(Circulation. 1997;96:3443-3449.)
© 1997 American Heart Association, Inc.
Articles |
Percutaneous Transluminal Mitral Valvuloplasty Normalizes Baroreflex Sensitivity and Sympathetic Activity in Patients With Mitral Stenosis
From the Second Department of Internal Medicine, Yokohama City University School of Medicine, Yokohama 236, Japan.
Correspondence to Eiji Gotoh, MD, Second Department of Internal Medicine, Yokohama City University School of Medicine, 3–9, Fukuura, Kanazawa-ku, Yokohama 236, Japan. E-mail cf6e-gtu{at}asahi-net.or.jp
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Abstract |
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Background In patients with mitral stenosis, reduced cardiac output or altered pulmonary hemodynamics may increase sympathetic nerve activity. However, the magnitude of the increase in sympathetic activity in such patients and the effect of valvuloplasty on this activity are unknown.
Methods and Results We microneurographically measured muscle
sympathetic nerve activity before and after mitral valvuloplasty in 10
patients (mean±SEM age, 48±2 years) with mitral stenosis and
in 10 healthy volunteers (47±4 years); hemodynamic
variables were also measured. Baroreflex sensitivity was assessed
on the basis of the ratio of the change in heart rate or muscle
sympathetic activity to the change in mean arterial
pressure during intravenous infusion of sodium
nitroprusside or phenylephrine. At baseline, muscle
sympathetic activity was significantly higher in the patients with
mitral stenosis than in the control subjects (42.1±3.2 versus
26.1±3.7 bursts/min, P<.05). However, there was no
significant difference between the groups in sympathetic activity at 1
week after valvuloplasty. The reduction in sympathetic activity after
valvuloplasty was maintained for 
6 months and correlated with the
increase in cardiac index (r=.74,
P<.05). Baroreflex sensitivity was significantly lower
in the patients than in the control subjects, but after valvuloplasty
there was no significant difference in baroreflex sensitivity between
the groups.
Conclusions Sympathetic activity is increased in patients with mitral stenosis. Mitral valvuloplasty in such patients results in early and long-lasting normalization of sympathetic nerve activity, possibly because of an improvement in arterial baroreflex sensitivity.
Key Words: nervous system, autonomic • mitral valve • valvuloplasty • heart failure
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Introduction |
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Mitral valve stenosis increases left atrial pressure, which may significantly alter pulmonary hemodynamics. As the stenosis worsens, cardiac output is reduced. This situation may increase sympathetic nervous activity because generalized activation of the sympathetic nervous system has been demonstrated in patients with congestive heart failure1,2; however, whether patients with mitral stenosis have increased sympathetic activity remains to be established.
An increase in sympathetic nerve activity may cause many of the pathophysiological processes associated with mitral stenosis. Increased sympathetic activity has been reported to precipitate platelet aggregation,3 which may lead to intra-atrial production of emboli. Increased sympathetic outflow stimulates renin release from the kidney4 and causes retention of body fluids, which may promote pulmonary congestion. Sympathetic stimulation increases heart rate, which shortens the diastolic filling period and may cause cardiac ischemia. Thus, elevated sympathetic nerve activity may be an important risk factor for the development of clinical manifestations of mitral stenosis. Percutaneous transluminal mitral valvuloplasty, which is standard treatment for patients with mitral stenosis,5,6 may decrease sympathetic activity and improve the prognosis of patients with this condition. However, the effect of valvuloplasty on sympathetic activity is unknown.
In this study, we directly measured muscle sympathetic nerve activity microneurographically7,8 in patients with mitral stenosis and normal sinus rhythm before and after percutaneous transluminal mitral valvuloplasty. We also measured sympathetic nerve activity in healthy volunteers as a control. Furthermore, we examined the effects of mitral valvuloplasty on baroreceptor reflex sensitivity because reduced afferent activity from baroreceptor may increase sympathetic outflow.9–11
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Methods |
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Subjects
The study group comprised 10 patients with symptomatic mitral stenosis (3 men and 7 women; mean±SEM age, 48±2 years) and 10 age-matched normal control subjects (5 men and 5 women; 47±4 years). Age, sex, NHYA class, mitral valve area, and mitral valve pressure gradient for each patient are given in Table 1
. None of the patients had atrial
fibrillation, other continuous arrhythmias, or evidence of
coronary artery disease on coronary angiograms. After
admission, 4 patients were administered coumadin, which was continued
after valvuloplasty. All medications that had the potential to affect
sympathetic nerve activity (including diuretics, digitalis,
nitrates, ß-blockers, and ACE inhibitors) were
discontinued 2 weeks before the study. Control subjects were
age-matched healthy volunteers, as confirmed by physical and routine
laboratory examinations, and were not taking any medication.
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Written informed consent was obtained from each patient and control subject after a detailed explanation of the purpose and procedures of the study. The microneurographic method was approved by the Human Studies Committee of Yokohama City University School of Medicine, and the protocol of this study was approved by the Ethical Panel of the Second Department of Internal Medicine.
Transluminal Mitral Valvuloplasty
Right heart catheterization was performed
through the left femoral vein with a 7F Swan-Ganz thermodilution
catheter. A 5F pigtail catheter was inserted through the left femoral
artery to measure arterial and left ventricular
pressure. Transseptal left heart catheterization was
performed through the right femoral vein with an 8F Mullins transseptal
sheath, a dilator, and a Brockenbrough needle. Mitral valvuloplasty was
performed with a 20- to 26-mm Inoue balloon
catheter,5 which was inflated for 5 seconds.
Before and after valvuloplasty, cardiac output was measured with the
thermodilution method, and mitral valve area was calculated according
to the formula of Gorlin.12 Left ventriculography
was performed to assess the degree of mitral valve
regurgitation and to measure left
ventricular volume, as evaluated with the area-length
method (Mipron, Kontron Instruments). Cardiac echography was performed
to measure cardiac output and stroke volume before, immediately after,
1 week after, and 6 months after valvuloplasty.
Muscle Sympathetic Nerve Activity
In patients with mitral stenosis, muscle sympathetic
nerve activity was measured before, 1 week after, and 6 months after
mitral valvuloplasty. The subjects rested for 30 minutes in the prone
position, after which resting blood pressure, heart rate, and muscle
sympathetic nerve activity were measured for 20 minutes. The baseline
values for these variables were averaged over the last 5 minutes of
this period. Blood pressure was measured every minute with an automated
sphygmomanometer (BP-203i, Nippon Colin). ECGs and muscle sympathetic
nerve activity were continuously monitored throughout the study.
Multiunit recordings of muscle sympathetic nerve activity were
obtained from a muscle fascicle of the tibial nerve at the popliteal
fossa.13 To record muscle sympathetic nerve
activity, a tungsten microelectrode (shaft diameter, 200 µm)
with an uninsulated tapered tip of 1 to 5 µm and an impedance of
5 M
(model 26–08-1, Frederik Haer) was manually inserted through
the skin. Spike potentials, amplified by amplifiers (DPA-21E and
DPA-100D, Dia Medical), were monitored on an oscilloscope (VC-10, Nihon
Kohden) and a loudspeaker and were continuously recorded on
magnetic tapes, which were later played back for analysis. The
recorded activity was fed through a band-pass filter (FV-664,
Negative Feedback Electronic Instruments) with a band width of 700 to
3000 Hz. The filtered neurogram was passed through an integrator (model
1333, NEC San-ei) with a time constant of 0.1 second to obtain the mean
voltage neurogram of muscle sympathetic nerve activity.
The peaks of the mean voltage neurogram were identified as muscle sympathetic nerve vasomotor activity according to the following previously defined criteria7,13,14: (1) weak electrical stimulation (1 to 3 V, 0.2 months, 1 Hz) of the tibial nerve through the electrode caused involuntary muscle contractions but not paresthesia; (2) tapping or stretching the muscle and tendon supplied by the impaled fascicle of the tibial nerve elicited afferent mechanoreceptor discharge, whereas stroking the skin in the distribution of the tibial nerve did not; and, finally, (3) peaks showed a characteristic pulse-synchronous "spontaneous" discharge during phases II and III of the Valsalva maneuver.
Quantitative Analysis of Muscle Sympathetic Nerve
Activity
For quantitative analysis of muscle sympathetic nerve
activity, the mean voltage neurogram of muscle sympathetic nerve
activity was displayed, together with the ECG, on a multidot thermal
recorder (Omnicorder, model 8 M14; NEC San-ei). Records were
divided into 1-minute periods, and for each period, the number of
bursts was determined from the tracing. Sympathetic bursts with an
amplitude three times higher than that of the basal noise were
identified through inspection of the mean voltage neurogram, and the
muscle sympathetic nerve activity was expressed as bursts/min and
bursts/100 heartbeats.
Baroreceptor Reflex Function
Baroreceptor reflex function for heart rate and muscle
sympathetic nerve activity was assessed through the use of
intravenous infusions of pressor and depressor agents.
Phenylephrine was intravenously infused at
doses of 0.5, 1.0, and 1.5 µg ·
kg-1 · min-1.
Nitroprusside was also intravenously infused at doses of
0.25, 0.5, 1.0, and 1.5 µg · kg-1
· min-1. Each infusion lasted for 5 minutes. A
recovery time of 30 minutes was allowed between the end of the first
infusion and the beginning of the second infusion. Mean blood pressure,
heart rate, and muscle sympathetic nerve activity were averaged over
the 5 minutes before and the 5 minutes during each infusion. The mean
ratios of the changes in heart rate and muscle sympathetic nerve
activity in response to changes in mean arterial pressure
were calculated for all doses of phenylephrine and
nitroprusside. Then, the average values of the mean ratios during
phenylephrine or nitroprusside infusion were calculated to
estimate average baroreflex sensitivity.
Measurement of Plasma Norepinephrine Levels
Blood samples were collected in chilled tubes containing
EDTA-2Na and promptly centrifuged. Plasma
norepinephrine levels were measured by
high-performance liquid chromatography with an
electrochemical detector.15 This assay was
sensitive to 10 pg/mL with a coefficient of variation of
10%.
Statistical Analysis
The significance of differences in hemodynamic
variables between before and after mitral valvuloplasty was
assessed with two-tailed paired Student's t tests. The
statistical significance of differences in mean muscle sympathetic
nerve activity was assessed by two-way repeated-measures ANOVA using
the computer program StatView, Version 4.02 (Abacus Concepts), and the
Newman-Keuls test was performed to assess the statistical significance
of difference between mean values. The significance of differences in
baroreflex sensitivity indices and plasma norepinephrine
concentrations between patients with mitral stenosis and normal
control subjects was assessed with two-tailed unpaired Student's
t tests, and that of differences in variables between
patients before and after valvuloplasty was assessed with two-tailed
paired Student's t test. Correlations between baseline
values or changes in muscle sympathetic nerve activity after
valvuloplasty and those in hemodynamic variables
were tested with the Spearman rank-correlation coefficient. Values of
P<.05 were considered to indicate statistical
significance.
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Results |
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Mitral Valvuloplasty
As shown in Table 2
, mitral valve
area increased significantly after mitral valvuloplasty in all
patients, and the mitral valve pressure gradient was significantly
reduced. The degree of mitral regurgitation was
unchanged in 8 patients and worsened angiographically from grade 1 to
grade 2 in 2 patients. For interatrial septal shunt, the
pulmonary-to-systemic blood flow ratio after
percutaneous mitral valvuloplasty was 1.1±0.0. Thus,
mitral valvuloplasty was considered successful in all patients.
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Hemodynamics
Hemodynamic data before and after mitral
valvuloplasty are also shown in Table 2
. Mean arterial
pressure and heart rate showed no significant change after
valvuloplasty, whereas cardiac index and stroke index increased
significantly and total peripheral resistance index
decreased significantly. Left atrial and mean pulmonary
arterial pressure decreased significantly, and
pulmonary vascular resistance index decreased slightly but not
significantly. Right atrial pressure was not significantly altered.
Valvuloplasty significantly increased left ventricular
end-diastolic volume index but did not change left
ventricular end-diastolic pressure.
Muscle Sympathetic Nerve Activity
Baseline muscle sympathetic nerve activity was significantly
higher in patients with mitral stenosis than in healthy control
subjects (43.6±3.2 versus 28.0±5.0 bursts/min; 63.0±5.0 versus
40.0±4.5 bursts/100 heartbeats). After valvuloplasty, muscle
sympathetic nerve activity significantly decreased, and there was no
significant difference between patients and control subjects either 1
week or 6 months after valvuloplasty (Figs 1 and 2).
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) and patients with
mitral stenosis (MS, 
) before, 1 week after, and 6 months
after percutaneous transluminal mitral valvuloplasty
(PTMV). MSNA was assessed as bursts/min (left) or bursts/100 heartbeats
(right). Values represent mean±SEM. *P<.05
versus healthy control subjects. 
P<.05 versus before
PTMV. Baseline MSNA was higher in patients with MS than in normal
control subjects. MSNA was within the normal range both 1 week and 6
months after PTMV.
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Plasma Norepinephrine Concentration
Baseline plasma norepinephrine concentration did not
significantly differ between patients with mitral stenosis and
normal control subjects (335.1±54.5 versus 253.0±38.9 pg/mL).
One week after valvuloplasty, plasma norepinephrine
concentration decreased significantly, and there was no significant
difference between patients (221.4±42.7 pg/mL) and control
subjects (246.0±48.5 pg/mL).
Relationship Between Muscle Sympathetic Nerve Activity and
Hemodynamic Variables
Before mitral valvuloplasty, significant correlations were found
between baseline muscle sympathetic nerve activity and baseline cardiac
index (r=.64), stroke index (r=.53), and total
peripheral resistance index (r=.54). However,
there was no significant correlation between baseline muscle
sympathetic nerve activity and baseline arterial blood
pressure, heart rate, left atrial pressure, pulmonary
arterial pressure, right atrial pressure, or
pulmonary vascular resistance index. After valvuloplasty, the
decrease in muscle sympathetic nerve activity significantly correlated
with the increases in cardiac index and stroke index and with the
decrease in total peripheral resistance index (Fig 3).
However, there was no significant correlation between the decrease in
muscle sympathetic nerve activity and the decreases in left atrial
pressure, mean pulmonary arterial pressure, or
pulmonary vascular resistance index. The decrease in muscle
sympathetic nerve activity did not significantly correlate with the
changes in mean arterial pressure, heart rate, or left
ventricular end-diastolic volume or
pressure.
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Baroreceptor Reflex Function
The relations between the changes in mean arterial
pressure and those in heart rate and muscle sympathetic nerve activity
are shown in Fig 4. Before valvuloplasty,
the baroreflex sensitivity indices for heart rate and muscle
sympathetic nerve activity were significantly lower in patients with
mitral stenosis than in healthy control subjects (Table 3).
After valvuloplasty, however, this impaired sensitivity was restored
for both variables, and there was no significant difference in
baroreflex sensitivity between patients and healthy control subjects.
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), patients with mitral stenosis (MS) before
valvuloplasty (
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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In this study, we examined the effect of percutaneous transluminal mitral valvuloplasty on muscle sympathetic nerve activity in patients with mitral stenosis and normal sinus rhythm. There were four key observations. First, muscle sympathetic nerve activity was higher in patients with mitral stenosis than in control subjects, which provides evidence for the first time that central sympathetic outflow to the skeletal muscle is increased in patients with mitral stenosis. Second, muscle sympathetic nerve activity decreased to normal levels by 1 week after successful transluminal mitral valvuloplasty and remained within the normal range for an additional 6 months. Third, the reduction in muscle sympathetic nerve activity after valvuloplasty was closely related to the improvement in cardiac index. Finally, the sensitivity of the baroreceptor reflex was significantly impaired in patients with mitral stenosis but normalized with improvement in mitral stenosis after valvuloplasty.
Sympathetic activity may be increased in association with a reduction in cardiac index in such patients because a significant decrease in stroke index has been related to sympathetic activation in patients with congestive heart failure.16 On the other hand, in patients with mitral stenosis, an increase in left atrial or pulmonary arterial pressure may inhibit sympathetic activity through cardiopulmonary mechanisms. In our study, muscle sympathetic nerve activity at rest was significantly elevated in patients with mitral stenosis. In addition, sympathetic activity was negatively correlated with cardiac index but not with left atrial or pulmonary arterial pressure. Therefore, cardiac index appears to be an important determinant of sympathetic activity.
In the present study, plasma norepinephrine concentrations at rest were not higher in the patients than in the control subjects. Ikeda et al17,18 also reported no significant difference in plasma norepinephrine concentrations at rest between patients with mitral stenosis and normal control subjects. The findings for muscle sympathetic nerve activity appear to be inconsistent with those for plasma norepinephrine concentration. Plasma norepinephrine concentration is considered a relatively insensitive index of sympathetic activity because only small amounts of norepinephrine released from peripheral sympathetic nerve endings reach the systemic circulation.19,20 Furthermore, plasma norepinephrine concentration may not be a reliable index of sympathetic activity in patients with cardiac dysfunction or low cardiac output because increased norepinephrine clearance has been reported under these conditions.21,22 Available evidence thus indicates that measurement of plasma norepinephrine concentrations cannot always be used to detect differences in sympathetic activity between patients and control subjects. In our study, after valvuloplasty, plasma norepinephrine concentration decreased significantly, suggesting that not only skeletal muscle but also generalized sympathetic activity is reduced by mitral valvuloplasty. However, because there are limitations in the estimation of generalized sympathetic nerve activity on the basis of plasma norepinephrine concentration, further investigations are required before firm conclusions can be drawn.
Surgical mitral valve replacement or commissurotomy may damage cardiac
autonomic nerves, and the surgical procedure itself may influence
sympathetic nerve activity.23 However,
percutaneous transluminal mitral valvuloplasty is less
invasive than open surgery and therefore may minimally affect cardiac
autonomic nerves. After percutaneous transluminal
mitral valvuloplasty, all patients showed significant increases in
mitral valve area and significant decreases in mitral pressure
gradient, changes that indicate a successful outcome of valvuloplasty.
At 1 week after successful mitral valvuloplasty, the elevated muscle
sympathetic activity decreased significantly to the normal range. This
reduction in sympathetic activity was maintained for 6 months.
Therefore, valvuloplasty appears to normalize increased levels of
sympathetic nerve activity in both the short and long term.
The reduction in muscle sympathetic nerve activity after mitral valvuloplasty significantly correlated with the increase in cardiac index in this study. This relationship is consistent with previous findings in patients with congestive heart failure.16 Ferguson et al24 reported that treatment of congestive heart failure with digitalis decreased muscle sympathetic nerve activity and increased cardiac output. In addition, Minami et al25 reported that cardiac surgery reduced plasma norepinephrine concentrations in patients with heart failure. Furthermore, cardiac transplantation has been reported to normalize resting plasma norepinephrine concentrations in patients with severe heart failure.26 Here again, cardiac output appears to be a major determinant of sympathetic activity.
Mitral valvuloplasty reduces left atrial and pulmonary arterial pressure, which may increase sympathetic activity through a mechanism mediated by the cardiopulmonary baroreflex. However, in our study, there was no significant correlation between the decrease in left atrial or pulmonary arterial pressure after valvuloplasty and the decrease in muscle sympathetic nerve activity after valvuloplasty. Thus, pulmonary hemodynamic changes after valvuloplasty are unlikely to affect sympathetic nerve activity. As reported previously,27 cardiopulmonary baroreflex function may not be intact in patients with mitral stenosis.
A reduction in afferent activity from the baroreceptor is considered a possible cause of sympathetic activation.10,28 In our study, baroreflex-mediated changes in heart rate and muscle sympathetic nerve activity produced by changes in arterial pressure were significantly less in patients with mitral stenosis than in normal control subjects. This suggests that the sensitivity of the arterial baroreflex, cardiopulmonary baroreflex, or both were impaired in such patients. As stated above, however, the cardiopulmonary baroreflex apparently is not intact in patients with mitral stenosis. We therefore speculate that the sensitivity of the arterial baroreflex is primarily decreased in these patients. In addition, the impaired baroreflex sensitivity was normalized after mitral valvuloplasty. Consequently, decreased baroreflex sensitivity in patients with mitral stenosis appears to be reversible. Furthermore, baroreceptor dysfunction may contribute to elevated sympathetic activity in patients with mitral stenosis, and the reduction in sympathetic activity after valvuloplasty may be related to the improvement in baroreflex sensitivity. Baroreflex sensitivity has been reported to be impaired in patients with congestive heart failure.29 In addition, cardiac transplantation in patients with severe heart failure normalized cardiac output and reversed impaired arterial baroreflex sensitivity as early as 2 weeks after the procedure.30 The relationship between impaired baroreflex sensitivity and elevated sympathetic nerve activity in patients with congestive heart failure29 is quite similar to that in patients with mitral stenosis. Thus, a reduction in cardiac output may decrease afferent activity from the baroreceptor and increase sympathetic activity.
In conclusion, central sympathetic outflow to the skeletal muscle was increased in patients with mitral stenosis. This increased sympathetic activity fell to the normal range after valvuloplasty, which increased cardiac index and baroreflex sensitivity. An improvement in baroreflex sensitivity, mainly arterial, may contribute to the normalization of sympathetic activity after valvuloplasty.
Received April 29, 1997; revision received July 29, 1997; accepted August 2, 1997.
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