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PubMed2004

1/f scaling in heart rate requires antagonistic autonomic control.

We present systematic evidence for the origins of 1/f -type temporal scaling in human heart rate. The heart rate is regulated by the activity of two branches of the autonomic nervous system: the parasympathetic (PNS) and the sympathetic (SNS) nervous systems. We examine alterations in the scaling property when the balance between PNS and SNS activity is modified, and find that the relative PNS suppression by congestive heart failure results in a substantial increase in the Hurst exponent H towards random-walk scaling 1/ f(2) and a similar breakdown is observed with relative SNS suppression by primary autonomic failure. These results suggest that 1/f scaling in heart rate requires the intricate balance between the antagonistic activity of PNS and SNS.

Adaptation, Physiological↗
PubMed1997

Influence of duration of rapid ventricular pacing on ventricular refractoriness in the presence of propafenone and lidocaine.

Propafenone and lidocaine have a rate dependent negative dromotropic effect on intraventricular conduction. We investigated the use dependent actions of propafenone and lidocaine on intraventricular conduction in isolated guinea pig hearts perfused by the method of Langendorff. Of primary interest was how the number of stimuli of the conditioning train (S1) might influence the ventricular effective refractory period (VERP) when refractoriness is assessed at a high pacing rate. Propafenone (0.3 microM) and lidocaine (50 microM) caused a comparable prolongation of the intraventricular conduction time during sinus rhythm. During ventricular pacing in the presence of propafenone an abrupt decrease of the pacing cycle length (220 to 120 ms) resulted in an initial peak of rate dependent prolongation of the QRS interval that subsequently decreased to a stable steady-state level. Lidocaine also induced a rate dependent increase of the intraventricular conduction time up to a steady-state level. The time constant, characterizing the changes of the intraventricular conduction time after shortening the ventricular pacing cycle length from 220 to 120 ms was significantly (P < 0.01) longer in the presence of propafenone (tau = 31 +/- 4 beats; mean +/- SEM; n = 11) than for lidocaine (tau = 3 +/- 1; n = 10). Both drugs caused the greatest increase of the VERP when the number of conditioning stimuli (S1, interstimulus interval = 120 ms) was in the range of their respective time constant. However, when the number of conditioning stimuli was further increased, VERP progressively diminished. These effects may be explained by a shortening of the action potential during high rates that results in a decreased binding of propafenone to Na+ channels and by the direct shortening of repolarization period by lidocaine (Class IB drug).

Action Potentials↗
PubMed2005

Heart rate turbulence: a new predictor for risk of sudden cardiac death.

Initial acceleration and a subsequent deceleration of sinus rhythm following a ventricular ectopic beat with a compensatory pause has been termed heart rate turbulence (HRT). The changes in sinus rhythm are thought to be mediated by a baroreflex response to the lower stroke volume of the ectopic beat. HRT is vagally mediated and abolished by atropine, whereas beta-blockers have no effect. HRT has been shown to be an independent and powerful predictor of mortality after myocardial infarction. In patients on beta-blockers, it scores better than left ventricular ejection fraction (LVEF) in its predictive value. Two common measures of HRT are turbulence onset and turbulence slope. When both these measures are abnormal, it is as powerful a predictor of mortality as LVEF. HRT correlates with other indices of cardiac autonomic functions like baroreflex sensitivity and heart rate variability. A composite autonomic index including all these three has been shown to be a powerful predictor of mortality. In patients undergoing direct percutaneous intervention for myocardial infarction, HRT improves in those attaining successful reperfusion. Abnormal values for HRT have been noted in patients with dilated cardiomyopathy and Chagas disease. Diabetic and elderly individuals are more likely to have blunted HRT. HRT cannot be measured in patients lacking ventricular ectopic beats and in patients presenting with atrial fibrillation.

Arrhythmias, Cardiac↗
PubMed1996

Power spectrum analysis contribution to the detection of cardiovascular dysautonomia in multiple sclerosis.

In multiple sclerosis (MS) autonomic cardiovascular dysfunction is an uncommon, but potentially dangerous event, to which studies of spectral analysis of heart rate variability have not been applied, yet. MATERIAL AND METHODS--We studied 16 patients with definite MS (11 women and 5 men, mean age 30.3 +/- 7.4 yrs., mean EDSS 2.06 +/- 1.42) and 16 sex- and age-matched healthy controls. Besides cardiovascular reflex tests (valsalva manoeuvre, deep breathing, lying to standing, Blood Pressure response to standing and sustained handgrip), each underwent spectral analysis of the R-R interval short-term variability at rest and after tilting, to detect three components: very low frequency (VLF), low frequency (LF) and high frequency (HF). A recent brain MRI was obtained from patients, to compare plaque characteristics with spectral parameters. RESULTS--At cardiovascular reflexes, only four patients (25%) showed an impairment, mostly of a mild degree. VLF and LF at rest were lower in MS subjects than in controls (p < 0.01). No significant correlation was found between spectral parameters and lesion area or localization as detected on MRI. CONCLUSIONS--Spectral analysis could usefully flank reflex tests to detect autonomic subclinical cardiovascular abnormalities.

Adult↗
PubMed1986

Maternal heart rate and stroke volume in the pygmy goat: effects of exercise and cardiac autonomic blockade.

To determine the normal maternal heart rate and stroke volume response to exercise and the role of the autonomic nervous system in this response, pregnant and non-pregnant pygmy goats were studied at rest, during and following treadmill exercise, and after autonomic blockade. Resting heart rates, stroke volumes and cardiac outputs were 10%, 60%, and 76% higher in pregnant compared to non-pregnant animals (P less than 0.05, 0.001, and 0.001 respectively). During exercise, heart rate and stroke volume rose in both pregnant and non-pregnant animals by similar amounts. Immediately post-exercise, stroke volume in pregnant animals dropped precipitously below resting levels by 15% (P less than 0.005) but cardiac output was preserved by heart rate. This fall in stroke volume was not seen in control animals. Autonomic blockade lowered resting and exercise heart rates in both groups without changing stroke volume. The elevations in heart rate and stroke volume in pregnancy are not primarily mediated via the autonomic nervous system. Although the maternal cardiac output response to exercise appears normal, the post-exercise fall in stroke volume, presumed secondary to a reduction in preload, could potentially be harmful to both mother and fetus.

Animals↗
PubMed1968

Circulatory effects of chloralose-urethane and sodium pentobarbitone anaesthesis in the rabbit.

1. The effects of chloralose-urethane and sodium pentobarbitone anaesthesia on heart rate, blood pressure and cardiac output were studied in normal rabbits, in animals given atropine and in animals without functioning autonomic effectors. The findings under anaesthesia were compared during spontaneous and artificial intermittent positive pressure respiration.2. The circulatory effects of chloralose-urethane and sodium pentobarbitone anaesthesia differed significantly for the first hour after induction of anaesthesia. During the subsequent 3 hr of maintained anaesthesia differences in the circulatory effects of the two anaesthetics were small.3. The direct local effects of these anaesthetics were assessed during the maintenance phase from the responses of animals without functioning autonomic effectors. With both anaesthetics there was peripheral vasodilatation and minimal effects on heart rate.4. The autonomic activity in the normal animal was assessed by comparing the changes in normal, atropinized and ;de-efferented' rabbits without functioning autonomic effectors. During chloralose-urethane anaesthesia there was reduction in cardiac vagal efferent activity and no change in cardiac sympatho-adrenal activity. With both anaesthetics there was an increase in peripheral sympatho-adrenal constrictor activity, tending to minimize the local vasodilator effects.

Anesthesia, Intravenous↗
PubMed1990

Influence of cardiac innervation on intrinsic heart rate in dogs.

Intrinsic heart rate is defined as the rate at which the heart beats when all cardiac neural and hormonal inputs are removed. We determined the effect of prevailing autonomic innervation of the heart on the intrinsic heart rate in chronically maintained, sedated, normally innervated dogs (n = 14), and in 14 other dogs that had previously (greater than 12 day) undergone complete surgical cardiac denervation. Intrinsic rate was determined in both groups using the following two procedures: 1) pharmacological effector blockade; and 2) pharmacological ganglionic blockade. The intrinsic rate determined by effector blockade was 142.9 +/- 7.2 (SE) beats/min in the dogs with intact cardiac innervation. When the same treatment was given after total surgical cardiac denervation, intrinsic rate was 97.9 +/- 4.8 beats/min. Intrinsic heart rate was significantly (P less than 0.05) lower in surgically denervated dogs. Ganglionic blockade in surgically denervated animals yielded an intrinsic rate of 90.0 +/- 8.5 beats/min, which was again significantly lower than the corresponding value of 128.4 +/- 5.5 beats/min in normal dogs. There was no difference in the intrinsic heart rate as determined by effector vs. ganglionic blockade in either group of dogs. An additional six dogs were subjected to selective surgical sinoatrial nodal parasympathectomy; their intrinsic rate (effector blockade) in the conscious state was 115.8 +/- 4.3 beats/min; this was significantly lower than the corresponding value for normal dogs and significantly greater than in dogs subject to total surgical cardiac denervation. The lower rate observed in the totally denervated and selectively denervated dogs after effector and/or ganglionic blockades implies that intrinsic heart rate depends on the level or nature of prevailing autonomic activity.

Animals↗
PubMed1990

Autonomic neural regulation of intact Purkinje system of dogs.

To characterize autonomic influences on the Purkinje system in vivo, we measured Purkinje relative refractory period (PRRP) in response to sympathetic (SNS) and vagal nerve stimulation (VNS). Effects of SNS on PRRP were primarily mediated via beta-adrenergic mechanisms because shortening of PRRP during SNS [from 215 +/- 7 (SE) to 202 +/- 8 ms, P less than 0.01] was entirely blocked by metoprolol (1 mg/kg). Vagal influences in the ambient state did not prolong PRRP, even when effective refractory period of adjacent muscle did prolong. When VNS was augmented with physostigmine, PRRP prolonged from 205 +/- 12 to 212 +/- 13 ms, P less than 0.05. Similar provocation of parasympathetic effects on PRRP occurred when VNS was performed during SNS; PRRP prolonged from 188 +/- 9 to 193 +/- 9 ms, P less than 0.05. Also, when alpha-adrenergic stimulation was produced by phenylephrine infusion (25 micrograms.kg-1.min-1) in the presence of metoprolol (1 mg/kg), which prolonged PRRP from 242 +/- 8 to 246 +/- 9 ms, P less than 0.05, the addition of VNS further prolonged PRRP from 246 +/- 9 to 253 +/- 9 ms, P less than 0.05. Thus some refractory period responses in the Purkinje system were similar to adjacent muscle, because beta-adrenergic activation shortened refractory period and vagal stimulation antagonized the shortening. Findings unique to Purkinje tissue were refractory period prolongation by vagal stimulation when facilitated by concurrent prolongation of refractory period during alpha-adrenergic stimulation.

Animals↗
PubMed1996

Effects of constant cardiac autonomic nerve stimulation on heart rate variability.

Heart rate variability is used to assess cardiac autonomic tone. We bought to determine the relationship of graded direct stimulation of efferent cardiac autonomic nerves on heart rate variability in an anesthetized canine model. Time and frequency domain variables were measured at denervated baseline and during electrical stimulation of the vagi and ansae subclaviae over a wide range of frequencies. Vagal and ansae stimuli produced significant changes in heart rate that correlated with the intensity of stimulation. Vagal stimulation resulted in small increases in time domain indexes of heart rate variability and in the power spectrum from 0.04 to 0.40 Hz, but with no correlation between stimulus intensity and changes in these indexes. By contrast, ansae stimulation had no effect on time or frequency domain measures. In the absence of central modulation of autonomic outflow, indexes of heart rate variability reflect the presence of vagal input but do not correlate with the level of vagal tone and are unaffected by changes in mean sympathetic tone.

Animals↗
PubMed1997

Sleep and circadian influences on cardiac autonomic nervous system activity.

To assess the separate contributions of the sleep and circadian systems to changes in cardiac autonomic nervous system (ANS) activity, 12 supine subjects participated in two 26-h constant routines, which were counterbalanced and separated by 1 wk. One routine did not permit sleep, whereas the second allowed the subjects to sleep during their normal sleep phase. Parasympathetic nervous system activity was assessed with respiratory sinus arrhythmia as measured from the spectral analysis of cardiac beat-to-beat intervals. Sympathetic nervous system activity was primarily assessed with the preejection period as estimated from impedance cardiography, although the 0.1-Hz peak from the spectral analysis of cardiac beat-to-beat intervals, the amplitude of the T wave in the electrocardiogram, and heart rate were also measured. Respiratory sinus arrhythymia showed a 24-h rhythm independent of sleep, whereas preejection period only showed a 24-h rhythm if sleep occurred. Thus the findings indicate that parasympathetic nervous system activity is mostly influenced by the circadian system, whereas sympathetic nervous system activity is mostly influenced by the sleep system.

Adult↗
PubMed2002

Cardiovascular alterations and autonomic imbalance in an experimental model of depression.

Depressed patients with and without a history of cardiovascular pathology display signs, such as elevated heart rate, decreased heart rate variability, and increased physiological reactivity to environmental stressors, which may indicate a predisposition to cardiovascular disease. The specific physiological mechanisms associating depression with such altered cardiovascular parameters are presently unclear. The current study investigated cardiovascular regulation in the chronic mild stress rodent model of depression and examined the specific autonomic nervous system mechanisms underlying the responses. Sprague-Dawley rats exposed to a series of mild, unpredictable stressors over 4 wk displayed anhedonia (an essential feature of human depression), along with elevated resting heart rate, decreased heart rate variability, and exaggerated pressor and heart rate responses to air jet stress. Results obtained from experiments studying autonomic blockade suggest that cardiovascular alterations in the chronic mild stress model are mediated by elevated sympathetic tone to the heart. The present findings have implications for the study of pathophysiological links between affective disorders and cardiovascular disease.

Animals↗
PubMed2001

Time delay of vagally mediated cardiac baroreflex response varies with autonomic cardiovascular control.

To examine whether changes in autonomic activity have an effect on the latency of the vagally mediated cardiac baroreflex response in humans, we investigated the effects of neck suction fluctuating sinusoidally at 0.2 Hz on R-R intervals (known to be mediated mainly by vagal activity) in the supine position, during 15 degrees head-down tilt and 60 degrees head-up tilt, and during vagotonic (2 microg/kg) and vagolytic (10 microg/kg) doses of atropine while the subjects breathed at 0.25 Hz. The phase shift between fluctuations in neck chamber pressure and in R-R interval was calculated by complex transfer function analysis and was used as a measure of the time delay between carotid baroreceptor stimulation and cardiac effector response. Cardiac baroreflex responsiveness increased significantly during low-dose atropine and decreased during head-up tilt or 10 microg/kg atropine. With increasing tilt angle, the time delay between cyclic baroreceptor stimulation and oscillations in R-R interval increased from 0.32 +/- 0.27 s (head down), to 0.59 +/- 0.25 s (supine position, P < 0.05 vs. head down), and to 0.86 +/- 0.27 s (head up, P < 0.01 vs. supine). Low-dose atropine had a similar effect to head-down tilt on baroreflex latency, whereas 10 microg/kg atropine increased the time delay markedly to 1.24 +/- 0.30 s. Our results demonstrate that changes in autonomic activity, generated either by gravitational stimulus or by atropine, not only affect baroreflex responsiveness but also have a major influence on the latency of the vagally mediated carotid baroreceptor-heart rate reflex. The prolonged baroreflex latency during decreased parasympathetic function may contribute to an unstable regulation of heart rate in patients with cardiac disease.

Adult↗
PubMed1998

Determinants of ventricular arrhythmias in hemodialysis patients. Evaluation of the effect of arrhythmogenic substrate and autonomic imbalance.

BACKGROUND/AIMS: In chronic hemodialysis patients, we evaluated determinants of repetitive ventricular tachyarrhythmias which included late potentials and heart rate variability. METHODS: We compared the presence of late potentials and heart rate variability obtained by ambulatory electrocardiogram (ECG), findings of echocardiography, and laboratory data between patients with and those without ventricular arrhythmias of Lown class 4A or 4B. Ambulatory ECG was recorded for 24 h from the beginning of hemodialysis. Heart rate variability was evaluated by the standard deviation of the normal RR interval (SDNN). RESULTS: Thirty patients (17%) had ventricular arrhythmias of Lown class 4A or 4B. They were older than patients without such arrhythmias (p=0.0021). Left-ventricular wall motion score (2.0+/-3.9 and 0.3+/-1.2, respectively, p < 0.0001) and left-ventricular mass index (167 +/-59 and 140+/-44 g/m2, respectively, p=0.0053) were larger in patients with ventricular arrhythmias of Lown class 4A or 4B than in those without. Stepwise logistic regression analysis was performed to select variables related to ventricular arrhythmias of Lown class 4A or 4B from the following 8 candidate variables; age, sex, presence of ischemic heart disease, diabetic nephropathy as the primary renal disease, presence of late potentials, SDNN, left-ventricular wall motion score and left-ventricular mass index. Higher left-ventricular wall motion score (p < 0.0001), older age (p=0.0022) and male sex (p=0.0235) were the variables associated with ventricular arrhythmias of Lown class 4A or 4B. CONCLUSION: In patients receiving hemodialysis, predominantly with chronic glomerulonephritis, ventricular arrhythmias of Lown class 4A or 4B were not associated with arrhythmogenic substrate revealed by late potentials or autonomic dysfunction assessed by heart rate variability. Left-ventricular wall motion abnormalities, age and sex were significant factors.

Autonomic Nervous System Diseases↗
PubMed1996

Incomplete reentry and epicardial breakthrough patterns during atrial fibrillation in the sheep heart.

BACKGROUND: The mechanisms underlying atrial fibrillation and its initiation are not fully understood. Our hypothesis is that atrial fibrillation results from complex activation involving the subendocardial muscle network. METHODS AND RESULTS: We have used video imaging to study the sequence of activation on the surface of the right atrium of the Langendorff-perfused sheep heart during pacing, atrial fibrillation, and its initiation. We recorded transmembrane potentials simultaneously from over 20,000 sites. We observed two types of patterns of wave propagation during the initiation of atrial fibrillation. The first type resulted from heterogeneties of refractoriness and transmural propagation near the stimulating electrode. The second type involved heterogeneity in conduction away from the pacing site. During atrial fibrillation, the average period of activation was 138 +/- 25 ms (n = 6), and complete reentrant pathways were never observed. Propagation patterns were characterized by a combination of incomplete reentry, breakthrough patterns, and wave collisions. Incomplete reentry occurred when waves propagated around thin lines of block and then terminated. Breakthrough patterns were frequent and occurred every 215 ms on average. The location of these breakthrough sites and the lines of block during incomplete reentry were not randomly distributed but appeared to be related to preferential propagation in the underlying subendocardial muscle structures. A computer model of atrial free wall connected to a pectinate muscle suggested that subendocardial muscles lead to epicardial breakthrough patterns that act to destabilize reentry. CONCLUSIONS: These results suggest that the complex three-dimensional structure of the atria plays a major role in the activation sequences during atrial fibrillation and its initiation.

Action Potentials↗
PubMed1988

Selective functional characteristics of rate-induced fatigue in rabbit atrioventricular node.

The slowly developing rate-induced prolongation in atrioventricular nodal conduction time, termed "fatigue," was selectively studied using specifically designed stimulation protocols in isolated rabbit heart preparations. A nodal recovery curve (A2H2 versus H1A2 intervals; nodal conduction time of each premature beat plotted against corresponding recovery time) was obtained before and after a stable and nearly maximum fatigue had been reached by driving the atrium for 5 minutes at a fast rate close to the upper limit of 1:1 nodal conduction. The fatigue uniformly prolonged all A2H2 intervals (12.3 +/- 1.3 msec) and systematically increased the minimum H1A2 interval at which complete nodal block occurred (24.8 +/- 4.0 msec) (p less than 0.01, n = 6). To study the rate and time dependence of fatigue, nodal conduction times were obtained during three rapid 5-minute pacings corresponding to 50%, 75%, and 100% shortening of the pacing interval in the 1:1 nodal conduction range. The respective maximum fatigue-induced increases in conduction time were 5.4 +/- 1.8, 9.0 +/- 2.7, and 12.5 +/- 2.1 msec (p less than 0.01, n = 6). However, the pacing interval had no significant effect on the time required to reach either 50% (17.1 +/- 3.5 seconds) or 90% (92.6 +/- 15.4 seconds) of the fatigue observed after 5 minutes of fast rate. At the termination of any rapid stimulation, the fatigue effect dissipated with a time course that was inverse but symmetrical to that of its induction. These findings support the existence of an independent, slow, nodal memory process by which the conduction time changes according to past events with a long time constant.

Animals↗
PubMed1976

Total cardiac denervation in diabetic autonomic neuropathy.

Total loss of the autonomic regulation of heart rate is described in a 28-year-old diabetic with extensive autonomic neuropathy. The patient had an almost fixed heart rate that barely responded to any of the tests that stimulate or inhibit the autonomic nerves. Its behavior was similar to that of the transplanted heart.

Adult↗