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(Circulation. 1997;96:1835-1842.)
© 1997 American Heart Association, Inc.
Articles |
Impact of Acute Mental Stress on Sympathetic Nerve Activity and Regional Blood Flow in Advanced Heart Failure
Implications for `Triggering' Adverse Cardiac Events
From the Division of Cardiology, Department of Medicine, and the Division of Nuclear Medicine and Biophysics, Department of Pharmacology, University of California, Los Angeles School of Medicine (C.K.H); and the Division of Nuclear Medicine and Biophysics, Albert-Ludwigs-University, School of Medicine, Freiburg, Germany (E.U.N.).
Correspondence to Holly R. Middlekauff, MD, UCLA Department of Medicine, Division of Cardiology, 47-123 CHS, 10833 Le Conte Ave, Los Angeles, CA 90095.
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Abstract |
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Background Evidence is accumulating that specific "triggers," such as intense psychological stress, may precipitate myocardial infarction and sudden death. Patients with advanced heart failure have increased resting sympathoexcitation, which has been directly related to increased mortality. The impact of triggers on sympathetic nerve activity and regional blood flow in heart failure has not been examined in patients with heart failure.
Methods and Results Twenty-seven patients with heart failure (NYHA functional class III or IV) and 26 age-matched normal control subjects were studied. Muscle sympathetic nerve activity, heart rate, mean arterial pressure, forearm blood flow, and renal blood flow were measured during mental stress testing with mental arithmetic and Stroop color word test. Patients with heart failure had elevated levels of resting muscle sympathetic nerve activity and heart rate. Mental stress significantly increased muscle sympathetic nerve activity and heart rate in both patients with heart failure and control subjects, although the magnitude of increases tended to be blunted in patients with heart failure. Nevertheless, absolute levels of sympathetic activity in patients with heart failure remained significantly higher than levels in control subjects during mental stress. The decrease in renal blood flow in patients with heart failure was similar to that of control subjects, despite greater resting renal vasoconstriction. The increase in forearm blood flow during mental stress testing in patients with heart failure was blunted compared with that of control subjects.
Conclusions Patients with heart failure do not have augmented muscle sympathetic nerve activity responses to mental stress, despite elevated resting levels of sympathetic activity, but they do have markedly higher absolute levels of sympathetic nerve activity during mental stress as well as at rest.
Key Words: death, sudden • kidney • heart failure • nervous system, autonomic • stress
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Introduction |
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Evidence is accumulating that specific "triggers," such as intense psychological or physical stress, may precipitate myocardial infarction and sudden death.1 2 3 4 In animals and humans, acute psychological stress elicits a "defense reaction," characterized by a marked increase in sympathetic nerve activity, which may, in susceptible individuals, trigger these adverse cardiac events.5 6 7 8 9 The increase in sympathetic nerve activity in humans during mental stress is thought to reflect the balance between two opposing forces: (1) central nervous system arousal, which is sympathoexcitatory, and (2) arterial baroreflex activation, which is sympathoinhibitory.8 10
Patients with advanced heart failure have increased cardiac mortality, which has been directly related to the level of resting sympathoexcitation.11 The impact of triggers on sympathetic nerve activity in heart failure has not been investigated. Although their exposure to physical stress is often necessarily limited, patients with heart failure may be particularly likely to experience psychological stress and be susceptible to its adverse sequelae.12 13 In patients with heart failure, impaired baroreflex restraint of muscle sympathetic nerve activity and heart rate has been described,14 15 which may lead to unopposed, and thus exaggerated, increases in muscle sympathetic nerve and heart rate responses during acute episodes of mental stress. The first goal of this investigation was to test the hypothesis that acute episodes of mental stress in patients with advanced heart failure produce exaggerated sympathetic and heart rate responses.
The marked sympathetic excitation elicited during the defense reaction in animals serves to prepare the animal for "flight or fight" by increasing blood flow to skeletal muscle beds.9 16 As a result of this increase in sympathetic nerve activity, a constellation of hemodynamic responses follows, including increased heart rate, cardiac output, and mean arterial pressure, as well as decreased renal blood flow, all working in concert to increase limb (skeletal muscle) blood flow.5 6 7 8 9 16 In normal humans, the defense reaction can be elicited by standard mental stress tests.17 In patients with heart failure, in whom resting forearm and renal vasoconstriction are the rule, the regional vascular responses during mental stress may have important hemodynamic consequences but have not yet been defined. The second goal of this investigation was to test the hypothesis that acute episodes of mental stress in patients with advanced heart failure are associated with blunted forearm vasodilatation and further renal vasoconstriction.
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Methods |
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Study Population
After written informed consent was obtained, a total of 27 advanced congestive patients with heart failure and 26 age-matched normal control subjects participated in two protocols. Seventeen patients with heart failure (mean±SD age, 50.3±11.8 years) and 16 control subjects (mean age, 42.1±14.3 years, P=NS) were enrolled in the study of muscle sympathetic nerve activity and forearm blood flow during mental stress. Ten patients with heart failure (mean age, 52.1±6.9 years) and 10 control subjects (mean age, 46.7±14.1 years, P=NS) were enrolled in the study of renal cortical blood flow during mental stress. The study protocols were approved by the UCLA Human Subject Protection Committee. Control subjects were healthy as confirmed by medical history and physical examinations, complete blood count, blood urea nitrogen, and serum creatinine and were not taking medications. In patients with heart failure, the etiology of heart failure was coronary artery disease in 14 patients and idiopathic dilated cardiomyopathy in 13 patients. Medications, including vasodilators, diuretics, and digoxin, were discontinued 24 to 36 hours before the study under medical supervision in the UCLA Clinical Research Center. All patients had advanced (New York Heart Association functional class III or IV) congestive heart failure and were undergoing heart transplantation evaluation. As measured by echocardiography, quantified mean left ventricular ejection fraction was 0.27±0.08. Patients and control subjects abstained from caffeine for 24 hours before the study but otherwise were on an uncontrolled diet. These studies were performed in the postabsorptive state.
Measurements and Procedures
Muscle Sympathetic Nerve Activity
Muscle sympathetic nerve activity was directly recorded from
the peroneal nerve using the technique of
microneurography.18 19 20 21 Multiunit postganglionic muscle
sympathetic nerve recordings were made using a tungsten
microelectrode (tip diameter, 5 to 15 µm). The signals were
amplified by a factor of 50 000 to 100 000 and bandpassed filtered
(700 to 2000 Hz). For recording and analysis, nerve
activity was rectified and integrated (time constant, 0.1 second) to
obtain a mean voltage display of sympathetic nerve activity that was
recorded on paper.
Forearm Blood Flow
Forearm blood flow was measured using venous occlusion
plethysmography. The arm was elevated above the heart level. A
mercury-filled Silastic tube attached to a low-pressure transducer was
placed around the forearm and connected to a plethysmograph (Hokanson).
Sphygmomanometer cuffs were placed around the wrist and upper arm. At
15-second intervals, the upper arm cuff was inflated above venous
pressure for 7 to 8 seconds. Forearm blood flow (mL ·
min-1 · 100 mL of
tissue-1) was determined on the basis of a
minimum of four separate readings. Forearm vascular resistance (units)
was estimated by dividing mean arterial pressure (one third
of pulse pressure plus diastolic pressure) by forearm blood
flow.
Positron Emission Tomography Measurement of Renal Cortical
Blood Flow
Positron emission tomography (PET) measurement of renal cortical
blood flow has been validated in animals using the microsphere
technique.22 23 In our laboratory, PET measurement of
renal blood flow is highly reproducible, with intraindividual
variation of repeated PET measurement of renal blood flow only
2%.24
Renal cortical blood flow was measured based on dynamic PET using the blood flow agent O-15 water, as previously described.24 In brief, after obtaining a 30-minute blank scan and a 20-minute transmission image for photon attenuation correction, O-15 water emission images were acquired on a Siemens/CTI model 931/08-12 tomograph. The subjects were injected with 30 mCi of O-15 water over 30 seconds into a peripheral vein while acquisition of the serial transaxial tomographic images was started. The acquisition protocol was completed in 5 minutes and consisted of twelve 10-second, four 30-second, and one 60-second frame. Time-activity curves of the renal cortex were generated by region of interest analysis and corrected for dead time of the scanner and partial volume effects.24 Renal cortical blood flow was then estimated by fitting the time-activity curves measured by PET to the one-compartment model for O-15 water. All analyses were performed by a single investigator (E.U.N.) who was blinded to the experimental conditions. Renal cortical vascular resistance (arbitrary units) was estimated by dividing mean arterial pressure (one third of pulse pressure plus diastolic pressure) by renal cortical blood flow.
Miscellaneous Measurements
Blood pressure was monitored noninvasively from an automatic
blood pressure cuff. Heart rate was monitored continuously through lead
II of the ECG.
Mental Stress Testing
Mental stress was elicited in two ways: Stroop color word test
and mental arithmetic.17 25 During the Stroop color word
test, subjects were shown a series of names of colors written in a
different color ink from the color specified. Subjects were asked to
identify the color of the ink, not read the word. During verbally
administered mental arithmetic testing, subjects were asked to rapidly
subtract a one- or two-digit number from a three- or four-digit number,
depending on the subject's skill level. Throughout each mental stress
test, subjects were urged to work more quickly and gently chastised for
incorrect answers. Because sympathetic nerve response to mental stress
is influenced strongly by perception of task difficulty,26
each subject was asked to assess task difficulty on completion of the
protocol, using a standard five-point scale of 0, not stressful; 1,
somewhat stressful; 2, stressful; 3, very stressful; and 4, very, very
stressful.
Experimental Protocols
Protocol 1. Muscle Sympathetic Nerve Activity, Heart Rate, Mean
Arterial Pressure, and Forearm Blood Flow During Acute
Mental Stress (16 Control Subjects, 17 Patients With Heart
Failure)
All studies were performed in a quiet, temperature-controlled
(72°F) room at approximately the same time of day. The arm was
positioned for venous plethysmography, and the leg was positioned for
microneurography. After an adequate nerve recording site was
obtained, the subject rested quietly for 10 minutes. Baseline muscle
sympathetic nerve activity, blood pressure, forearm blood flow, and
heart rate were then recorded for 2 minutes. Acute mental stress
testing (either color word test or mental arithmetic) was then
performed for 4 minutes. Muscle sympathetic nerve activity, blood
pressure, forearm blood flow, and heart rate were recorded
continuously during the mental stress test and during a 4-minute
recovery period. After a 15-minute rest period to allow
physiological parameters to return to
baseline, the protocol was repeated using the other mental stress test.
The order of the mental stress tests was varied; Stroop color word test
was performed first in 19 subjects, and mental arithmetic was performed
first in 14 subjects.
Protocol 2. Renal Cortical Blood Flow During Acute Mental Stress
(10 Control Subjects, 10 Patients With Heart Failure)
Control subjects and patients with heart failure were studied in
the supine position in the PET scanner. The subject rested during the
20-minute transmission scan. Then, renal cortical blood flow was
determined with PET O-15 water as described above. Baseline
measurements of blood pressure and heart rate were made. Acute mental
stress testing with the Stroop color word test was performed for 4
minutes. At 1.5 minutes of mental stress, O-15 water was administered
for measurement of renal cortical blood flow. Blood pressure and heart
rate were measured continuously.
Statistical Analysis
Muscle sympathetic bursts were identified by visual inspection
and expressed as burst frequency (bursts per minute) and total activity
(units per minute). Statistical analysis was performed using
paired Student's t tests and two-group repeated measure
ANOVA. Absolute changes and percent changes were analyzed, and
the results were similar. The data are presented as mean±SEM
percent change or mean absolute change. Probability values of <.05
were considered statistically significant.
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Results |
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Basal Measurements
Baseline sympathetic nerve and hemodynamic data from the color word test and mental arithmetic were similar; baseline color word test data are shown on Table 1
. Muscle sympathetic nerve activity and
heart rate were significantly greater in patients with heart failure
than in control subjects, but mean arterial pressure did
not differ between the groups. Baseline renal cortical blood flow and
forearm blood flow were significantly lower in patients with heart
failure than in control subjects, and baseline renal cortical and
forearm vascular resistance were significantly greater in patients with
heart failure than in control subjects.
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Muscle Sympathetic Nerve Responses to Mental Stress
In control subjects compared with patients with heart
failure, the perception of severity of the color word test (2.5±0.8
versus 1.6±1.0, P=NS) or mental arithmetic test (1.9±0.9
versus 2.0±0.8, P=NS) was not different. During the mental
stress, muscle sympathetic nerve activity increased in both patients
with heart failure and control subjects, although the magnitude of the
increase was greater in the control subjects (Table 2, Fig 1). During
recovery from the mental stress, muscle sympathetic nerve activity
remained elevated in control subjects but not in patients with heart
failure (Table 2, Fig 1).
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During the mental stress, heart rate increased in both patients with
heart failure and control subjects, although the magnitude of the
increase tended to be greater in the control subjects (Fig 2). During recovery from mental stress,
heart rate remained elevated in patients with heart failure but
returned promptly to baseline levels in control subjects (Fig 2).
During mental stress, mean arterial pressure increased in
both control subjects and patients with heart failure (Fig 3).
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Forearm Blood Flow Responses to Mental Stress
During mental stress, forearm blood flow increased in both
patients with heart failure and control subjects, although the increase
was significantly greater in control subjects (Table 2
, Fig 4A and 4B). During mental stress, forearm
vascular resistance decreased in both patients with heart failure and
control subjects, although the decrease was greater in control subjects
(Table 2, Fig 4C and 4D).
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Renal Blood Flow Response to Mental Stress
Baseline heart rate was greater in patients with heart failure
than in control subjects (77±5 versus 62±3 bpm, P=.006),
but mean arterial pressure was not different between the
groups (85±6 versus 82±3 mm Hg, P=NS). During mental
stress, the increase in heart rate was similar between the groups
(heart failure versus control, 12±2% versus 15±4%;
P=NS), and the increase in mean arterial
pressure was similar between the groups (heart failure versus control,
9±3% versus 10±3%; P=NS). Renal cortical blood flow
decreased and renal vascular resistance increased to a similar degree
in both patients with heart failure and control subjects (Table 2, Fig 5).
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Discussion |
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The major new findings of this study are that during acute mental stress in patients with heart failure, (1) muscle sympathetic nerve activity increases despite elevated levels at baseline. The increase in muscle sympathetic nerve activity is not exaggerated, and in fact tends to be blunted, compared with that of age-matched control subjects. During recovery from mental stress, muscle sympathetic nerve activity immediately returns to baseline, which is in contrast to control subjects, in whom muscle sympathetic nerve activity remains elevated. (2) Heart rate increases during mental stress, despite elevated levels at baseline. The increase in heart rate during mental stress is not exaggerated, and in fact tends to be blunted, compared with that of control subjects, but during recovery heart rate remains elevated in patients with heart failure, which is in contrast to control subjects, in whom heart rate rapidly returns to baseline. (3) The decrease in renal blood flow and increase in renal vascular resistance is similar to that of control subjects despite greater resting renal vasoconstriction in patients with heart failure, and (4) the increase in forearm blood flow and decrease in forearm vascular resistance during mental stress testing is blunted compared with that of control subjects.
Muscle Sympathetic Nerve Activity
Acute mental stress did not elicit an exaggerated increase in
muscle sympathetic nerve activity in patients with heart failure; in
contrast, the increase in muscle sympathetic nerve activity tended to
be blunted. In prior studies, the magnitude of the increase in muscle
sympathetic nerve activity during mental stress has been found to be
most closely related to the level of perceived stress, increasing with
increased perception of task difficulty.26 In our study,
perception of stress during the color word test tended to be less in
the patients with heart failure than in the control subjects, but the
difference was not significant. There was no difference in perceived
stress between patients with heart failure and control subjects during
mental arithmetic, yet the sympathetic responses during each task were
the same. Thus, difference between stress perception seems an unlikely
explanation for the blunted sympathetic responses in patients with
heart failure.
In our study, resting muscle sympathetic nerve activity was markedly increased in patients with heart failure compared with control subjects, a finding that is in agreement with numerous earlier studies.20 27 28 It is possible that sympathetic nerve activity at rest in patients with heart failure is at near-maximal levels and therefore unable to increase further, despite an acute excitatory stimulus. However, several other investigators have demonstrated that during the cold pressor test, which is another sympathoexcitatory maneuver independent of the baroreflexes, the capacity for further significant sympathetic activation is preserved in patients with heart failure. During the cold pressor test, the increase in sympathetic nerve activity in patients with heart failure is not blunted compared with that in control subjects.29 30
Although the magnitude of the increase in muscle sympathetic nerve
activity is not exaggerated, and in fact tends to be blunted, in
patients with heart failure compared with control subjects during acute
mental stress testing, the absolute level of muscle sympathetic nerve
activity attained during mental stress is markedly increased in heart
failure compared with control subjects (Table 2). These extremely high
absolute levels of muscle sympathetic nerve activity during mental
stress contribute to systemic vasoconstriction and to circulating
levels of plasma norepinephrine and thus may contribute to
cardiac adrenergic activation. In addition, Wallin and
colleagues31 reported a close correlation between muscle
sympathetic nerve activity and cardiac sympathetic activation
(estimated by cardiac norepinephrine spillover) at rest
and during acute mental stress. Thus, marked increases in muscle
sympathetic nerve activity in patients with heart failure may have
important implications for the cardiac manifestations of acute mental
stress.
Heart Rate
In our study, heart rate increased during mental stress in both
patients with heart failure and control subjects, although the
magnitude of increase in heart rate tended to be greater in the control
subjects. This pattern mirrors the pattern of muscle sympathetic nerve
activity during mental stress in patients with heart failure compared
with control subjects.
During recovery, however, there was a dissociation of heart rate and muscle sympathetic nerve activity. In control subjects during recovery, muscle sympathetic nerve activity remained elevated, in contrast to heart rate, which rapidly returned to baseline. In heart failure, heart rate and muscle sympathetic nerve activity were also dissociated but in the opposite fashion; that is, during recovery, muscle sympathetic nerve activity returned rapidly to baseline, but heart rate remained elevated. During mental stress, neural regulation of heart rate in patients with heart failure and control subjects may differ. In control subjects, the rise in heart rate during mental stress and its rapid return to basal levels during recovery may reflect fluctuations in cardiac vagal activity. In patients with heart failure, cardiac vagal activity is attenuated; therefore, a blunted recovery of heart rate would be predicted. In patients with heart failure, the rise in heart rate during mental stress and its slow return to baseline during recovery may be sympathetically mediated. During recovery from exercise in control subjects and patients with heart failure, the rate of recovery of heart rate to basal levels is directly related to restoration of cardiac vagal tone.32 Slow restoration of baseline heart rate after exercise is associated with low intrinsic cardiac vagal nerve activity at rest.32 During acute mental stress in patients with heart failure, cardiac sympathetic nerve activity is increased, and the already diminished cardiac vagal activity is virtually eliminated. This acute combination of autonomic factors may trigger life-threatening events in susceptible patients with heart failure.
Renal Cortical Blood Flow
Renal cortical blood flow was markedly diminished and renal
cortical vascular resistance was markedly elevated at rest in patients
with heart failure compared with control subjects. In animal studies
during mental stress, acute renal vasoconstriction is the
rule.5 16 To date, the renal blood flow response during
acute mental stress has not been measured in humans due to the
technical difficulties in measuring rapid changes in renal blood flow.
Using dynamic PET imaging with the blood flow agent O-15
water,22 23 24 we found that during acute mental stress
testing in humans, renal cortical blood flow decreased and renal
cortical vascular resistance increased. In patients with heart failure,
despite resting renal vasoconstriction, we found that during acute
mental stress the decrease in renal blood flow and increase in renal
vascular resistance was marked; in fact, it was not different from the
degree of renal vasoconstriction evoked in control subjects, in whom
basal renal cortical blood flow was almost twice that of patients with
heart failure. Renal sympathetic nerve activity is increased at rest in
patients with heart failure, often in association with activation of
the renin-angiotensin system, leading to renal
vasoconstriction, fluid retention, and progressive heart failure
symptoms. Our results demonstrate that mental stress exacerbates this
renal vasoconstriction in heart failure, contributing to the
neurohumoral and circulatory abnormalities that characterize heart
failure.
Forearm Blood Flow
In our study, resting forearm blood flow in patients with heart
failure was diminished, which is consistent with findings
reported in numerous earlier studies.33 34 Although both
patients with heart failure and control subjects responded with an
increase in forearm blood flow and decrease in forearm vascular
resistance during mental stress, this response was
blunted in patients with heart failure. In animals and humans during
acute mental stress, an immediate and dramatic increase in limb
(skeletal muscle) blood flow is characteristic.9 16 This
prompt vasodilatation in humans is blocked by atropine,
consistent with an effect mediated by cholinergic vasodilator
nerves. Dietz and colleagues35 recently reported that the
nitric oxide synthase blocker
NG-monomethyl-L-arginine
blunted blood flow response to mental stress in normal humans and that
both
NG-monomethyl-L-arginine and
atropine caused a greater reduction in forearm blood flow than atropine
alone. These investigators concluded that the rapid forearm
vasodilation that occurs at the onset of mental stress is likely
mediated by cholinergic stimulation of the vascular
endothelium.35 In patients with heart
failure, abnormalities of forearm blood flow and
endothelial function have been described at rest and in
response to specific stimuli, such as exercise.34 36 We
speculate that the blunted increase in forearm blood flow during acute
mental stress is attributable to abnormalities either of cholinergic
neural activation during mental stress, endothelial
release of nitric oxide, or both.
Study Limitations
In this study, we did not measure cardiac sympathetic nerve
activity directly and instead have used muscle sympathetic nerve
activity as an estimate of cardiac sympathetic nerve activity. Muscle
sympathetic nerve activity is highly correlated to cardiac
norepinephrine spillover at rest, and changes in muscle
sympathetic nerve activity and cardiac norepinephrine
spillover during mental stress are qualitatively
similar.31
In summary, during mental stress in patients with heart failure, muscle sympathetic nerve activity increases significantly, despite already increased levels at rest. This increase in muscle sympathetic nerve activity is not exaggerated, and in fact tends to be blunted, compared with that of age-matched control subjects. Nevertheless, absolute levels of muscle sympathetic nerve activity in patients with heart failure at rest were significantly higher than the peak levels of muscle sympathetic nerve activity in control subjects during acute mental stress. In patients with heart failure, heart rate also increases during mental stress and remains elevated during recovery, likely indicative of an increased cardiac sympathetic nerve activity and attenuated return of cardiac vagal activity. In addition, despite basal renal vasoconstriction at rest, renal blood flow decreases further during mental stress. The augmentation of forearm blood flow produced during mental stress in patients with heart failure is blunted compared with that of control subjects. Thus, acute mental stress in patients with heart failure is associated with adverse autonomic and hemodynamic responses, with potentially deleterious clinical sequelae.
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Acknowledgments |
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This work was supported in part by US Public Health Services grant M01-RR-00865-20S1A1 (Dr Middlekauff) and the Laubisch Fund (Dr Middlekauff). Dr Negrao was supported by FAPESP, Heart Institute–HCFMUSP, and the University of San Paulo. The authors are indebted to Leila Terada and Julie A. Walden, MN, for facilitating patient enrollment; to the PET technologists for performing the PET scanning; and to the nurses and staff of the UCLA Clinical Research Center for excellent patient care.
Received December 16, 1996; revision received April 21, 1997; accepted April 28, 1997.
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