to 0.44, p <0.001 for all correlations). On Cox's univariate regression analysis, the RRs for abnormal values of TO, TS, and the combination of abnormal TO and TS were 1.86 (95% confidence interval [CI] 0.96 to 3.61, p = 0.065), 4.08 (95% CI 2.11 to 7.89, p <0.0001), and 6.87 (95% CI 3.06 to 15.45, p <0.0001), respectively. The composite autonomic index (combined TO, TS, BRS, and SDNN) was the strongest risk predictor: for all 4 abnormal factors, RR 16.79 (95% CI 6.01 to 46.89, p <0.0001). On multivariate analysis, abnormal TO and TS, and left ventricular ejection fraction remained as independent predictors: RRs 4.07 (95% CI 1.70 to 9.77, p = 0.0017) and 3.53 (95% CI 1.76 to 7.06, p = 0.0004), respectively. In a separate model, the composite autonomic index was the strongest multivariate risk predictor: RR 8.67 (95% CI 2.72 to 7.65, p = 0.0003) for all abnormal factors, and adjusted for left ventricular ejection fraction. Thus, this study confirms the independent value of HR turbulence in predicting fatal cardiac arrest and nonfatal cardiac arrest in a low-risk post-acute myocardial infarction population. By combining HR turbulence, BRS, and SDNN, a comprehensive assessment of cardiac autonomic reflexes and modulation can be obtained.
This study evaluated whether small shifts in cardiac autonomic balance with standing, as measured by heart rate variability (HRV), were prospectively associated with incident coronary heart disease (CHD) and mortality. Both Black and White men and women aged 45-64 years from the Atherosclerosis Risk in Communities Study (n = 9,267) were followed from 1987 to 1997 for myocardial infarction (n = 296), fatal CHD (n = 63), and non-CHD mortality (n = 533). HRV indices and mean R-R interval length (inverse of heart rate) were measured in the supine and standing positions for 2 minutes each; HRV shift was calculated as the difference between positions. After adjustment for demographic characteristics and medication use, HRV in each position was significantly inversely related to events in Cox proportional hazards models. With the exception of R-R interval length shift and myocardial infarction (hazard ratio = 1.42, 95% confidence interval: 1.02, 1.98 for the smallest vs. the largest quartile), there was no association between HRV shift and the other events. Despite clinical research suggesting that HRV shift with standing is a more sensitive measure of autonomic balance than is HRV in one position, simple measures such as heart rate change and supine and standing HRV were better predictors of events.