Exploring directionality in spontaneous heart period and systolic pressure variability interactions in humans: implications in the evaluation of baroreflex gain

2005 ◽  
Vol 288 (4) ◽  
pp. H1777-H1785 ◽  
Author(s):  
Giandomenico Nollo ◽  
Luca Faes ◽  
Alberto Porta ◽  
Renzo Antolini ◽  
Flavia Ravelli

Although in physiological conditions RR interval and systolic arterial pressure (SAP) are likely to interact in a closed loop, the traditional cross-spectral analysis cannot distinguish feedback (FB) from feedforward (FF) influences. In this study, a causal approach was applied for calculating the coherence from SAP to RR ( Ks-r) and from RR to SAP ( Kr-s) and the gain and phase of the baroreflex transfer function. The method was applied, compared with the noncausal one, to RR and SAP series taken from 15 healthy young subjects in the supine position and after passive head-up tilt. For the low frequency (0.04–0.15 Hz) spectral component, the enhanced FF coupling ( Kr-s = 0.59 ± 0.21, significant in 14 subjects) and the blunted FB coupling ( Ks-r = 0.17 ± 0.17, significant in 4 subjects) found at rest indicated the prevalence of nonbaroreflex mechanisms. The tilt maneuver recovered FB influences ( Ks-r = 0.47 ± 0.16, significant in 14 subjects), which were stronger than FF interactions ( Ks-r = 0.34 ± 0.19, significant in 9 subjects). At the respiratory frequency, the RR-SAP regulation was balanced at rest ( Ks-r = 0.30 ± 0.18 and Kr-s = 0.29 ± 0.20, significant in 11 and 8 subjects) and shifted toward FB mechanisms after tilt ( Ks-r = 0.35 ± 0.19 and Kr-s = 0.19 ± 0.11, significant in 14 and 8 subjects). The causal baroreflex gain estimates were always lower than the corresponding noncausal values and decreased significantly from rest to tilt in both frequency bands. The tilt-induced increase of the phase lag from SAP to RR suggested a shift from vagal to sympathetic modulation. Thus the importance of nonbaroreflex interactions pointed out the necessity of accounting for causality in the cross-spectral analysis of the interactions between cardiovascular variables in healthy humans.

2002 ◽  
Vol 283 (3) ◽  
pp. H1200-H1207 ◽  
Author(s):  
Giandomenico Nollo ◽  
Luca Faes ◽  
Alberto Porta ◽  
Barbara Pellegrini ◽  
Flavia Ravelli ◽  
...  

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 (χs/t) or vice versa (χt/s), and the global synchronization (χ) 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 (χt/s= 0.072 ± 0.037 and χs/t = 0.054 ± 0.028) to tilt (χt/s = 0.125 ± 0.071 and χs/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: χt/s = 0.041 ± 0.023 and χs/t = 0.069 ± 0.042; AMI: χt/s = 0.050 ± 0.030 and χs/t = 0.089 ± 0.053). Tilting blunted the unbalance in old subjects (χt/s = 0.065 ± 0.052 and χs/t = 0.069 ± 0.044) but not in AMI patients (χt/s = 0.040 ± 0.019 and χs/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.


1994 ◽  
Vol 266 (3) ◽  
pp. H1112-H1120 ◽  
Author(s):  
S. Guzzetti ◽  
C. Cogliati ◽  
C. Broggi ◽  
C. Carozzi ◽  
D. Caldiroli ◽  
...  

The heart period (R-R) variability power spectrum presents two components, at low (LF; approximately 0.10 Hz) and high (approximately 0.25 Hz) frequencies, whose reciprocal powers appear to furnish an index of sympathovagal interaction modulating heart rate. In addition, the LF component of the systolic arterial pressure variability spectrum furnishes a marker of sympathetic modulation of vasomotor activity. The contribution of spinal and supraspinal neural circuits to the genesis of these rhythmic oscillatory components remains largely unsettled. Therefore we performed spectral analysis of R-R and systolic arterial pressure variabilities in 15 chronic neurologically complete quadriplegic patients (QP) and in 15 control subjects during resting conditions, controlled respiration, and head-up tilt. At rest, in seven QP the LF component was undetectable in both cardiovascular variability spectra; in two QP this component was present only in R-R variability spectrum, whereas the remaining six showed a significantly reduced LF in both signals. In QP, the LF component, when present, underwent paradoxical changes with respect to controls, decreasing during tilt and increasing during controlled respiration. In five QP in whom the recording session was repeated after 6 mo, a significant increase in LF was observed in both variability spectra. These data confirm the finding that a disconnection of sympathetic outflow from supraspinal centers can cause the disappearance of the LF spectral component. However, LF presence in some QP supports the hypothesis of a spinal rhythmicity likely to be modulated by the afferent sympathetic activity.


Cephalalgia ◽  
1995 ◽  
Vol 15 (6) ◽  
pp. 504-510 ◽  
Author(s):  
M De Marinis ◽  
S Strano ◽  
M Granata ◽  
C Urani ◽  
S Lino ◽  
...  

Twenty-four hour ECG Holter and blood-pressure monitorings were performed in eight patients suffering from cluster headache. Spectral analysis of heart-rate fluctuation was used to assess the autonomic balance under basal conditions, after head-up tilt, and during a spontaneous attack. Normal autonomic balance was found at rest and during sympathetic activation obtained with head-up tilt in the interparoxysmal period. Before the onset of headache, an increase in the low-frequency (LF) component of the power spectrum was apparent in all patients. This sign of sympathetic activation was followed by an increase in the high-frequency (HF) component that developed about 2000 beats after the onset of headache and rapidly overcame the LF component until the end of pain. Significant differences were found when comparing the spectral parameters [total spectral values (TP), power of the LF and HF components and LF/HF ratio] obtained before, during and after headache. During the attack, blood pressure increased and heart rate decreased in all subjects. There appears to be a primary activation of both sympathetic and parasympathetic functions in cluster headache attacks. The sympathetic component seems to be involved mostly in the development of the attack, whereas the parasympathetic activation seems to occur, following the onset of the attack, independently of the pain.


2011 ◽  
Vol 300 (2) ◽  
pp. R378-R386 ◽  
Author(s):  
Alberto Porta ◽  
Aparecida M. Catai ◽  
Anielle C. M. Takahashi ◽  
Valentina Magagnin ◽  
Tito Bassani ◽  
...  

In physiological conditions, heart period (HP) affects systolic arterial pressure (SAP) through diastolic runoff and Starling's law, but, the reverse relation also holds as a result of the continuous action of baroreflex control. The prevailing mechanism sets the dominant temporal direction in the HP-SAP interactions (i.e., causality). We exploited cross-conditional entropy to assess HP-SAP causality. A traditional approach based on phases was applied for comparison. The ability of the approach to detect the lack of causal link from SAP to HP was assessed on 8 short-term (STHT) and 11 long-term heart transplant (LTHT) recipients (i.e., less than and more than 2 yr after transplantation, respectively). In addition, spontaneous HP and SAP variabilities were extracted from 17 healthy humans (ages 21–36 yr, median age 29 yr; 9 females) at rest and during graded head-up tilt. The tilt table inclinations ranged from 15 to 75° and were changed in steps of 15°. All subjects underwent recordings at every step in random order. The approach detected the lack of causal relation from SAP to HP in STHT recipients and the gradual restoration of the causal link from SAP to HP with time after transplantation in the LTHT recipients. The head-up tilt protocol induced the progressive shift from the prevalent causal direction from HP to SAP to the reverse causality (i.e., from SAP to HP) with tilt table inclination in healthy subjects. Transformation of phases into time shifts and comparison with baroreflex latency supported this conclusion. The proposed approach is highly efficient because it does not require the knowledge of baroreflex latency. The dependence of causality on tilt table inclination suggests that “spontaneous” baroreflex sensitivity estimated using noncausal methods (e.g., spectral and cross-spectral approaches) is more reliable at the highest tilt table inclinations.


2018 ◽  
Vol 111 (2) ◽  
pp. 95-100 ◽  
Author(s):  
Michela Anna Pia Ciliberti ◽  
Francesco Santoro ◽  
Luigi Flavio Massimiliano Di Martino ◽  
Antonio Cosimo Rinaldi ◽  
Giuseppe Salvemini ◽  
...  

2005 ◽  
Vol 289 (5) ◽  
pp. H1968-H1975 ◽  
Author(s):  
Rubens Fazan ◽  
Mauro de Oliveira ◽  
Valdo José Dias da Silva ◽  
Luis Fernando Joaquim ◽  
Nicola Montano ◽  
...  

The goal of this study was to determine the baroreflex influence on systolic arterial pressure (SAP) and pulse interval (PI) variability in conscious mice. SAP and PI were measured in C57Bl/6J mice subjected to sinoaortic deafferentation (SAD, n = 21) or sham surgery ( n = 20). Average SAP and PI did not differ in SAD or control mice. In contrast, SAP variance was enhanced (21 ± 4 vs. 9.5 ± 1 mmHg2) and PI variance reduced (8.8 ± 2 vs. 26 ± 6 ms2) in SAD vs. control mice. High-frequency (HF: 1–5 Hz) SAP variability quantified by spectral analysis was greater in SAD (8.5 ± 2.0 mmHg2) compared with control (2.5 ± 0.2 mmHg2) mice, whereas low-frequency (LF: 0.1–1 Hz) SAP variability did not differ between the groups. Conversely, LF PI variability was markedly reduced in SAD mice (0.5 ± 0.1 vs. 10.8 ± 3.4 ms2). LF oscillations in SAP and PI were coherent in control mice (coherence = 0.68 ± 0.05), with changes in SAP leading changes in PI (phase = −1.41 ± 0.06 radians), but were not coherent in SAD mice (coherence = 0.08 ± 0.03). Blockade of parasympathetic drive with atropine decreased average PI, PI variance, and LF and HF PI variability in control ( n = 10) but had no effect in SAD ( n = 6) mice. In control mice, blockade of sympathetic cardiac receptors with propranolol increased average PI and decreased PI variance and LF PI variability ( n = 6). In SAD mice, propranolol increased average PI ( n = 6). In conclusion, baroreflex modulation of PI contributes to LF, but not HF PI variability, and is mediated by both sympathetic and parasympathetic drives in conscious mice.


1987 ◽  
Vol 65 (10) ◽  
pp. 2048-2052 ◽  
Author(s):  
John P. Finley ◽  
Sherwin T. Nugent ◽  
Wiebke Hellenbrand

The variation in instantaneous heart rate is most prominent in infants and younger subjects. In a preliminary study of the effects of maturation on heart rate, we compared the heart rate variations of 29 children and young adults in three groups between 5 and 24 years of age. We used spectral analysis to determine the intensity of the variations in each of the two main frequency bands in which variations occur: HF, 0.15–0.45 Hz, and LF, 0.03–0.15 Hz. Three-minute segments of continuous instantaneous heart rate were recorded for each subject in standing and supine positions. The group mean LF and HF amplitudes and the L/H ratio decreased between 5 and 10 years of age in both positions, significantly for LF and L/H in the supine position (p < 0.05). Half of the youngest group of children had adult LF amplitude values by 5 years of age; the others had much higher levels, indicating increased low frequency variation at this age. Thus the high variation in heart rate in very young subjects is most prominent in the LF range. These preliminary results, considered with previous pharmacological studies, suggest that many children have a significant decrease in sympathetic activity between 5 and 10 years of age and possibly a slight decrease in parasympathetic activity. Spectral analysis of heart rate appears a promising technique for investigating the development of neural control of the heart.


2006 ◽  
Vol 100 (3) ◽  
pp. 792-799 ◽  
Author(s):  
Shizue Masuki ◽  
John H. Eisenach ◽  
Frank A. Dinenno ◽  
Michael J. Joyner

In the present study, we assessed whether heart rate (HR) or arterial pressure fluctuations are enhanced in healthy young humans with reduced α-adrenergic vasoconstrictor responses and, if so, whether this occurs for both α1- and α2-adrenergic receptor-mediated vasoconstriction. Arterial pressure (brachial artery catheter) and HR (ECG) were monitored continuously, and α1- and α2-adrenergic responsiveness was determined by assessing the effects of brachial artery infusions of phenylephrine (α1-adrenergic agonist) and dexmedetomidine (α2-adrenergic agonist), respectively, on forearm blood flow (strain gauge plethysmography). α1-Adrenergic responsiveness varied markedly among the subjects ( n = 20) and was inversely correlated with coefficient of variation for HR ( R2 = 0.37, P < 0.01), whereas the responsiveness was not correlated with the coefficient of variation for either systolic or diastolic arterial pressure. α1-Adrenergic responsiveness was inversely and more strongly correlated with baroreflex sensitivity ( R2 = 0.62, P < 0.0001), determined from beat-to-beat changes in HR and systolic arterial pressure, than the coefficient of variation for HR. On the other hand, α2-adrenergic responsiveness was not correlated with any of the parameters determined above. These results suggest that, in healthy young subjects, the enhanced HR response to changes in systolic pressure helps maintain the stability of arterial blood pressure when α1-adrenergic responsiveness is reduced.


2013 ◽  
Vol 114 (2) ◽  
pp. 203-210 ◽  
Author(s):  
André Diedrich ◽  
Alexandra A. Crossman ◽  
Larry A. Beightol ◽  
Kari U. O. Tahvanainen ◽  
Tom A. Kuusela ◽  
...  

Because it is likely that, in healthy human subjects, baroreflex mechanisms operate continuously, independent of experimental interventions, we asked the question, In what ways might study of unprovoked, very infrequent muscle sympathetic bursts inform baroreflex physiology? We closely examined arterial pressure and R-R interval responses of 11 supine healthy young subjects to arterial pressure ramps triggered by large isolated muscle sympathetic bursts. We triggered data collection sweeps on the beginnings of sympathetic bursts and plotted changes of arterial pressure (finger volume clamp or intra-arterial) and R-R intervals occurring before as well as after the sympathetic triggers. We estimated baroreflex gain from regression of R-R intervals on systolic pressures after sympathetic bursts and from the transfer function between cross-spectra of systolic pressure and R-R intervals at low frequencies. Isolated muscle sympathetic bursts were preceded by arterial pressure reductions. Baroreflex gain, calculated with linear regression of R-R intervals on systolic pressures after bursts, was virtually identical to baroreflex gain, calculated with the cross-spectral modulus [mean and (range): 24 (7–43) vs. 24 (8–45) ms/mmHg], and highly significant, according to linear regression ( r2 = 0.91, P = 0.001). Our results indicate that 1) since infrequent human muscle sympathetic bursts are almost deterministically preceded by arterial pressure reductions, their occurrence likely reflects simple baroreflex physiology, and 2) the noninvasive low-frequency modulus reliably reproduces gains derived from R-R interval responses to arterial pressure ramps triggered by infrequent muscle sympathetic bursts.


2006 ◽  
Vol 291 (6) ◽  
pp. R1579-R1591 ◽  
Author(s):  
Sanja Milutinović ◽  
David Murphy ◽  
Nina Japundžić-Žigon

Although it has been suggested that vasopressin (VP) acts within the central nervous system to modulate autonomic cardiovascular controls, the mechanisms involved are not understood. Using nonpeptide, selective V1a, V1b, and V2 antagonists, in conscious rats, we assessed the roles of central VP receptors, under basal conditions, after the central application of exogenous VP, and after immobilization, on cardiovascular short-term variability. Equidistant sampling of blood pressure (BP) and heart rate (HR) at 20 Hz allowed direct spectral analysis in very-low frequency (VLF-BP), low-frequency (LF-BP), and high-frequency (HF-BP) blood pressure domains. The effect of VP antagonists and of exogenous VP on body temperature (Tb) was also investigated. Under basal conditions, V1a antagonist increased HF-BP and Tb, and this was prevented by metamizol. V1b antagonist enhanced HF-BP without affecting Tb, and V2 antagonist increased VLF-BP variability which could be prevented by quinapril. Immobilization increased BP, LF-BP, HF-BP, and HF-HR variability. V1a antagonist prevented BP and HR variability changes induced by immobilization and potentiated tachycardia. V1b antagonist prevented BP but not HR variability changes, whereas V2 antagonist had no effect. Exogenous VP increased systolic arterial pressure (SAP) and HF-SAP variability, and this was prevented by V1a and V1b but not V2 antagonist pretreatment. Our results suggest that, under basal conditions, VP, by stimulation of V1a, V1b, and cognate V2 receptors, buffers BP variability, mostly due to thermoregulation. Immobilization and exogenous VP, by stimulation of V1a or V1b, but not V2 receptors, increases BP variability, revealing cardiorespiratory adjustment to stress and respiratory stimulation, respectively.


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