The interactions between systolic arterial pressure (SAP) and R-R interval (RR) fluctuations after acute myocardial infarction (AMI) were investigated by measures of synchronization separating the feedback from the feedforward control and capturing both linear and nonlinear contributions. The causal synchronization, evaluating the ability of RR to predict SAP (Xs/t) or vice versa (Xt/s), and the global synchronization (X) were estimated at rest and after head-up tilt in 35 post-AMI patients, 20 young and 12 old. Significance and nonlinearity of the coupling were assessed by surrogate data analysis. Tilting increased the number of young subjects in which RR-SAP link was significant (from 17 to 19) and linear (from 11 to 18). In AMI, both significance and linearity of the coupling were low at rest (26 significant and 24 nonlinear) and further reduced after tilt (17 significant and 16 nonlinear). Old subjects showed a partial recovery of linearity after tilt (rest: 1 linear of 7 significant; tilt: 5 linear of 8 significant). In young subjects, the causal synchronization indexes were balanced and increased from rest (Xt/s = 0.072 ± 0.037 and Xs/t = 0.054 ± 0.028) to tilt (Xt/s = 0.125 ± 0.071 and Xs/t = 0.108 ± 0.053). On the contrary, in old subjects and AMI patients, the feedforward was prevalent to the feedback coupling at rest (old: Xt/s = 0.041 ± 0.023 and Xs/t = 0.069 ± 0.042; AMI: Xt/s = 0.050 ± 0.030 and Xs/t = 0.089 ± 0.053). Tilting blunted the unbalance in old subjects (Xt/s = 0.065 ± 0.052 and Xs/t = 0.069 ± 0.044) but not in AMI patients (Xt/s = 0.040 ± 0.019 and Xs/t = 0.060 ± 0.040). Thus, after AMI, nonlinear mechanisms are elicited in RR-SAP interactions. Furthermore, the neural regulation of the cardiovascular system resulted in imbalance as a consequence of impaired feedback and enhanced feedforward control mechanisms.
Nollo, G., Faes, L., Porta, A., Pellegrini, B., Ravelli, F., Del Greco, M., et al. (2002). Evidence of unbalanced regulatory mechanism of heart rate and systolic pressure after acute myocardial infarction. AMERICAN JOURNAL OF PHYSIOLOGY. HEART AND CIRCULATORY PHYSIOLOGY, 283(3 52-3), H1200-H1207.
Evidence of unbalanced regulatory mechanism of heart rate and systolic pressure after acute myocardial infarction
Faes, Luca;Porta, Alberto;
2002-01-01
Abstract
The interactions between systolic arterial pressure (SAP) and R-R interval (RR) fluctuations after acute myocardial infarction (AMI) were investigated by measures of synchronization separating the feedback from the feedforward control and capturing both linear and nonlinear contributions. The causal synchronization, evaluating the ability of RR to predict SAP (Xs/t) or vice versa (Xt/s), and the global synchronization (X) were estimated at rest and after head-up tilt in 35 post-AMI patients, 20 young and 12 old. Significance and nonlinearity of the coupling were assessed by surrogate data analysis. Tilting increased the number of young subjects in which RR-SAP link was significant (from 17 to 19) and linear (from 11 to 18). In AMI, both significance and linearity of the coupling were low at rest (26 significant and 24 nonlinear) and further reduced after tilt (17 significant and 16 nonlinear). Old subjects showed a partial recovery of linearity after tilt (rest: 1 linear of 7 significant; tilt: 5 linear of 8 significant). In young subjects, the causal synchronization indexes were balanced and increased from rest (Xt/s = 0.072 ± 0.037 and Xs/t = 0.054 ± 0.028) to tilt (Xt/s = 0.125 ± 0.071 and Xs/t = 0.108 ± 0.053). On the contrary, in old subjects and AMI patients, the feedforward was prevalent to the feedback coupling at rest (old: Xt/s = 0.041 ± 0.023 and Xs/t = 0.069 ± 0.042; AMI: Xt/s = 0.050 ± 0.030 and Xs/t = 0.089 ± 0.053). Tilting blunted the unbalance in old subjects (Xt/s = 0.065 ± 0.052 and Xs/t = 0.069 ± 0.044) but not in AMI patients (Xt/s = 0.040 ± 0.019 and Xs/t = 0.060 ± 0.040). Thus, after AMI, nonlinear mechanisms are elicited in RR-SAP interactions. Furthermore, the neural regulation of the cardiovascular system resulted in imbalance as a consequence of impaired feedback and enhanced feedforward control mechanisms.File | Dimensione | Formato | |
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