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Biomedical subjects

R D Berger

Publications and source records attributed to R D Berger.

At least 37 records · Page 2Linked to original sources
PubMed1999

Ventricular pacing with premature excitation for treatment of hypertensive-cardiac hypertrophy with cavity-obliteration.

BACKGROUND: Hypertensive left ventricular hypertrophy with supranormal systolic ejection and distal cavity obliteration (HHCO) can result in debilitating exertional fatigue and dyspnea. Dual-chamber pacing with ventricular preactivation generates discoordinate contraction, which can limit cavity obliteration and thereby increase potential ejection reserve. Accordingly, we hypothesized that pacing may improve exercise tolerance long-term in this syndrome. METHODS AND RESULTS: Dual-chamber pacemakers were implanted in 9 patients with exertional dyspnea caused by HHCO. Intrinsic atrial rate was sensed, and ventricular preactivation was achieved by shortening the atrial-ventricular delay. Pacing was on or off for successive 3-month periods (randomized, double-blind, crossover design), followed by 6 additional pacing-on months. Metabolic exercise testing, quality-of-life assessment, and rest and dobutamine-stress echocardiographic/Doppler data were obtained. After 3 months of pacing-on, exercise duration rose from 324+/-133 to 588+/-238 s (mean+/-SD; P=0.001, with 7 of 9 patients improving >/=30%), and maximal oxygen consumption increased from 13.6+/-2.9 to 16.7+/-3.3 mL of O(2). min(-1). kg(-1) (P<0.02). Both parameters were little changed from baseline during the pacing-off period. Improved exercise capacity persisted at 1-year follow-up. Clinical symptoms and activities of daily living improved during the pacing-on period and stayed improved at 1 year, but they were little changed during the pacing-off period. Despite similar basal values, stroke volume (P<0.001) and cardiac output (P<0.02) increased with dobutamine stimulation 2 to 3 times more after 1 year of follow-up as compared with baseline. CONCLUSIONS: Long-term dual-chamber pacing can improve exercise capacity, cardiac reserve, clinical symptoms, and activities of daily living in patients with HHCO. This therapy may provide a novel alternative for patients in whom traditional pharmacological treatment proves inadequate.

Cardiac Output↗
PubMed1998

Interaction between neuronal nitric oxide synthase and inhibitory G protein activity in heart rate regulation in conscious mice.

Nitric oxide (NO) synthesized within mammalian sinoatrial cells has been shown to participate in cholinergic control of heart rate (HR). However, it is not known whether NO synthesized within neurons plays a role in HR regulation. HR dynamics were measured in 24 wild-type (WT) mice and 24 mice in which the gene for neuronal NO synthase (nNOS) was absent (nNOS-/- mice). Mean HR and HR variability were compared in subsets of these animals at baseline, after parasympathetic blockade with atropine (0.5 mg/kg i.p.), after beta-adrenergic blockade with propranolol (1 mg/kg i.p.), and after combined autonomic blockade. Other animals underwent pressor challenge with phenylephrine (3 mg/kg i.p.) after beta-adrenergic blockade to test for a baroreflex-mediated cardioinhibitory response. The latter experiments were then repeated after inactivation of inhibitory G proteins with pertussis toxin (PTX) (30 microgram/kg i.p.). At baseline, nNOS-/- mice had higher mean HR (711+/-8 vs. 650+/-8 bpm, P = 0.0004) and lower HR variance (424+/-70 vs. 1,112+/-174 bpm2, P = 0.001) compared with WT mice. In nNOS-/- mice, atropine administration led to a much smaller change in mean HR (-2+/-9 vs. 49+/-5 bpm, P = 0.0008) and in HR variance (64+/-24 vs. -903+/-295 bpm2, P = 0.02) than in WT mice. In contrast, propranolol administration and combined autonomic blockade led to similar changes in mean HR between the two groups. After beta-adrenergic blockade, phenylephrine injection elicited a fall in mean HR and rise in HR variance in WT mice that was partially attenuated after treatment with PTX. The response to pressor challenge in nNOS-/- mice before PTX administration was similar to that in WT mice. However, PTX-treated nNOS-/- mice had a dramatically attenuated response to phenylephrine. These findings suggest that the absence of nNOS activity leads to reduced baseline parasympathetic tone, but does not prevent baroreflex-mediated cardioinhibition unless inhibitory G proteins are also inactivated. Thus, neuronally derived NO and cardiac inhibitory G protein activity serve as parallel pathways to mediate autonomic slowing of heart rate in the mouse.

Animals↗
PubMed1998

Predictors of fluoroscopy time and estimated radiation exposure during radiofrequency catheter ablation procedures.

The objective of this study was to identify factors that predict fluoroscopy duration and radiation exposure during catheter ablation procedures. The patient population included 859 patients who participated in the Atakr Ablation System clinical trial at 1 of 9 centers (398 male and 461 female patients, aged 36 +/- 21 years). Each patient underwent catheter ablation of an accessory pathway, the atrioventricular junction, or atrioventricular nodal reentrant tachycardia using standard techniques. The duration of fluoroscopy was 53 +/- 50 minutes. Factors identified as independent predictors of fluoroscopy duration included patient age and sex, the success or failure of the ablation procedure, and the institution at which the ablation was performed. Catheter ablation in adults required longer fluoroscopy exposure than it did in children. Men required longer durations of fluoroscopy exposure than did women. The mean estimated "entrance" radiation dose was 1.3 +/- 1.3 Sv. The dose needed to cause radiation skin injury was exceeded during 22% of procedures. The overall mean effective absorbed dose from catheter ablation procedures was 0.025 Sv for female patients and 0.017 Sv for male patients. This degree of radiation exposure would result in an estimated 1,400 excess fatal malignancies in female patients and 2,600 excess fatal malignancies in male patients per 1 million patients.

Adolescent↗
PubMed1998

Comparison of adenosine effects on atrioventricular node reentry and atrioventricular reciprocating tachycardias.

BACKGROUND: Adenosine is an established first line therapy for the treatment of narrow complex tachycardias. The two most common etiologies of paroxysmal supraventricular tachycardia (SVT) are atrioventricular node reentry tachycardia (AVNRT) and atrioventricular reciprocating tachycardia (AVRT). HYPOTHESIS: We postulated that adenosine might have different effects on the termination of AVNRT vs. AVRT, and that these differences might assist in the noninvasive differentiation between these diagnoses. METHODS: Fifty-nine patients referred for the diagnosis and treatment of SVT were included in the study. All patients had SVT induced during electrophysiology testing, and each patient received adenosine during SVT. The adenosine dose, time to tachycardia termination, and site of tachycardia termination were recorded. Seventeen patients required isoproterenol administration to initiate SVT. This subset of patients was compared with those not requiring isoproterenol. RESULTS: There was no statistically significant difference in the adenosine dose or time to tachycardia termination when comparing patients with AVNRT with those with AVRT. All patients with AVNRT had termination of tachycardia in the antegrade direction with final activation in the atria. Patients requiring isoproterenol for tachycardia initiation experienced tachycardia termination significantly faster than those not requiring isoproterenol, although there was no difference in the dose of adenosine required for termination. CONCLUSION: These data demonstrate that patients with dual AV node physiology and AVNRT do not have altered sensitivity to adenosine compared with patients with AVRT and normal AV nodes. Further investigation will be required to determine the clinical utility of the significantly shorter time to tachycardia termination for patients receiving isoproterenol.

Adenosine↗
PubMed1998

Beat-to-beat repolarization lability identifies patients at risk for sudden cardiac death.

INTRODUCTION: Recent studies have implicated repolarization lability in the genesis of malignant ventricular arrhythmias. However, few data exist on assessment of temporal QT interval variability and its relation to arrhythmogenesis. We tested the ability of the QT variability index (QTVI), a measure of beat-to-beat QT interval fluctuations measured on a single ECG lead, to identify patients presenting with malignant ventricular arrhythmias and predict their subsequent occurrences. METHODS AND RESULTS: We measured the QTVI in 95 patients presenting for electrophysiologic study (EPS). The ability of the QTVI to identify patients with sudden cardiac death (SCD) or sustained monomorphic ventricular tachycardia (MVT) on presentation and during follow-up of 23.7+/-14.3 months was compared with spatial QT dispersion, T wave alternans ratio during atrial pacing, MVT inducibility at EPS, signal-averaged ECG, heart rate variability, and ejection fraction. The QTVI was higher in patients with heart disease than in controls (-0.7+/-0.7 vs -1.1+/-0.5, P < 0.05), and higher in patients presenting with SCD than in other patients with heart disease (0.0+/-0.6 vs -0.8+/-0.5, P < 0.05). The QTVI was the only clinical variable that identified patients who presented with SCD (P = 0.004, odds ratio = 12.5) on stepwise, logistic multiple regression. Fourteen patients had arrhythmic events during follow-up. In a Kaplan-Meier analysis of arrhythmic events, QTVI> or =0.1 was a discriminator for higher risk of arrhythmic events (P < 0.05). CONCLUSIONS: (1) This noninvasive measure of temporal repolarization lability identified patients with SCD and predicted arrhythmia-free survival. (2) Further studies are needed to determine the mechanisms that mediate beat-to-beat QT interval variability.

Death, Sudden, Cardiac↗
PubMed1997

Beat-to-beat QT interval variability: novel evidence for repolarization lability in ischemic and nonischemic dilated cardiomyopathy.

BACKGROUND: Dilated cardiomyopathy (DCM) is associated with a high incidence of malignant ventricular arrhythmias and sudden death. Abnormalities in repolarization of ventricular myocardium have been implicated in the development of these arrhythmias. Spatial heterogeneity in repolarization has been studied in DCM, but temporal fluctuations in repolarization in this setting have been largely ignored. We sought to test the hypothesis that beat-to-beat QT interval variability is increased in DCM patients compared with control subjects. METHODS AND RESULTS: Eighty-three patients with ischemic and nonischemic DCM and 60 control subjects served as the study population. Beat-to-beat QT interval variability was measured by automated analysis on the basis of 256-second records of the surface ECG. A QT variability index (QTVI) was calculated for each subject as the logarithm of the ratio of normalized QT variance to heart rate variance. The coherence between heart rate and QT interval fluctuations was determined by spectral analysis. In patients, ejection fractions were assessed by echocardiography or ventriculography, and spatial QT dispersion was determined from the standard 12-lead ECG. DCM patients had greater QT variance than control subjects (60.4+/-63.1 versus 25.7+/-24.8 ms2, P<.0001) despite reduced heart rate variance (6.7+/-7.8 versus 10.5+/-10.4 bpm2, P=.01). The QTVI was higher in DCM patients than in control subjects, with a high degree of significance (-0.43+/-0.71 versus -1.29+/-0.51, P<10[-12]). QTVI did not correlate with ejection fraction or spatial QT dispersion but did depend on New York Heart Association functional class. QTVI did not differ between DCM patients with ischemic and those with nonischemic origin. Coherence between heart rate and QT interval fluctuations at physiological frequencies was lower in DCM patients compared with control subjects (0.28+/-0.14 versus 0.39+/-0.18, P<.0001). CONCLUSIONS: DCM is associated with beat-to-beat fluctuations in QT interval that are larger than normal and uncoupled from variations in heart rate. QT interval variability increases with worsening functional class but is independent of ejection fraction. These data indicate that DCM leads to temporal lability in ventricular repolarization.

Adult↗
PubMed1997

Comparison of heart rate variability in patients with chronic fatigue syndrome and controls.

Recent studies have reported a close association between chronic fatigue syndrome and neurally mediated hypotension. We hypothesized that this association may result from an abnormality in autonomic function among patients with chronic fatigue syndrome, which may be detectable using an analysis of heart rate variability. We prospectively studied 19 patients who fulfilled the Centers for Disease Control criteria for chronic fatigue syndrome and 11 controls. Each subject underwent a two-stage tilt-table test while wearing a Holter monitor. Heart rate variability was assessed in the supine baseline position and during upright tilt using frequency domain parameters. In the baseline supine position, high frequency (HF) power, low frequency (LF) power, and the ratio of low frequency power to high frequency power (LF/HF ratio) were similar. In both patient groups, upright tilt resulted in a similar decrease in HF power, increase in LF power, and increase in the LH/HF ratio. In conclusion, autonomic function, as assessed using an analysis of heart rate variability, does not differ in the baseline supine state, nor in response to upright tilt among patients with chronic fatigue syndrome and healthy controls.

Adult↗
PubMed1997

Signal-averaged intracardiac electrograms: a new method to detect kent potentials.

INTRODUCTION: In patients with manifest accessory pathways, Kent potentials are often difficult to identify even at sites of successful catheter ablation, due largely to signal noise and catheter instability. We hypothesized that signal averaging the intracardiac electrogram recorded from the ablation catheter over a number of beats would improve the signal-to-noise ratio of the electrogram and aid in the detection of Kent potentials at accessory pathway locations. METHODS AND RESULTS: We retrospectively analyzed distal-pair electrograms recorded from 9 successful, 6 transiently successful, and 10 failed ablation sites in 10 patients with manifest accessory pathways who underwent catheter ablation. We developed custom software to finely align 20 to 30 consecutive sinus beats and compute the signal average of the electrogram (SAE) for each site. Kent potentials were classified as probable, possible, or absent in the raw ablation site electrogram and the SAE base on morphologic criteria. A measure of beat-to-beat signal instability, the variability quotient (VQ), was also computed for each site. Probable Kent potentials were found in the raw ablation site electrogram at only 2 of the 15 successful and transiently successful sites, but were found in the SAE at 10 of these sites (P = 0.008). Eight of the 9 successful sites had VQ < 0.2, suggesting stable catheter-tissue contact, while 3 of the 6 transiently successful sites had VQ > 0.2, indicating unstable contact. CONCLUSIONS: Signal averaging the intracardiac ablation site electrogram enhances detection of Kent potentials at accessory pathway locations. Catheter instability can be quantified by signal variability analysis and, when high, may predict lack of successful ablation even at sites where Kent potentials are present.

Adolescent↗
PubMed1996

Temperature monitoring during radiofrequency ablation.

Thermal injury is the primary mechanism of lesion formation during radiofrequency catheter ablation procedures. Irreversible tissue injury requires heating to approximately 50 degrees C. Temperatures above 100 degrees C result in coagulum formation. Because of this importance of temperature during radiofrequency catheter ablation procedures, temperature monitoring has been proposed as a tool to facilitate catheter ablation procedures. The results of recent clinical studies demonstrate that electrode temperatures do not differ at successful and failed ablation sites, electrode temperature does not predict or eliminate the possibility of arrhythmia recurrence, and closed-loop temperature control decreases but does not eliminate the development of coagulum nor guarantees that target temperatures will be achieved. These observations are due in large part to the important distinctions between electrode temperature, the temperature at the electrode-tissue interface, and the temperature at the ablation target. Nonetheless, temperature monitoring and temperature control are valuable tools during radiofrequency ablation procedures as they provide important information regarding the adequacy of tissue heating, minimize the development of coagulum, and maximize lesion size.

Animals↗
PubMed1996

Catheter ablation of coexistent bundle branch and interfascicular reentrant ventricular tachycardias.

INTRODUCTION: Bundle branch reentry and interfascicular reentry are potential mechanisms of ventricular tachycardia in the setting of a dilated cardiomyopathy. We report a patient with myotonic dystrophy who presented with near syncope, in whom both of these mechanisms were present, leading to two different wide complex tachycardias. METHODS AND RESULTS: Electrophysiologic study demonstrated infra-Hisian conduction system disease and inducible bundle branch reentrant ventricular tachycardia. Catheter ablation of the right bundle eliminated bundle branch reentry. However, following this, the patient had inducible interfascicular reentry, which subsequently occurred spontaneously while still hospitalized. Catheter ablation of the left posterior fascicle successfully eliminated this second tachycardia, and the patient has had no further arrhythmias. CONCLUSIONS: This report is of an unusual patient with coexistent bundle branch reentry and interfascicular reentry producing two different forms of sustained ventricular tachycardia. This is the first report of catheter ablation of the left posterior fascicle for elimination of conduction system reentry.

Adult↗
PubMed1996

Recurrence of conduction following radiofrequency catheter ablation procedures: relationship to ablation target and electrode temperature. The Atakr Multicenter Investigators Group.

INTRODUCTION: More than 1 in 10 patients may develop recurrence of conduction after undergoing a successful radiofrequency catheter ablation procedure. The physiologic basis for recurrence following successful ablation procedures remains uncertain. The purpose of this study was to evaluate the role of electrode temperature as a predictor of recurrence following radiofrequency catheter ablation procedures. METHODS AND RESULTS: The subjects of this study were 538 patients who underwent a successful attempt at radiofrequency catheter ablation of AV nodal reentrant tachycardia, an accessory pathway, and/or the AV junction. Patients were followed for a mean of 215 +/- 138 days. Conduction recurred in 35 (6.5%) of the 538 patients. Recurrence of conduction occurred in 25 (9.3%) of 270 patients undergoing ablation of an accessory pathway, 7 (3.5%) of 201 patients undergoing ablation of AV nodal reentrant tachycardia, and in 3 (4.5%) of 67 patients undergoing ablation of the AV junction. The electrode temperature achieved at successful sites associated with recurrence was not different from the temperature achieved at successful sites without recurrence (61.1 +/- 8.9 vs 61.6 +/- 9.1; P = 0.8). The likelihood of developing a recurrence was higher following ablation of accessory pathways than following ablation of AV nodal reentrant tachycardia or the AV junction (P = 0.03). Patients experiencing a recurrence following ablation of an accessory pathway had longer procedure durations (P = 0.0001). Ablation of left free-wall pathways was associated with a lower incidence of recurrence as compared with all other locations (P = 0.008). CONCLUSION: The results of this study suggest that electrode temperature at the successful ablation site cannot be used to identify patients at highest risk of recurrence.

Adolescent↗
PubMed1995

Role of atrial contraction in diastolic pressure elevation induced by rapid pacing of hypertrophied canine ventricle.

The mechanism of diastolic pressure elevation induced by acute rapid pacing in pressure-load hypertrophied left ventricles (LVs) remains incompletely understood. It has been ascribed to abnormalities of coronary flow, metabolism, and calcium cycling. However, rapid pacing also alters the timing of atrial and ventricular stimulation relative to the diastolic filling period, and this could also influence diastolic pressures. To test the role of such mechanical factors, LV pressure-volume hemodynamics were measured in closed-chested anesthetized dogs during and after abrupt cessation of rapid atrial pacing. Twenty-one dogs were studied: 6 dogs with LV hypertrophy (LVH) induced by perinephritic hypertension, 5 sham-operated normotensive dogs, and 10 acute normotensive control dogs. In LVH dogs, but not in sham-operated or control dogs, end-diastolic pressure rose progressively with increasing heart rate from 5.6 +/- 3.1 mm Hg at baseline to 22.6 +/- 8.1 mm Hg at 220 beats per minute. In all hearts, rapid pacing shifted the timing of left atrial contraction so that it occurred near the onset of LV filling rather than at end diastole. However, in LVH hearts, early LV diastolic pressure and peak atrial pressure were also markedly elevated. Most striking, immediately after terminating the pacing, diastolic pressure declined to near baseline. This rapid pressure decline occurred just when atrial systole would have ensued and before ventricular activation would have followed had pacing continued. Thus, diastolic pressure elevation resolved before a change in ventricular pacing rate. The role of atrial contraction was further explored by simultaneous atrioventricular pacing. This shifted the time of atrial systole so that it occurred during LV isovolumic contraction, while maintaining the identical LV pacing rate. This change eliminated the diastolic pressure elevation found previously. Further analysis revealed that the pressure increase during rapid pacing was not due simply to partial LV filling imposed on a relaxing ventricle or to hypertension or an intact pericardium. These data indicate that mechanical effects of atrioventricular interaction play an important role in tachycardia-induced diastolic dysfunction in this model of LVH and can be more causative than ischemia or metabolic factors in this setting.

Animals↗
PubMed1994

Sudden cardiac death in heart failure. The role of abnormal repolarization.

Congestive heart failure is a common, highly lethal cardiovascular disorder claiming over 200,000 lives a year in the United States alone. Some 50% of the deaths in heart failure patients are sudden, and most of these are probably the result of ventricular tachyarrhythmias. Methods designed to identify patients at risk have been remarkably unrewarding, as have attempts to intervene and prevent sudden death in these patients. The failure to impact favorably on the incidence of sudden death in heart failure patients stems largely from a lack of understanding of the underlying mechanisms of arrhythmogenesis. This article explores the role of abnormalities of ventricular repolarization in heart failure patients. We will examine evidence for the hypothesis that alteration of repolarizing K+ channel expression in failing myocardium predisposes to abnormalities in repolarization that are arrhythmogenic. The possible utility of novel electrophysiological and ECG measures of altered ventricular repolarization will be explored. Understanding the mechanism of sudden death in heart failure may lead to effective therapy and more accurate identification of patients at greatest risk.

Action Potentials↗
PubMed1993

A time domain approach for the fluctuation analysis of heart rate related to instantaneous lung volume.

This paper presents a time domain technique for estimating transfer characteristics from fluctuations of instantaneous lung volume (ILV) to heart rate (HR). An effective procedure for estimating the impulse response of HR to ILV is proposed. Pre- and post-processing procedures, including prefiltering of the HR signal, preenhancement of the high frequency content of the ILV signal, and post-filtering of the estimated impulse response, together with a random breathing technique, are shown to effectively reduce spurious transfer gain so as to get a stable estimate of the impulse response. Analysis of the data collected from fourteen healthy male subjects in various conditions revealed that there are three components in the impulse response: fast positive, delayed slow negative, and oscillatory. The effects of the autonomic blocking agents propranolol and atropine on these transfer characteristics are also described.

Atropine↗
PubMed1991

Spectral analysis of heart rate in diabetic autonomic neuropathy. A comparison with standard tests of autonomic function.

Power spectral analysis of the heart rate was compared with standard tests of autonomic function performed on 15 insulin-dependent diabetic patients with symptoms of autonomic dysfunction. The high-frequency power, low-frequency power, and total power of the heart rate power spectrum measured in the supine position--possible measures of parasympathetic nervous system function--were significant predictors of the expiratory-inspiratory ratio, the beat-to-beat heart rate difference on deep respiration, the standard deviation of the resting heart rate, the 30:15 ratio, and the Valsalva ratio. The change in low-frequency power on moving from the supine to upright position, a possible measure of sympathetic nervous system function, was a modest predictor of the systolic and diastolic blood pressure fall in response to postural change, but a poor predictor of the blood pressure response to isometric exercise and a cold stimulus. This study supports the role of heart rate power spectral analysis as a clinical test of autonomic function in patients with known or suspected autonomic failure.

Adult↗
PubMed1991

Transfer function analysis of the circulation: unique insights into cardiovascular regulation.

We have demonstrated previously that transfer function analysis can be used to precisely characterize the respiratory sinus arrhythmia (RSA) in normal humans. To further investigate the role of the autonomic nervous system in RSA and to understand the complex links between respiratory activity and arterial pressure, we determined the transfer functions between respiration, heart rate (HR), and phasic, systolic, diastolic, and pulse arterial pressures in 14 healthy subjects during 6-min periods in which the respiratory rate was controlled in a predetermined but erratic fashion. Pharmacological autonomic blockade with atropine, propranolol, and both, in combination with changes in posture, was used to characterize the sympathetic and vagal contributions to these relationships, as well as to dissect the direct mechanical links between respiration and arterial pressure from the effects of the RSA on arterial pressure. We found that 1) the pure sympathetic (standing + atropine) HR response is characterized by markedly reduced magnitude at frequencies greater than 0.1 Hz and a phase delay, whereas pure vagal (supine + propranolol) modulation of HR is characterized by higher magnitude at all frequencies and no phase delay; 2) both the mechanical links between respiration and arterial pressure and the RSA contribute significantly to the effects of respiration on arterial pressure; 3) the RSA contribution to arterial pressure fluctuations is significant for vagal but not for sympathetic modulation of HR; 4) the mechanical effects of respiration on arterial pressure are related to the negative rate of change of instantaneous lung volume; 5) the mechanical effects have a higher magnitude during systole than during diastole; and 6) the mechanical effects are larger in teh standing than the supine position. Most of these findings can be explained by a simple model of circulatory control based on previously published experimental transfer functions from our laboratory.

Adult↗
PubMed1990

Heart rate and muscle sympathetic nerve variability during reflex changes of autonomic activity.

Low-frequency (less than 0.15 Hz) fluctuations of heart rate are increased by maneuvers, such as standing or hemorrhage, that increase sympathetic outflow to the heart and vasculature. To test the hypothesis that low-frequency heart rate fluctuations provide an index of sympathetic efferent activity, we compared power spectral measures of heart rate variability with two measures of sympathetic outflow, peroneal nerve sympathetic activity and antecubital vein plasma norepinephrine concentrations. Autonomic outflow was varied with graded stepwise infusions of nitroprusside and phenylephrine, which lowered or raised average diastolic pressures by approximately 15 mmHg. Before vasoactive drug infusions, no spectral measure of heart rate variability correlated significantly with muscle sympathetic activity, plasma norepinephrine concentration, average heart rate, or arterial pressure. During increases of muscle sympathetic activity and probable reductions of cardiac vagal activity induced by nitroprusside, the fraction of heart rate spectral power at low frequencies, but not the absolute value, correlated significantly with muscle sympathetic activity and plasma norepinephrine. However, during reductions of muscle sympathetic activity and probable elevations of cardiac vagal activity induced by phenylephrine, no measure of heart rate variability correlated significantly with muscle sympathetic activity. These findings can be explained by a model of heart rate control in which low-frequency heart rate fluctuations result from changing levels of both the sympathetic and parasympathetic inputs to the sinoatrial node.

Adult↗