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(Circulation. 1995;92:3206-3211.)
© 1995 American Heart Association, Inc.
Articles |
Sympathetic Activation and Loss of Reflex Sympathetic Control in Mild Congestive Heart Failure
Presented in part at the 66th Scientific Sessions of the American Heart Association, Atlanta, Ga, November 8-11, 1993, and published in Abstract form in Circulation (1993;88[suppl I]:I-572).
From the Cattedra di Medicina Interna, Ospedale S. Gerardo, Monza; the Istituto di Clinica Medica, Centro di Fisiologia Clinica e Ipertensione, Ospedale Maggiore and Università di Milano; and Centro Auxologico Italiano, Milano, Italy.
Correspondence to Prof Giuseppe Mancia, Centro Fisiologia Clinica e Ipertensione, Policlinico, Via F Sforza 35, 20122 Milano, Italy.
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Abstract |
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 Top Abstract IntroductionMethods Results Discussion References |
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Background Baroreflex control of sympathetic activity is impaired in severe congestive heart failure (CHF), probably causing the marked sympathetic activation typical of this condition. Little information exists, however, as to whether baroreflex impairment and related sympathetic activation also occur in mild CHF.
Methods and Results We studied 19 patients (age, 57.5±2.2 years, mean±SEM) with CHF in New York Heart Association (NYHA) class III or IV and with a marked reduction in left ventricular ejection fraction (LVEF, 30.1±1.5% from echocardiography) and 17 age-matched patients with CHF in NYHA class I or II and with an only slightly reduced LVEF (44.9±3.3%) that never was <40%. Seventeen age-matched healthy subjects served as control subjects. Primary measurements included beat-to-beat arterial blood pressure (with the Finapres technique), heart rate (from ECG), and postganglionic muscle sympathetic nerve activity (MSNA, from microneurography at the peroneal nerve). Measurements were performed at baseline and during baroreceptor stimulation (intravenous phenylephrine infusion), baroreceptor deactivation (intravenous nitroprusside infusion), and cold-pressor test. Baseline blood pressure was similar in the three groups, whereas heart rate was progressively greater from control subjects to patients with mild and severe CHF. MSNA (bursts per 100 heart beats) increased significantly and markedly from control subjects to patients with mild and severe CHF (47.1±2.9 versus 64.4±6.2 and 82.1±3.4, P<.05 and P<.01, respectively). Heart rate and MSNA were progressively reduced by phenylephrine infusion and progressively increased by nitroprusside infusion. Compared with control subjects, the responses were strikingly impaired in severe CHF patients, but a marked impairment also was seen in mild CHF patients. On average, baroreflex sensitivity in mild CHF patients was reduced by 59.1±5.5% (MSNA) and 64.8±4.8% (heart rate). In contrast, reflex responses to the cold-pressor test were similar in the three groups.
Conclusions These results demonstrate that in mild CHF patients the baroreceptor inhibitory influence on heart rate and MSNA is already markedly impaired. This impairment may be responsible for the early sympathetic activation that occurs in the course of CHF.
Key Words: heart failure • baroreceptors • reflex • nervous system
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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In patients with severe CHF, plasma norepinephrine concentration, plasma norepinephrine spillover from sympathetic nerve terminals, and sympathetic nerve firing directly measured from the peroneal nerve are markedly increased,1 2 3 4 and baroreceptor modulation of the heart and peripheral sympathetic drive is strikingly reduced.5 6 7 8 9 Thus, severe CHF is characterized by sympathetic activation that probably is due, at least in part, to an impairment of reflex restraint of sympathetic tone.
Recent studies have shown that plasma norepinephrine concentration and sympathetic nerve traffic also may be increased in patients classified as being in NYHA class I or II , ie, with symptoms of mild CHF.10 11 12 13 14 In most studies, however, sympathetic activity was measured by plasma norepinephrine concentration, namely by an index of sympathetic activity that is particularly fallible in CHF because norepinephrine increases depend heavily on a reduced tissue clearance instead of on an increased nerve terminal secretion.3 15 Furthermore, in the three studies4 9 12 in which sympathetic activity was directly measured by microneurography, the population of mild CHF patients had a striking reduction in LVEF (average values, 19±1.7%, 21±1%, and 19±2%, respectively, mean±SEM), raising the possibility that a severe rather than a mild heart failure condition was responsible for the sympathetic activation. Finally, no study has compared the baroreflex in mild and severe CHF to determine to what extent a baroreflex impairment occurs in the early phase of this condition and thus leads to an early sympathetic activation. Because sympathetic activation carries a prognostic importance in CHF,2 16 this information is of primary clinical relevance.
The present investigation was undertaken to address these issues. We studied two groups of patients, one with severe CHF and the other with CHF belonging to NYHA class I or II but with only a moderate reduction in cardiac function. Sympathetic activity was measured by both plasma norepinephrine and direct microneurographic recording of sympathetic nerve traffic. Baroreflex function was examined for baroreceptor activities ranging from above to below baseline activity and for baroreceptor influences on both HR and sympathetic nerve traffic. This allowed a thorough characterization of the stimulus-response curves of the reflex.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Our study was performed in 53 subjects (50 men, 3 women) ranging in age from 32 to 72 years who had a body mass index
25
kg/m2. Seventeen hospitalized subjects recovering from
noncardiovascular diseases and in good clinical
condition (age, 54.1±2.8 years) served as control subjects. The
remaining 36 subjects (age, 58.2±1.8 years) were hospital inpatients
with CHF in NYHA class I or II (n=17; age, 59.1±2.9 years) or
class
III or IV (n=19; age, 57.5±2.2 years) caused by either
idiopathic
dilated cardiomyopathy (n=21) or coronary
heart disease (n=15). The two groups will hereafter be referred to as
patients with mild and severe CHF, respectively. All subjects included in the study were normotensive and in sinus rhythm. The CHF patients had chest radiographic evidence of a cardiothoracic ratio >0.55 and an echocardiographic evidence (see below) of an increased LVEDD and a reduced LVEF. The patients in NYHA class I or II were recruited only if their LVEFs were not <40%. No subject had a history of myocardial infarction in the 6 months before the study or clinical or laboratory evidence of valvular heart disease, renal insufficiency, diabetes mellitus, or any other condition known to affect autonomic modulation of the cardiovascular system.17 The control subjects were physically untrained and under no drug treatment. The CHF patients were treated with furosemide, digitalis, angiotensin-converting enzyme inhibitors, or vasodilators in various combinations and doses. Drug treatment was withdrawn at least 7 days before the study, except digitalis was maintained in 7 patients with severe CHF. In both control subjects and CHF patients, blood counts, serum electrolytes, and renal laboratory function tests were normal.
The study protocol was approved by the Ethics Committee of our institution. All subjects agreed to participate after being informed of the study nature and purpose.
Measurements
BP, CVP, HR, Respiration Rate, and
Echocardiography
BP was measured three times by a mercury
sphygmomanometer, with
the first and fifth Korotkoff sounds taken to identify systolic
and diastolic values, respectively. In addition,
arterial BP was monitored in all subjects by a finger
photoplethysmographic device (Finapres Ohmeda 2300) capable of
providing accurate and reproducible beat-to-beat
systolic and diastolic values.18 19 In
11 control subjects and 14 CHF patients (11 with mild CHF and 3 with
severe CHF), CVP was measured by a catheter placed in the right atrium
from an antecubital vein of the right arm and connected with a
transducer (model P23XL, Gould Instruments) positioned at the midchest
level. HR was monitored continuously by a cardiotachometer triggered by
the R wave of an ECG lead. Respiration rate was monitored by a
strain-gauge pneumograph positioned at the midchest level.
Measurements included an echocardiogram performed in M mode after selection of the measurement section by a B-mode scan. This allowed us to assess LVEDD and to calculate LVEF.20 Echocardiographic data were collected by a single operator unaware of the experimental design. The within-operator coefficient of variation of the LVEDD measurements (ie, the within-operator reproducibility) was 6%.
Sympathetic Nerve
Traffic
Multiunit recording of efferent MSNA was obtained
through a tungsten microelectrode inserted into the right or left
peroneal nerve, as previously
described.21 22 23 The nerve
signal was amplified x70 000, fed through a bandpass filter (700 to
2000 Hz), and integrated with a custom nerve traffic analysis
system (Bioengineering Department, University of Iowa). Integrated
nerve activity was monitored by a loudspeaker, displayed on a storage
oscilloscope (model 511A, Tektronix), and recorded with BP, CVP,
HR, and respiratory movements on thermic paper by an ink polygraph
(Gould 3800, Gould Instruments). The muscle nature of the MSNA was
assessed according to the criteria outlined
previously,21 23 and the recording was accepted
only if the signal-to-noise ratio exceeded the value of 3.
Under baseline resting conditions, MSNA was quantified as bursts per minute and bursts per 100 heart beats. Several studies have shown this quantification to be highly reproducible, ie, to differ by only 4.3% when assessed on two separate occasions by a single investigator.22 In our laboratory, this value amounts to 3.8%, and MSNA quantification also shows a long-term reproducibility.24 This was confirmed in 9 control subjects of the present study in whom MSNA values were 33.5±2.8 and 34.6±2.7 bursts per minute and 48.9±3.4 and 50.1±3.2 bursts per 100 heart beats when assessed in two different experimental sessions spaced by an interval of 16.4±1.3 months.
Neurohumoral Variables
Plasma norepinephrine was
assayed by
high-performance liquid
chromatography.25 PRA, plasma AVP, and
plasma ANP were assayed by
radioimmunoassay.26 27 28 All
measurements were obtained from a blood sample drawn from a cannula
placed in an antecubital vein of the arm contralateral to that used for
sphygmomanometric and finger BP measurements.
Baroreflex
and Cold-Pressor Test
Baroreceptor modulation of MSNA and HR was
assessed by the
technique based on infusion of vasoactive drugs.17
Briefly, phenylephrine was infused incrementally through
the cannula placed in an antecubital vein at the doses of 0.3, 0.6, and
0.9
µg·kg-1·min-1.
Nitroprusside was also infused incrementally in an antecubital vein at
doses of 0.4, 0.8, and 1.2
µg·kg-1·min-1.
Each infusion was maintained for 5 minutes, and the drug initially
infused was randomly selected. The end of the first infusion was
separated from the beginning of the second infusion by a recovery time
of 45 minutes. MAP (diastolic pressure plus one third of
pulse pressure), MSNA, and HR were averaged for 5 minutes before
infusion and for 5 minutes of each step infusion. Baroreceptor
modulation of MSNA and HR was estimated by calculation of the absolute
and percent change in MSNA and the absolute change in HR in relation to
the change in MAP induced by each dose of phenylephrine and
nitroprusside. The average ratio between MSNA or HR changes and MAP
changes was also calculated separately for the three infusions of
phenylephrine and nitroprusside. This was taken as the
measure of baroreflex sensitivity during baroreceptor stimulation and
deactivation.
Cold-pressor test was performed 45 minutes after the end of the second vasoactive drug infusion by immersion of the hand not used for BP measurements in iced water (3°C) for 2 minutes. MAP, MSNA, and HR were averaged for 5 minutes before and 2 minutes during the cold-pressor test.
Protocol and Data Analysis
CHF patients and control subjects
were taken to the laboratory
in the morning after a light breakfast, put in the supine position, and
fitted with the intravenous cannulas, microelectrodes for
MSNA recording, and other measuring devices. A blood sample was
then drawn, and the three sphygmomanometric BP measurements were
obtained. After a 30-minute interval, BP, CVP, HR, respiratory rate,
and MSNA were measured continuously during (1) an initial 10-minute
baseline resting condition, (2) infusion of one vasoactive drug, (3) a
second 10-minute baseline resting condition, (4) infusion of the second
vasoactive drug, (5) a 5-minute resting condition, and (6)
cold-pressor test.
Data were calculated by a single investigator unaware of the patient classification. Values from individual subjects were averaged for the different groups and expressed as mean±SEM. The statistical significance of the differences in mean values was assessed by two-way ANOVA. The two-tailed t test for unpaired observations was used to locate the difference between groups; the two-tailed t test for paired observations was used to locate the difference between resting conditions and baroreceptor stimulation, baroreceptor deactivation, and cold-pressor test. Bonferroni's correction for multiple comparisons was used.29 Correlations between different variables were analyzed by the Spearman method. A value of P<.05 was taken as the level of statistical significance.29
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Baseline Data
Table 1
shows the hemodynamic,
echocardiographic, and neurohumoral data in mild and
severe CHF patients and the corresponding values observed in control
subjects. MAP was superimposable in the three groups, but all other
variables showed a tendency to be progressively modified from
control subjects to patients with mild and severe CHF. The increases in
HR, PRA, AVP, and plasma norepinephrine observed in mild
CHF patients versus control subjects were not statistically
significant, whereas the differences in LVEF, ANP, and MSNA between the
three groups all were statistically significant. For MSNA, this was the
case when MSNA was expressed as both bursts per minute and as bursts
per 100 heart beats (ie, corrected for HR values). In CHF patients,
MSNA displayed a significant, although modest, inverse correlation with
LVEF (r=-.41, P<.04), a direct correlation
with ANP (r=.40, P<.02) and PRA
(r=.34, P<.05), but no relation with LVEDD,
norepinephrine, or AVP. No correlation was found between
LVEDD (or LVEF) and ANP, PRA, norepinephrine, or AVP. No
significant correlation between these variables was found in
control subjects.
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Baroreceptor Reflex
As Fig 1 shows, infusion
of the three incremental
doses of phenylephrine caused a progressive increase in
MAP, a progressive decrease in HR, and a progressive reduction in MSNA,
whereas infusion of the three incremental doses of nitroprusside had
opposite effects. The changes in HR and MSNA induced by
phenylephrine or nitroprusside were markedly and
significantly reduced in patients with severe CHF compared with those
seen in control subjects. A less pronounced significant reduction in
the HR and MSNA responses, however, was also observed in patients with
mild CHF. The HR and MSNA baroreflex sensitivities during baroreceptor
stimulation and deactivation (see "Methods") were significantly
reduced in patients with both mild and severe CHF compared with control
subjects (Fig 2). CVP was progressively
reduced and increased by stepwise nitroprusside and
phenylephrine infusions, respectively. The changes were
small, similar in control subjects and CHF patients, and not
significant for the lowest dose of vasoactive drugs infused (Table
2).
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, solid lines) and
patients with mild (
, dashed lines) and severe (
, dotted
lines) CHF were always significantly different (P<.01,
control subjects vs severe CHF patients; P<.05, control
subject vs mild CHF patients) but not between patients with mild and
severe CHF (P<.01).
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In all CHF patients pooled, no relation existed between resting HR values and the sensitivity of the baroreceptor-HR reflex (r=-.29 and r=-.01 for phenylephrine and nitroprusside, respectively; P=NS). In contrast, there was a significant inverse relation between resting sympathetic nerve traffic and the sensitivity of the baroreceptor-MSNA (r=-.32 for phenylephrine, P<.05; r=-.63 for nitroprusside, P<.001).
Cold-Pressor Test
Cold-pressor test induced an increase in
MAP, HR, and MSNA.
The magnitude of the HR and MSNA increases was slightly less in
patients with mild or severe CHF than in control subjects, but the
differences between groups were not statistically significant (Fig
3).
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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Our observations provide new information on sympathetic activity and baroreceptor control of the heart and sympathetic firing in patients with mild CHF. These two issues are discussed separately.
Sympathetic Activity
In our study, plasma norepinephrine was
progressively
greater from control subjects to patients with mild and severe CHF, but
the difference was significant only between patients with severe CHF
and control subjects. In contrast, sympathetic nerve traffic was
progressively and significantly increased from control subjects to
patients with mild or severe CHF. Thus, sympathetic activity increases
progressively with the severity of CHF, but an activation is already
manifest in a stage of the disease where symptoms are only mild. This
finding confirms the results reported in previous
studies.10 13 It adds to previous evidence, however,
the
observation than an increase in sympathetic activity occurs not only
when symptoms of CHF are mild but also when, as in our patients,
cardiac function is only slightly affected. Sympathetic activation is
thus a really early phenomenon of a CHF condition.
The increase of sympathetic nerve traffic but not of plasma norepinephrine in patients with mild CHF deserves further considerations. It is clear from this observation that microneurography is a more sensitive marker of the sympathetic activation in the early stage of CHF than plasma norepinephrine. We can speculate that this might reflect an increase of sympathetic activity only to skeletal muscle circulation, ie, to the circulation innervated by the sympathetic fibers recorded from the peroneal nerve.21 However, this does not fit with the evidence that skeletal muscle circulation is a predominant contributor to plasma norepinephrine.30 31 Thus, a more likely explanation is that in the initial stage of CHF there is already a generalized sympathetic activation; however, the degree of this activation is too modest to allow the small fraction of norepinephrine escaping sympathoeffector junctions to modify norepinephrine levels in the blood stream. This amounts to saying that the sensitivity of plasma norepinephrine in detecting increases in sympathetic activity may be limited,30 32 which has indeed been shown in hypertensive subjects in whom a generalized but modest sympathetic activation induced by baroreceptor unloading was not accompanied by a significant plasma norepinephrine increase33 and in obese normotensive subjects in whom baseline sympathetic activation was detected by sympathetic burst rate but not by plasma norepinephrine levels.34 This limitation may disappear when sympathetic activation is more pronounced, and a correlation between increases in sympathetic burst rate and plasma norepinephrine has been shown repeatedly in patients with severe CHF.4 12
Our data also provide information on the appearance and progression of other humoral activations from mild to severe CHF. The most important findings are that ANP showed a progressive and significant increase from control subjects to patients with mild or severe CHF and a significant correlation with sympathetic nerve traffic, whereas PRA and AVP showed an increase only in patients with severe CHF and little or no correlation with sympathetic nerve traffic. These observations suggest that an increased ANP secretion may be another very early abnormality in CHF, whereas an increased secretion of renin and vasopressin might instead represent a later feature of this condition.14 35 36 37 38
Baroreflex Control of HR and Sympathetic Nerve
Traffic
Compared with control subjects, baroreceptor stimulation and
deactivation were virtually devoid of any reflex effect on HR and
sympathetic nerve traffic in patients with severe CHF. Both reflex
responses, however, also were clearly reduced in patients with mild
CHF, providing the first direct evidence that in the initial stage of
CHF the baroreflex also is impaired. Because the degree of this
impairment was correlated with the degree of sympathetic activation, it
is possible that the former and the latter phenomena are linked by a
cause-effect relation, ie, that the sympathetic activation is due
to a reduction of reflex sympathetic restraint.
The impairment of the baroreflex in patients with CHF deserves further comments. First, this impairment involved to a similar extent the baroreceptor ability to modulate HR and sympathetic nerve traffic. Because baroreceptor modulation of HR depends largely on the vagus,17 39 we can conclude that reflex control of both autonomic divisions is similarly impaired in patients with CHF. This is different from what occurs in patients with hypertension or diabetes in which the baroreceptor-HR reflex is impaired to a greater and earlier extent than baroreceptor control of sympathetic activity, peripheral vasculature, and blood pressure.17 40 41 42 Second, in patients with severe CHF, reflex responses to baroreceptor stimulation and deactivation were both markedly reduced; in patients with mild CHF, the responses to baroreceptor stimulation were more markedly affected than the responses to baroreceptor deactivation. This may be due to the fact that when the impairment is less pronounced, the baroreflex can operate more easily at or below its tonic level of activity than under conditions of maximal engagement, ie, when baroreceptor stimulation tests the "baroreflex reserve." Third, as expected from previous observations,9 17 43 in both control subjects and CHF patients CVP was increased during stepwise infusion of phenylephrine and was reduced during stepwise infusion of nitroprusside, indicating some involvement of volume cardiopulmonary receptors whose reflex influences also are impaired in patients with severe CHF.9 44 45 46 This raises the possibility that both arterial baroreceptors and cardiopulmonary receptors contributed to the early impairment of baroreflex control in patients with CHF, although the small magnitude of the CVP changes and their virtual absence during infusion of the lowest vasoactive drugs doses suggest that impairment of the arterial baroreflex component played an important role. Finally, because the HR and sympathetic responses to cold-pressor test were similar in control subjects and patients with severe and mild CHF, the baroreflex impairment does not depend on a generalized alteration of autonomic cardiovascular control but on factors affecting specifically the central and/or afferent portions of the reflex arch. A possible "central" factor is angiotensin II, which blunts the baroreceptor sensitivity by crossing the blood-brain barrier at several fenestration sites where the baroreceptor input is integrated.47 48 A possible "afferent" factor is a reduction in arterial compliance, which makes baroreceptors less responsive to pressure stimuli. Indeed, a reduction in arterial compliance is the most likely factor in patients with mild CHF because, although plasma renin activity is increased primarily in patients with severe CHF (see also data in our patients), arterial compliance is strikingly reduced in patients with severe CHF but also is clearly reduced in patients with mild CHF.49
In conclusion, our observations show that compared with age-matched control subjects, subjects with mild symptoms of CHF and only a limited impairment of cardiac function have increased sympathetic nerve activity. Baroreceptor control of HR and sympathetic traffic also is impaired in patients with mild CHF, suggesting that the sympathetic activation is due to an early loss of reflex sympathetic restraint.
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Selected Abbreviations and Acronyms |
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Received December 12, 1994; revision received June 20, 1995; accepted July 27, 1995.
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 C. Rostagno, M. Felici, S. Caciolli, G. Olivo, M. Comeglio, G. Galanti, and G. G. N. Serneri Decreased Baroreflex Sensitivity Assessed from Phase IV of Valsalva Maneuver in Mild Congestive Heart Failure Angiology, August 1, 1999; 50(8): 655 - 664. [Abstract] [PDF]
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K. Narkiewicz, C. A. Pesek, P. J. H. van de Borne, M. Kato, and V. K. Somers Enhanced Sympathetic and Ventilatory Responses to Central Chemoreflex Activation in Heart Failure Circulation, July 20, 1999; 100(3): 262 - 267. [Abstract] [Full Text] [PDF]
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G Grassi and G Mancia Sympathetic overactivity and exercise intolerance in heart failure: a cause-effect relationship Eur. Heart J., June 2, 1999; 20(12): 854 - 855. [PDF]
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C.F. Notarius, S. Ando, G.A. Rongen, and J.S. Floras Resting muscle sympathetic nerve activity and peak oxygen uptake in heart failure and normal subjects Eur. Heart J., June 2, 1999; 20(12): 880 - 887. [Abstract] [PDF]
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L. Rudas, A. A. Crossman, C. A. Morillo, J. R. Halliwill, K. U. O. Tahvanainen, T. A. Kuusela, and D. L. Eckberg Human sympathetic and vagal baroreflex responses to sequential nitroprusside and phenylephrine Am J Physiol Heart Circ Physiol, May 1, 1999; 276(5): H1691 - H1698. [Abstract] [Full Text] [PDF]
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G Tjeerdsma, M T Meinardi, W T A van der Graaf, M P van den Berg, N H Mulder, H J G M Crijns, E G E de Vries, and D J van Veldhuisen Early detection of anthracycline induced cardiotoxicity in asymptomatic patients with normal left ventricular systolic function: autonomic versus echocardiographic variables Heart, April 1, 1999; 81(4): 419 - 423. [Abstract] [Full Text]
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 G. S. Pepper and R. W. Lee Sympathetic Activation in Heart Failure and Its Treatment With {beta}-Blockade Arch Intern Med, February 8, 1999; 159(3): 225 - 234. [Abstract] [Full Text] [PDF]
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G. Grassi, D. Spaziani, G. Seravalle, G. Bertinieri, R. Dell'Oro, C. Cuspidi, and G. Mancia Effects of Amlodipine on Sympathetic Nerve Traffic and Baroreflex Control of Circulation in Heart Failure Hypertension, February 1, 1999; 33(2): 671 - 675. [Abstract] [Full Text] [PDF]
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G. Hasenfuss Animal models of human cardiovascular disease, heart failure and hypertrophy Cardiovasc Res, July 1, 1998; 39(1): 60 - 76. [Abstract] [Full Text] [PDF]
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B. P.M. Imholz, W. Wieling, G. A. van Montfrans, and K. H. Wesseling Fifteen years experience with finger arterial pressure monitoring:: assessment of the technology Cardiovasc Res, June 1, 1998; 38(3): 605 - 616. [Abstract] [Full Text] [PDF]
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G. Grassi, G. Seravalle, M. Colombo, G. Bolla, B. M. Cattaneo, F. Cavagnini, and G. Mancia Body Weight Reduction, Sympathetic Nerve Traffic, and Arterial Baroreflex in Obese Normotensive Humans Circulation, May 26, 1998; 97(20): 2037 - 2042. [Abstract] [Full Text] [PDF]
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D. H. Silber, G. Sutliff, Q. X. Yang, M. B. Smith, L. I. Sinoway, and U. A. Leuenberger Altered mechanisms of sympathetic activation during rhythmic forearm exercise in heart failure J Appl Physiol, May 1, 1998; 84(5): 1551 - 1559. [Abstract] [Full Text] [PDF]
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G. Grassi, M. Colombo, G. Seravalle, D. Spaziani, and G. Mancia Dissociation Between Muscle and Skin Sympathetic Nerve Activity in Essential Hypertension, Obesity, and Congestive Heart Failure Hypertension, January 1, 1998; 31(1): 64 - 67. [Abstract] [Full Text] [PDF]
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G. Grassi, B. M. Cattaneo, G. Seravalle, A. Lanfranchi, and G. Mancia Baroreflex Control of Sympathetic Nerve Activity in Essential and Secondary Hypertension Hypertension, January 1, 1998; 31(1): 68 - 72. [Abstract] [Full Text] [PDF]
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R. Willenbrock, H. Stauss, M. Scheuermann, K. J. Osterziel, T. Unger, and R. Dietz Effect of chronic volume overload on baroreflex control of heart rate and sympathetic nerve activity Am J Physiol Heart Circ Physiol, December 1, 1997; 273(6): H2580 - H2585. [Abstract] [Full Text] [PDF]
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K. Ashino, E. Gotoh, S.-i. Sumita, A. Moriya, and M. Ishii Percutaneous Transluminal Mitral Valvuloplasty Normalizes Baroreflex Sensitivity and Sympathetic Activity in Patients With Mitral Stenosis Circulation, November 18, 1997; 96(10): 3443 - 3449. [Abstract] [Full Text]
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P. Ponikowski, T. P. Chua, M. Piepoli, D. Ondusova, K. Webb-Peploe, D. Harrington, S. D. Anker, M. Volterrani, R. Colombo, G. Mazzuero, et al. Augmented Peripheral Chemosensitivity as a Potential Input to Baroreflex Impairment and Autonomic Imbalance in Chronic Heart Failure Circulation, October 21, 1997; 96(8): 2586 - 2594. [Abstract] [Full Text]
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H. R. Middlekauff, A. H. Nguyen, C. E. Negrao, E. U. Nitzsche, C. K. Hoh, B. A. Natterson, M. A. Hamilton, G. C. Fonarow, A. Hage, and J. D. Moriguchi Impact of Acute Mental Stress on Sympathetic Nerve Activity and Regional Blood Flow in Advanced Heart Failure : Implications for `Triggering' Adverse Cardiac Events Circulation, September 16, 1997; 96(6): 1835 - 1842. [Abstract] [Full Text]
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G. Grassi, B. M. Cattaneo, G. Seravalle, A. Lanfranchi, M. Pozzi, A. Morganti, S. Carugo, and G. Mancia Effects of Chronic ACE Inhibition on Sympathetic Nerve Traffic and Baroreflex Control of Circulation in Heart Failure Circulation, August 19, 1997; 96(4): 1173 - 1179. [Abstract] [Full Text]
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G. Grassi, B. M. Cattaneo, G. Seravalle, A. Lanfranchi, G. Bolla, and G. Mancia Baroreflex Impairment by Low Sodium Diet in Mild or Moderate Essential Hypertension Hypertension, March 1, 1997; 29(3): 802 - 807. [Abstract] [Full Text]
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S.-i. Ando, H. R. Dajani, B. L. Senn, G. E. Newton, and J. S. Floras Sympathetic Alternans: Evidence for Arterial Baroreflex Control of Muscle Sympathetic Nerve Activity in Congestive Heart Failure Circulation, January 21, 1997; 95(2): 316 - 319. [Abstract] [Full Text]
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B. Rundqvist, M. Elam, Y. Bergmann-Sverrisdottir, G. Eisenhofer, and P. Friberg Increased Cardiac Adrenergic Drive Precedes Generalized Sympathetic Activation in Human Heart Failure Circulation, January 7, 1997; 95(1): 169 - 175. [Abstract] [Full Text]
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G. E. Newton and J. D. Parker Cardiac Sympathetic Responses to Acute Vasodilation: Normal Ventricular Function Versus Congestive Heart Failure Circulation, December 15, 1996; 94(12): 3161 - 3167. [Abstract] [Full Text]
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