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Biomedical subjects

A Malliani

Publications and source records attributed to A Malliani.

At least 91 records · Page 5Linked to original sources
PubMed1994

Power spectral analysis of cardiovascular variability in patients at risk for sudden cardiac death.

The time series of successive heart periods present important variations around its mean value, determining the phenomenon of heart rate variability (HRV), assessed with both time and frequency domain approaches. A low standard deviation of the heart period (a time domain index of HRV) is a powerful prognostic indicator of sudden coronary death in patients recovering from acute myocardial infarction. Spectral analysis of HRV usually demonstrates two major components: indicated as LF (low frequency, approximately 0.1 Hz) and HF (high frequency, approximately 0.25 Hz). They are defined by center frequency and associated power, which is expressed in msec2 or normalized units. When assessed in normalized units, LF and HF provide quantitative indicators of neural control of the sinoatrial node. Numerous experimental and clinical studies have consistently indicated that the LF component is a marker of sympathetic modulation and HF a marker of vagal modulation; the LF/HF ratio is a synthetic index of sympathovagal balance. In the analysis of 24-hour Holter recordings of normal subjects, a circadian rhythmicity of spectral markers of sympathetic and vagal modulation is clearly present, with a sympathetic predominance during the day and a vagal predominance during the night. In patients recovering from an acute myocardial infarction, spectral analysis of HRV revealed an increased sympathetic and decreased vagal activity during early convalescence, and a return to their normal balance by 6 to 12 months. A clear increase of LF was also evident in patients studied within a few hours of the onset of symptoms related to an acute myocardial infarction, independent of its location. Similarly, LF increased during transient myocardial ischemia. An increase in markers of sympathetic activity has also been observed prior to episodes of malignant arrhythmias. Spectral analysis of HRV could help in the understanding of the role of abnormal neural mechanisms in sudden coronary death, thus contributing to its prevention.

Death, Sudden, Cardiac↗
PubMed1994

Influences of neural mechanisms on heart period and arterial pressure variabilities in quadriplegic patients.

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.

Adolescent↗
PubMed1994

Restraining effects of captopril on sympathetic excitatory responses in dogs: a spectral analysis approach.

This study was planned to clarify the effects of captopril administration on the autonomic control of the circulation in conscious dogs and in dynamic conditions using spectral analysis of R-R interval and systolic arterial pressure (SAP) variabilities. Changes in sympathovagal balance modulating the sinoatrial (SA) node were inferred, respectively, from the low (LFR-R)- and high-frequency (HFR-R) components of R-R variability; LFSAP furnished a marker of sympathetic vasomotor control. Increases in sympathetic activity were induced by three different experimental maneuvers [bilateral carotid occlusion (BCO), coronary artery occlusion (CAO), and dynamic exercise] capable of increasing sympathetic outflow to the SA node and to the vessels. Studies were performed both before and after intravenous captopril administration. During BCO, only LFSAP increased from 4.3 +/- 1.5 to 19.7 +/- 4.1 mmHg2; during CAO, both LFR-R and LFSAP increased, respectively, from 3 +/- 1 to 21 +/- 2 normalized units (nu) and from 4.1 +/- 1.3 to 7.2 +/- 1.5 mmHg2. Dynamic exercise at 2 and 4 km/h progressively raised LFR-R from 8 +/- 2 to 58 +/- 7 and 75 +/- 5 nu, respectively; LFSAP showed a parallel trend increasing from 2.5 +/- 0.7 to 8.04 +/- 1.9 and 12.7 +/- 2.2 mmHg2. In all experimental conditions, captopril significantly (P < 0.05) blunted the increase of LFSAP. A restraining effect on LFR-R was apparent only with CAO. Spectral analysis of cardiovascular variabilities indicates that, in the conscious dog, acute captopril administration has an important inhibitory effect on cardiac sympathetic excitatory mechanisms as well as on sympathetic vasomotor control.

Animals↗
PubMed1994

Power spectrum analysis of heart rate variability to assess the changes in sympathovagal balance during graded orthostatic tilt.

BACKGROUND: The powers of the low-frequency (LF) and high-frequency (HF) oscillations characterizing heart rate variability (HRV) appear to reflect, in their reciprocal relationship, changes in the state of the sympathovagal balance occurring during numerous physiological and pathophysiological conditions. However, no adequate information is available on the quantitative resolution of this methodology. METHODS AND RESULTS: We studied 22 healthy volunteers (median age, 46.5 years) who were subjected after a rest period to a series of passive head-up tilt steps randomly chosen from the following angles: 15 degrees, 30 degrees, 45 degrees, 60 degrees, and 90 degrees. From the continuous ECG, after appropriate analog-to-digital conversion, a personal computer was used to compute, with an autoregressive methodology, time and frequency domain indexes of RR interval variability. Spectral and cross-spectral analysis with the simultaneously recorded respiratory signal excluded its contribution to LF. Age was significantly correlated to variance and to the absolute values in milliseconds squared of very-low-frequency (VLF), LF, and HF components. The tilt angle was correlated to both LF and HF (expressed in normalized units [nu]) and to the LF-to-HF ratio (r = .78, -.72, and .68; respectively). Lower levels of correlation were found with HF (in ms2) and RR interval. No correlation was present between tilt angle and variance, VLF, or LF (in ms2). Individual analysis confirmed that the use of nu provided the greatest consistency of results. CONCLUSIONS: Spectral analysis of HRV, using nu or LF-to-HF ratio, appears to be capable of providing a noninvasive quantitative evaluation of graded changes in the state of the sympathovagal balance.

Adult↗
PubMed1994

[Methods for assessing the autonomic nervous system in man].

Assessment of baroreflex sensitivity and spectral analysis of heart rate variability are two methods capable of providing relevant information on neural mechanisms controlling heart period and on their alterations during several pathophysiological conditions such as coronary artery disease and cardiac insufficiency. These techniques provide complementary information: the former is based on a stimulus-response model which has in the activation of vagal fibers directed to the heart its main efferent component; the latter, by quantifying the spontaneous harmonic oscillations of heart period, furnishes indices of sympathetic and vagal modulation of sinus node.

Autonomic Nervous System↗
PubMed1994

Non-linear dynamics in the beat-to-beat variability of sympathetic activity in decerebrate cats.

Non-linear interactions between low-frequency rhythms (0.1 Hz) of beat-to-beat variability series of sympathetic discharge and respiratory rhythm (0.3 Hz) are observed in decerebrate artificially ventilated cats. Simple graphical tools as Poincaré and recurrence maps are used to detect, in a qualitative way, phase-locking phenomena. Non-parametric bispectral analysis is also carried out to quantify the degree of second-order coupling between oscillations at different frequencies.

Animals↗
PubMed1993

Early and late effects of exercise and athletic training on neural mechanisms controlling heart rate.

OBJECTIVE: This study addresses the long term and short term effects of heavy dynamic exercise on neural control of heart rate. METHODS: A group of healthy controls was compared with (1) a group of trained athletes during a period of yearly rest (detrained) and (2) a group of trained athletes at the peak of their training routine. Additionally, a group of 10 controls was studied 1, 24, and 48 h after a single bout of maximal dynamic exercise. Spectral analysis of RR interval variability provided markers of sympathetic (low frequency, LF, 0.10 Hz) and vagal (high frequency, HF, 0.25 Hz) modulation of the sinoatrial node. RESULTS: (1) In detrained athletes resting bradycardia was accompanied by a predominant HF rhythmic component suggestive of a prevailing vagal tone. (2) Trained athletes showed a resting bradycardia together with high LF values, thus suggesting a more complex neural interaction modulating heart rate. An additional longitudinal part of the study, performed on a group of detrained athletes who were examined for the second time after resuming training, confirmed the finding of a prevailing LF component in resting conditions. (3) In the 10 control subjects maximal dynamic exercise induced an increase in LF which outlasted the cessation of exercise up to 24 h, suggesting a persistent sympathetic activation. (4) Passive tilt, a manoeuvre which enhances sympathetic drive, produced a greater enhancement of the LF component in trained athletes than in control subjects. CONCLUSIONS: The cardiac sympathetic excitation outlasting heavy dynamic exercise may explain the coexistence of training bradycardia with signs of enhanced sympathetic activity in trained champion athletes.

Adolescent↗
PubMed1993

Evidence of functional alterations in sympathetic activity after myocardial infarction.

To assess whether the presence of areas of efferent sympathetic denervation might contribute to alterations in sympathetic and vagal neural regulatory activities observed after myocardial infarction, we attempted to correlate the changes in the spectral components of RR variability with the I-123 MIBG and Thallium-201 uptake defects. Ten patients with first and uncomplicated myocardial infarction were studied. Thallium-201 and I-123 MIBG scintigraphy as well as spectral analysis of heart rate variability were performed 7 days, 4, 12 and 30 months after the acute event. Regional abnormalities in I-123 MIBG uptake were more extensive than the perfusion defects indicated by Thallium-201 images and remained constant throughout the entire period of observation. In the early post-infarction period, spectral analysis of RR variability was characterized by a predominant LF (74 +/- 6 nu) and a smaller HF (16 +/- 3 nu) component indicating a sympathetic predominance. Thereafter, we observed a progressive reduction in LF and a gradual increase in HF which were consistent with a normalization of sympatho-vagal balance. These data indicate that after a myocardial infarction, the presence and persistence of areas of sympathetic functional denervation do not seem to play a major role in determining the changes in sympathetic and vagal neural regulatory activities directed to the heart.

3-Iodobenzylguanidine↗
PubMed1993

Effect of captopril on sympathetic preganglionic efferent activity in cats.

In 13 decerebrate cats, we studied the effects of captopril (10 mg/kg iv bolus) on the background discharge of thoracic preganglionic sympathetic fibers. After drug administration there was an initial reduction in systolic arterial pressure (SAP), which was followed by a later inhibition of sympathetic discharge (from 2.7 +/- 0.5 to 0.79 +/- 0.1 imp/0.1 s; P < 0.01). Captopril significantly reduced the excitatory response of sympathetic fibers to premature ventricular contraction (70 +/- 17 vs. 257 +/- 30%), inferior vena cava obstruction (176 +/- 56 vs. 315 +/- 85%) and asphyxia (143 +/- 20 vs. 245 +/- 51%). Vice versa the sympathetic response to aortic occlusion was unaffected (-58 +/- 8 vs. -62 +/- 6%). A similar reduction in sympathetic discharge was observed after captopril administration in anesthetized cats (n = 3). On the contrary, no changes in background neural discharge were noticed in decerebrate-spinalized cats (n = 5), despite comparable hemodynamic effects. These data indicate that captopril reduces sympathetic efferent activity and its responsiveness to excitatory stimuli. The lack of neural effects in decerebrate-spinalized cats is consistent with a brain stem site of action of captopril.

Animals↗
PubMed1993

[Behavior, sympathetic nervous system, and arterial hypertension].

The discharge of sympathetic and vagal outflows appears regulated, in general, by a reciprocal interaction, that is to say that the increased activity of one component is accompanied by the decreased activity of the other. A sympathetic excitation can depend on central neural mechanisms, on peripheral excitatory reflexes and on a reduced inhibition exerted by inhibitory reflex mechanisms. Behavioral studies can reveal conditions associated with an increased sympathetic activity and with an augmented arterial pressure. The use of a spectral methodology applied to the study of cardiovascular variability allows the quantification, on the whole, of the state of sympatho-vagal balance: in the course of essential arterial hypertension this equilibrium appears shifted towards a sympathetic predominance.

Behavior↗