(Circulation. 2001;103:96.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Effect of P-Wave Timing During Supraventricular Tachycardia on the Hemodynamic and Sympathetic Neural Response
From the University of Texas Southwestern Medical Center and Dallas Veterans Affairs Medical Center (M.H.H., J.D.Z., R.L.P., C.J.S., M.M.A., J.A.J.), Dallas, Tex; and University of North Texas Health Science Center at Fort Worth (S.L.W., M.L.S.), Department of Integrative Physiology, Fort Worth, Tex.
Correspondence to Mohamed H. Hamdan, MD, Dallas VA Medical Center, Division of Cardiology (111A), 4500 S Lancaster Rd, Dallas, TX 75216. E-mail Hamdan{at}ryburn.swmed.edu44195
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Background—Previous studies have shown the importance of the timing of atrial and ventricular systole on the hemodynamic response during supraventricular tachycardia (SVT). However, the reflex changes in autonomic tone during SVT remain poorly understood.
Methods and Results—Eleven patients with permanent dual-chamber pacemakers were enrolled in the study. Arterial blood pressure (BP), central venous pressure (CVP), and peripheral muscle sympathetic nerve activity (SNA) were recorded during DDD pacing at a rate of 175 bpm (cycle length 343 ms) with an atrioventricular (AV) interval of 30, 200 and 110 ms, simulating tachycardia with near-simultaneous atrial and ventricular systole, short-RP tachycardia (RP<PR), and long-RP tachycardia (RP>PR). Each pacing run was performed for 3 minutes separated by a 5-minute recovery period. All patients demonstrated an abrupt fall in BP, an increase in CVP, and an increase in SNA regardless of the AV interval. The decreases in SBP, DBP, and MAP and the increase in CVP were significantly less during long-RP tachycardia (AV interval 110 ms) than during the other 2 pacing modes (P<0.05), and the increase in SNA in 7 of the 11 patients was significantly greater during closely coupled atrial and ventricular systole than during long-RP tachycardia (P<0.05).
Conclusions—These data suggest that the superior maintenance of hemodynamic stability during long-RP tachycardia is accompanied by reduced sympathoexcitation, which is primarily mediated by the arterial baroreceptors, with a modest cardiopulmonary vasodepressor effect.
Key Words: pacing • nervous system, autonomic
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Supraventricular tachycardia (SVT) may result in disabling symptoms such as palpitations and shortness of breath, or it may be scarcely noticed. Hemodynamic tolerance of SVT is dependent on heart rate, ventricular performance, loading conditions, atrioventricular (AV) coupling, and autonomic nervous system–regulatory mechanisms. Previous studies have shown the importance of the timing of atrial and ventricular systole on blood pressure (BP), central venous pressure (CVP) and cardiac output.1 2 3 4 5 These studies demonstrated a greater fall in BP and cardiac output with closely coupled atrial and ventricular systole. However, the reflex changes in autonomic tone during tachycardia, in particular during simultaneous atrial and ventricular contractions, remain poorly understood. Although the fall in BP during SVT unloads extracardiac baroreceptors, resulting in a reflex increase in sympathetic nerve activity (SNA), the increase in cardiac filling pressures activates cardiac mechanoreceptors, leading to a reflex withdrawal of sympathetic tone. Furthermore, an atrial vasodepressor reflex triggered by the atrial contraction against closed AV valves has been suggested but remains unproved.6
The purpose of the present study was to examine the effect of atrial timing during simulated tachycardia on the hemodynamic and sympathetic neural responses. Two hypotheses were tested: (1) superior arterial BP maintenance during long-RP tachycardia (RP>PR) produces a reduced sympathoexcitation relative to short-RP tachycardia (RP<PR) and tachycardia with near-simultaneous atrial and ventricular systole and (2) tachycardia with near-simultaneous atrial and ventricular systole produces a vasodepressor effect that may be mediated by atrial receptors. Rapid dual-chamber pacing with varying AV intervals was performed to simulate SVT with almost simultaneous atrial and ventricular systole and short-RP and long-RP tachycardia. Arterial BP, CVP, and peripheral muscle SNA were continuously recorded during these interventions.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Study Patients
The study was performed at the Dallas Veterans Affairs Medical Center and Parkland Memorial Hospital. Both institutional review boards approved the study. Informed consent was obtained from all patients, and all procedures were in accordance with institutional guidelines. All patients with a dual-chamber pacemaker (Medtronic pacemaker models 7088 and 7960) were screened for the study. Patients were excluded if they had neuropathy, NYHA class III or IV congestive heart failure, recent myocardial infarction, or unstable angina. All patients had an echocardiogram performed within 6 months of the study to determine left ventricular function and chamber sizes. A total of 12 patients were enrolled. One patient developed atrial fibrillation soon after the first pacing sequence and therefore was excluded. The data for the remaining 11 patients form the material of this study.
Measurements
Patients were studied in the drug-free postabsorptive
state after informed consent was obtained. Efferent postganglionic
muscle SNA was recorded from the right peroneal nerve as
previously described.7
Briefly, a sterile microelectrode was inserted into a fascicle of the
peroneal nerve near the fibular head. The nerve signals were amplified,
filtered (700 to 2000 Hz), rectified, and discriminated. Raw nerve
signals were integrated to produce a mean voltage display for
quantitative analysis. The SNA was quantified as the total activity
derived from the sum of the area of the SNA bursts for a given time
period. Finger arterial BP was continuously monitored and recorded
according to the Penaz volume-clamp
method8 9 10
with a finger cuff (Ohmeda Monitoring System). CVP was continuously
recorded with a catheter placed in the superior vena cava via the right
antecubital vein. Heart rate was derived from continuous ECG recording
of 
2 leads.
Experimental Protocol
After adequate CVP, BP, and SNA recordings were
obtained, the following protocol was performed. The order of the 3
pacing runs (with different AV intervals) was randomized:
- 1. Baseline
measurements for a period of 5 minutes.
- 2. Dual-chamber pacing (DDD) at a
rate of 175 bpm (cycle length 343 ms) with an AV interval of 30 ms
(simulating tachycardia with near-simultaneous atrial and ventricular
systole).
- 3. Recovery for 5
minutes.
- 4. Dual-chamber pacing (DDD) at a rate of 175
bpm (cycle length 343 ms) with an AV interval of 200 ms for 3 minutes
(simulating short-RP tachycardia).
- 5. Recovery for 5
minutes.
- 6. Dual-chamber pacing (DDD) at a rate of 175
bpm (cycle length 343 ms) with an AV interval of 110 ms for 3 minutes
(simulating long-RP tachycardia).
- 7. Recovery for 5
minutes.
SNA, BP, and CVP were measured continuously
during the study. Data were analyzed during the last minutes of
recovery and pacing with each AV interval. Pacing was always done at
maximum output, and capture was confirmed through analysis of the
12-lead ECG. In addition to the hemodynamic and autonomic measurements,
arterial baroreflex-SNA gain was calculated during each pacing mode.
The gain was estimated from the initial changes in diastolic BP (DBP)
and SNA at the nadir of arterial BP in the first 20 seconds of each
pacing run (gain=
SNA/DBP).
Data Analysis
All data sets passed a test for normality with a
Smirnov-Komolgorov test; therefore, the following parametric tests were
used. A 1-way ANOVA with repeated measures design was used for all
comparisons between the 3 AV intervals for baseline data and the
hemodynamic changes during pacing. When a significant main effect was
obtained, the specific differences were determined through the
application of a least significant difference post hoc test.
Correlation analyses were performed by determination of the Pearson
linear correlation coefficients, and a forward progression stepwise
regression model was used to assess the relative contribution of
changes in hemodynamic variables to the SNA responses. For all tests,
statistical significance was set a priori at an 
level of
0.05.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Clinical Characteristics
All subjects were men with a mean age of 63±10 years. Left ventricular function was normal in 7 patients, mildly depressed in 2, and moderately depressed in 2. The clinical characteristics of all subjects, including the indications for pacing, are summarized in Table 1
.
|
Hemodynamic Response
Hemodynamic data were obtained for all 11 patients. The
results of dual-chamber pacing at baseline and during each AV interval
are shown in
Table 2. All values shown are at steady state. At the onset
of pacing, all patients demonstrated an abrupt fall in BP regardless of
the AV interval. After 30 to 60 seconds, BP gradually recovered and
reached a new baseline below the resting state
(Figure 1). The average changes in SBP, DBP, and mean
arterial BP (MAP) are summarized in
Figure 2. The decreases in SBP, DBP, and MAP were all
significantly less during long-RP tachycardia (AV interval 110 ms) than
during the other 2 pacing modes
(P<0.05). An abrupt increase
in CVP was noted at the onset of pacing regardless of the AV interval,
with a gradual decrease to a new baseline above the resting state. The
changes in CVP during pacing are summarized in
Figure 2. Similar to arterial BPs, the increase in CVP
during long-RP tachycardia (AV interval 110 ms) was significantly less
than during the other 2 pacing modes
(P<0.05). When pacing was
terminated, both arterial BP and CVP returned to prepacing levels
within 30 seconds. For all pacing conditions, the change in MAP
correlated inversely with the change in CVP
(r2=0.88,
P<0.001).
|
|
|
SNA Determination
SNA was obtained in 7 patients. In the remaining 4, the
data were discarded because of decreased signal-to-noise ratio or loss
of recording site during the study. SNA rose abruptly in all patients
with the onset of pacing and reached a steady state after 30 to 60
seconds
(Figure 1
). The percent change in SNA from baseline with
near-simultaneous atrial and ventricular systole or short-RP and
long-RP tachycardia was 39±11%, 52±13%, and 18±9%, respectively
(P<0.05). A summary of the
changes in SNA during pacing with different AV intervals is provided in
Figure 2. The increase in SNA was significantly less during
long-RP tachycardia (AV interval 110 ms) than during the other 2 pacing
modes (P<0.05). There was no
statistical difference between short-RP tachycardia and
near-simultaneous atrial and ventricular pacing
(P=0.21). However, this was
limited by a low statistical power (0.69). SNA returned to prepacing
baseline levels within 1 minute of termination of pacing. There was no
statistical significance between SNA at baseline and that at 1 minute
after pacing
(P<0.001).
The relative roles of arterial BP and CVP in the SNA
responses were assessed with a stepwise regression model. In the first
step of the forward regression model, DBP was entered with an
r2
value of 0.77 (P<0.001). In
the second step, CVP was entered and the
r2
value was increased to 0.89
(P<0.001). The slope estimates
for the regression model were -3.3 for DBP and -0.8 for
CVP.
Baroreflex Gain
Arterial baroreflex-SNA gain estimates tended to be
greater during long-RP tachycardia (1.4±0.7%/mm Hg) than during
short-RP tachycardia (1.1±0.7%/mm Hg) and during tachycardia with
near-simultaneous atrial and ventricular systole (0.9±0.6%/mm Hg),
but this trend was not significant
(P=0.22). For all pacing
conditions, the arterial baroreflex-SNA gain correlated modestly with
the change in CVP
(r2=0.39,
P=0.13), suggesting that a
modest vasodepressor effect of the increased cardiac filling
occurred.
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The major findings of the present study are that (1) SNA increased during all pacing modes, with the largest increase occurring during closely coupled atrial and ventricular systole; (2) the changes in SNA seem to parallel the changes in BP, suggesting a predominant arterial baroreflex control of sympathoexcitation with a modest cardiopulmonary vasodepressor effect; and (3) the lack of significant differences in SNA between tachycardia with near-simultaneous atrial and ventricular systole and short-RP tachycardia suggests that an atrial vasodepressor response does not appear to play an important role in SNA responses.
Hemodynamic Changes During SVT
The hemodynamic effects of SVT have been reported
previously in
detail.4 5 11 12
In summary, tachycardias, regardless of their mechanisms or cause,
result in decreased diastolic filling, stroke volume, and cardiac
output. The results are a decrease in BP and pulse pressure, which is
directly related to the tachycardia rate, cardiac function, and AV
synchrony. At any given rate, the timing of atrial systole has been
shown to alter the hemodynamic
response.1 11
Several authors have shown that closely coupled atrial and ventricular
systole results in increases in atrial pressures, A-wave magnitude, and
pulmonary pressure and decreases in cardiac index and
BP.4 12 13
The first combined electrophysiological and hemodynamic study that
assessed the hemodynamic consequences of SVT in which patients served
as their own control was reported by Goldreyer et
al.13 Eight patients with AV
nodal reentrant tachycardia were studied at baseline and during induced
tachycardia. Right atrial and pulmonary artery pressures increased
during SVT, whereas cardiac index and BP decreased. In addition, the
authors observed large atrial waves during tachycardia, presumably due
to atrial contraction against closed tricuspid valves. Subsequently,
several
authors11 14
demonstrated that patients with AV nodal reentrant tachycardia had
significantly higher mean and peak right atrial pressures during
tachycardia than did patients with circus movement tachycardia.
Furthermore, Sganzerla et al3
found a lesser degree of hypotension and a faster recovery of BP in
patients with atypical AV nodal reentrant tachycardia compared with
patients with typical AV nodal reentrant tachycardia. They attributed
these findings to the temporal relationship between atrial and
ventricular systole.
Our findings are consistent with these previous studies. We found that long-RP tachycardia was associated with the least drop in BP, whereas tachycardias with closely coupled atrial and ventricular systole (AV intervals 30 and 200 ms) resulted in a greater decrease in BP. Similarly, the increase in CVP was least with long-RP tachycardia and greatest with the other tachycardias. Therefore, in the present study, the autonomic responses to simulated SVT, as discussed later, are relevant to the previous experimental and clinical studies of hemodynamic function.
Autonomic Changes During SVT
During SVT, the fall in BP reduces the stretch on
the arterial baroreceptors, resulting in a decrease in the afferent
nerve traffic to the vasomotor centers. This in turn augments
sympathetic efferent tone and withdraws vagal efferent
tone.15 16
Previously, the evidence for activation of the sympathetic tone was
indirect and only qualitative as suggested by (1) BP recovery during
sustained tachycardia and (2) a brisk overshoot of the BP after
tachycardia
termination.17 18
Although the fall in BP during tachycardia leads to a reflex increase
in sympathetic activity through extracardiac
baroreceptors,15 16
the increase in cardiac filling pressures may result in opposite
effects.17 18 The
increase in filling pressure activates the cardiac mechanoreceptors,
leading to reflex withdrawal of sympathetic tone. We have previously
shown in humans that arterial baroreflex control predominates in
mediation of sympathoexcitation during ventricular
tachycardia19 and that
baroreflex gain predicts BP recovery during sustained ventricular
tachycardia.20 However, the
relative roles of cardiopulmonary and arterial baroreceptors in the
control of SNA and arterial BP during SVT and the effect of AV coupling
on these responses remain unknown. Leitch et
al12 explored the mechanism
of syncope in 22 patients with SVT. The authors found that the
tachycardia cycle length tended to be longer in patients with syncope
than in patients without syncope and that the former group had a
propensity toward vasodepressor syncope. They postulated that the
slower tachycardia rate might be related to inappropriate stimulation
of left ventricular stretch receptors by the reduced left ventricular
volume and increased adrenergic tone, similar to what is seen with
vasovagal syncope. In that study, the tachycardia rate was used as a
surrogate for sympathetic activity.
In the present study, we directly measured SNA
responses to address the role of arterial and cardiopulmonary
baroreceptors in the control of SNA when AV coupling is altered. We
found a significant increase in sympathetic activity during rapid
pacing with all 3 AV intervals. This was associated with a decrease in
BP and an increase in CVP. The increase in sympathetic tone despite an
increase in filling pressures suggests that the sympathetic response is
mainly mediated by the arterial baroreceptors and that the contribution
of the cardiopulmonary baroreceptors is minimal. This was further
demonstrated by the presence of a greater increase in sympathetic
activity during closely coupled atrial and ventricular systole compared
with long-RP tachycardias despite higher cardiac filling pressures.
Nevertheless, a greater role of cardiopulmonary baroreceptors in the
decrease in SNA may be implied by these data because of the large
decrease in arterial BP. A 20- to 30-mm Hg decrease in MAP alone would
be expected to produce a much greater increase in SNA than the 40% to
60% increase that we observed. Previous studies have shown that 15- to
20-mm Hg changes in MAP produced by nitroprusside infusion, lower body
negative pressure, or ventricular pacing will elicit increases in SNA
of 100% to
200%.19 21 22 23
We previously showed a prominent role of arterial baroreceptor control
of SNA during ventricular pacing in which the decreases in MAP were
modest.19 The lack of a
greater increase in SNA in the present study in which the decrease in
MAP averaged >20 mm Hg may imply a greater cardiopulmonary baroreflex
sympathoinhibition, or it may reflect an impairment in the arterial
baroreflex control of SNA in these patients.
Is There an Atrial Vasodepressor
Response?
The presence of an atrial vasodepressor response
triggered by large atrial waves during simultaneous atrial and
ventricular contractions has been suggested but remains
unproved.6 24 This
reflex has been implied as a potential cause of hypotension during
ventricular pacing. Erlebacher et
al6 found that the presence
of cannon A waves during ventricular pacing was associated with a
relative decrease in systemic vascular resistance with a significant
decrease in BP. The authors concluded that the hypotension was
primarily due to a vasodepressor reflex initiated by left atrial cannon
A waves.
During SVT, the A and V waves tend to be fused, giving rise to large atrial waves. These waves tend to be larger with closely coupled atrial and ventricular systole and are usually associated with a higher CVP and a lower BP. The present study was not designed to assess the presence of an atrial vasodepressor reflex. However, we have seen a greater increase in SNA during pacing with closely coupled atrial and ventricular systole compared with long-RP tachycardia, suggesting the predominance of arterially mediated sympathoexcitation. On the other hand, the difference between nearly simultaneous atrial and ventricular systole and short-RP tachycardia was not significant (P=0.21), although it was limited by a relatively low statistical power (0.69). The lack of differences in CVP between the conditions also limits the conclusions that can be made regarding an atrial vasodepressor effect. The stepwise regression model does provide some suggestion that there was a very modest vasodepressor effect; however, we cannot discern whether this was mediated specifically by atrial receptors. Our findings of a lesser arterial baroreflex-SNA gain during closely coupled atrial and ventricular systole compared with long-RP tachycardia also suggest a modest vasodepressor effect of the increased cardiac filling yet do not confirm or negate the presence of an atrial vasodepressor response.
Conclusions
Our data suggest that arterial baroreflex control
predominates in mediation of sympathoexcitation during rapid AV
sequential pacing regardless of the AV interval, with only modest
contribution of the cardiopulmonary baroreceptors. In addition, we
found a greater hemodynamic response with long-RP tachycardia compared
with pacing with closely coupled atrial and ventricular systole.
Finally, the existence of an atrial vasodepressor reflex was suggested
by a reduced baroreflex-SNA gain during simultaneous atrial and
ventricular pacing, but the importance of this effect appeared to be
minimal.
|
Acknowledgments |
|---|
This work was supported in part by a Medtronic fund (to M.H.H.) and NIH grant HL-49266 (to M.L.S.).
Received June 21, 2000; revision received August 11, 2000; accepted August 14, 2000.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. 1. Skinner N, Mitchell J, Wallace A, et al. Hemodynamic effects of altering the timing of atrial systole. Am J Physiol. 1963;205:499–503.
2. Naito M, Dreifus L, David D, et al. Reevaluation of the role of atrial systole to cardiac hemodynamics: evidence for pulmonary venous regurgitation during abnormal atrioventricular sequencing. Am Heart J. 1983;105:295–302.[Medline] [Order article via Infotrieve]
3.
Sganzerla P,
Fabbiocchi F, Grazi S, et al. Electrophysiologic and haemodynamic
correlates in supraventricular tachycardia.
Eur Heart J. 1989;10:32–39.
4. Gohl KP, Wortmann A, Bachmann K. Haemodynamic analysis of atrioventricular tachycardia. Eur Heart J. 1992;13(suppl E):99–103.
5.
Chen Y, Chen S, Tai
C, et al. Role of atrial electrophysiology and autonomic nervous system
in patients with supraventricular tachycardia and paroxysmal atrial
fibrillation. J Am Coll
Cardiol. 1998;32:732–738.
6. Erlebacher J, Danner R, Stelzer P. Hypotension with ventricular pacing: an atrial vasodepressor reflex in human beings. J Am Coll Cardiol. 1984;4:550–555.[Abstract]
7. Wallin BG, Eckberg DL. Sympathetic transients caused by abrupt alterations of carotid baroreceptor activity in humans. Am J Physiol. 1982;242:H185–H190.
8. Molhoek GP, Wesseling KH, Settels JJ, et al. Evaluation of the Penaz servo-plethysmo-manometer for the continuous, non-invasive measurement of finger blood pressure. Basic Res Cardiol. 1984;79:518–609.
9. Imholz BPM, Van Montfrans GA, Settels JJ, et al. Continuous non-invasive blood pressure monitoring. Cardiovasc Res. 1988;22:390–397.[Medline] [Order article via Infotrieve]
10. Friedman DB, Jensen FB, Matzen S, et al. Non-invasive blood pressure monitoring during head-up tilt using the Penaz principle. Acta Anaesthesiol Scand. 1990;34:519–522.[Medline] [Order article via Infotrieve]
11.
Klein L, Miles W,
Zipes D. Effect of atrioventricular interval during pacing or
reciprocating tachycardia on atrial size, pressure, and refractory
period. Circulation. 1990;82:60–68.
12.
Leitch J, Klein
G, Yee R, et al. Syncope associated with supraventricular tachycardia.
Circulation. 1992;85:1064–1071.
13.
Goldreyer B,
Kastor J, Kershbaum K. The hemodynamic effects of induced
supraventricular tachycardia in man.
Circulation. 1976;54:783–789.
14. Gursoy S, Steurer G, Brugada J, et al. Brief report: the hemodynamic mechanism of pounding in the neck in atrioventricular nodal reentrant tachycardia. N Engl J Med. 1992;327:772–774.[Medline] [Order article via Infotrieve]
15.
Mancia G, Ferrari
A, Gregorini L, et al. Circulatory reflexes from carotid and
extracarotid baroreceptors areas in man.
Circ Res. 1977;41:309–315.
16.
Scher AM. Carotid
and aortic regulation of arterial blood pressure.
Circulation. 1977;56:521–528.
17. Thoren P. Role of cardiac vagal C-fibers in cardiovascular control. Rev Physiol Biochem Pharmacol. 1979;86:1–94.[Medline] [Order article via Infotrieve]
18. Bishop VS, Malliani A, Thoren P. Cardiac mechanoreceptors. In: Shepherd JT, Abboud FM, Geiger SR, eds. Handbook of Physiology: The Cardiovascular System. Baltimore, Md: Williams & Wilkins; 1983:497–556.
19. Smith ML, Joglar JA, Wasmund SL, et al. Reflex control of sympathetic activity during simulated ventricular tachycardia in humans. Circulation. 1999;99:628–634.
20. Hamdan MH, Joglar JA, Page RL, et al. Baroreflex gain predicts blood pressure recovery during simulated ventricular tachycardia in humans. Circulation. 1999;99:381–386.
21.
Sundlof G, Wallin
BG. Effect of lower body negative pressure on human muscle nerve
sympathetic activity. J
Physiol. 1978;278:525–532.
22. Smith ML, Ellenbogen KA, Eckberg DL. Human sympathetic neural responses to induced ventricular tachycardia. J Am Coll Cardiol. 1991;18:1015–1024.[Abstract]
23. Dibner-Dunlap ME, Smith ML, Thames MD. Enalaprilat augments arterial and cardiopulmonary baroreflex control of sympathetic nerve activity in patients with heart failure. J Am Coll Cardiol. 1996;27:358–364.[Abstract]
24. Alicandri C, Fouad FM, Tarazi RC, et al. Three cases of hypotension and syncope with ventricular pacing: possible role of atrial reflexes. Am J Cardiol. 1978;42:137–142.[Medline] [Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  N. M. Segerson, S. L. Wasmund, M. Daccarett, M. L. Fabela, C. H. Hammond, G. Stoddard, M. L. Smith, and M. H. Hamdan The acute effect of atrioventricular pacing on sympathetic nerve activity in patients with normal and depressed left ventricular function Am J Physiol Heart Circ Physiol, September 1, 2008; 295(3): H1076 - H1080. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. L. Wasmund, J.-M. Li, R. L. Page, J. A. Joglar, R. C. Kowal, M. L. Smith, and M. H. Hamdan Effect of Atrial Fibrillation and an Irregular Ventricular Response on Sympathetic Nerve Activity in Human Subjects Circulation, April 22, 2003; 107(15): 2011 - 2015. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. S. Takata, S. L. Wasmund, M. L. Smith, J.-M. Li, J. A. Joglar, K. Banks, R. C. Kowal, R. L. Page, and M. H. Hamdan Serotonin Reuptake Inhibitor (Paxil) Does Not Prevent the Vasovagal Reaction Associated With Carotid Sinus Massage and/or Lower Body Negative Pressure in Healthy Volunteers Circulation, September 17, 2002; 106(12): 1500 - 1504. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||