(Circulation. 2000;102:1027.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Biventricular Pacing Decreases Sympathetic Activity Compared With Right Ventricular Pacing in Patients With Depressed Ejection Fraction
From the University of Texas Southwestern Medical Center and Dallas Veterans Affairs Medical Center (M.H.H., J.D.Z., J.A.J., C.J.S., K.R., R.L.P.), Dallas, Tex, and Department of Integrative Physiology (J.F.E., M.L.S.), University of North Texas Health Science Center at Fort Worth.
Correspondence to Mohamed H. Hamdan, MD, Dallas VA Medical Center, Division of Cardiology (111A), 4500 S Lancaster Road, Dallas, TX 75216. E-mail Hamdan{at}ryburn.swmed.edu
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Abstract |
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Background—Although there have been few studies in which the hemodynamic effects of right ventricular (RV) and left ventricular (LV) pacing were compared with those of biventricular (BV) pacing, the autonomic changes during these different pacing modes remain unknown. We hypothesized that BV pacing results in improved hemodynamics and a decrease in sympathetic nerve activity (SNA) compared with single-site pacing.
Methods and Results—Thirteen men with a mean ejection fraction of 0.28±0.7 were enrolled in the study. Arterial blood pressure (BP), central venous pressure (CVP), and SNA were recorded during 3 minutes of right atrial (RA)-RV, RA-LV, and RA-BV pacing at a rate 10 beats faster than sinus rhythm. BP was greater during LV (151±7/85±3 mm Hg) and BV (151±6/85±3 mm Hg) pacing than during RV pacing (146±7/82±3 mm Hg) (P<0.05). There were no differences in CVP among all pacing modes (P=0.27). SNA was significantly less (P<0.02) during both LV (606±35 U) and BV (582±41 U) pacing compared with RV pacing (685±32 U) (P<0.02). Although not statistically significant (P=0.08 to 0.14), there was a trend for patients with a narrow QRS to have a lower mean BP and higher SNA during LV pacing than during BV pacing (r=0.42 to 0.49).
Conclusions—LV-based pacing results in improved hemodynamics and a decrease in SNA compared with RV pacing in patients with LV dysfunction regardless of the QRS duration.
Key Words: heart failure • pacing • nervous system, autonomic
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Introduction |
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Conventional pacing of the right heart with a short atrioventricular (AV) delay was used as an adjunctive therapy in patients with drug-resistant congestive heart failure until prospective studies showed no improvement or even deterioration with pacing.1 2 3 Today, dual chamber pacing is used only for the treatment of symptomatic bradyarrhythmias. On the other hand, preliminary results with biventricular (BV) pacing have shown improvement in New York Heart Association (NYHA) functional class and exercise tolerance in patients with depressed ejection fraction and intraventricular conduction delay.4 This improvement is thought to be the result of correction of the electrical and mechanical asynchrony of the left heart. To our knowledge, few studies5 6 7 8 have compared the hemodynamic effect of single-site versus multisite pacing in patients with depressed ejection fraction, and no studies have considered the autonomic changes during these different pacing modes.
Therefore, the purpose of the present study was to compare BV pacing with right ventricular (RV) and left ventricular (LV) pacing in patients with depressed ejection fraction. Arterial blood pressure (BP), central venous pressure (CVP), and muscle sympathetic nerve activity (SNA) with microneurography were measured during sinus rhythm and single-site and multisite pacing at rates slightly above normal sinus rhythm. We hypothesized that BV pacing results in improved hemodynamics and a decrease in sympathetic activity compared with single-site pacing.
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Methods |
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Patients
The study was performed at the Dallas Veterans Affairs Medical Center and was approved by the institutional review board. Informed consent was obtained from all patients, and all procedures were conducted in accordance with institutional guidelines. All patients with a clinical indication for programmed electrical stimulation and a depressed ejection fraction (<0.35) were screened for the study. Patients were excluded if they had a history of insulin-dependent diabetes mellitus or a history or signs of peripheral neuropathy. A total of 13 patients were enrolled in the study, and the recordings from these subjects form the basis of the present study.
Experimental Protocol
After acceptable recordings of SNA were obtained, the
following protocol was performed. Arterial BP, CVP, and
sympathetic neural responses to 3 minutes of pacing were recorded
during right atrial (RA)-RV, RA-LV, and RA-BV pacing. The sequence was
chosen at random with a 1-minute recovery time and a 1-minute repeat
baseline value obtained between each pacing mode.
Electrophysiological Studies
Patients were studied in the drug-free postabsorptive state
after informed consent was obtained. Three quadripolar catheters were
inserted percutaneously and positioned in the high
lateral RA, RV apex, and across the tricuspid valve for His-bundle
recording. Next, a 2.5F multipolar catheter (Cardima Inc) was
introduced from the femoral vein via a guiding catheter and positioned
in the lateral cardiac vein for LV pacing. Atrial and
ventricular pacing thresholds were then measured, and
pacing was performed at twice diastolic pacing
threshold.
Measurements
Efferent, postganglionic muscle SNA was recorded from the
right peroneal nerve as previously described. Briefly, a sterile
microelectrode was inserted into a fascicle of the peroneal nerve near
the fibular head. The nerve signals were amplified, filtered (70 to
2000 Hz), rectified, and discriminated. Raw nerve signals were
integrated (time constant 0.05 s) to produce a mean voltage
display for quantitative analysis. Muscle sympathetic neural
bursts during sinus rhythm were readily recognized by their tight
temporal relationship to the sinus cardiac cycle, their increasing
frequency during Valsalva maneuvers, the occurrence of large bursts
accompanying premature ventricular beats, and their failure
to respond to arousal stimuli or stroking of the skin. The SNA was
quantified as the total activity derived from the sum of the area of
the SNA bursts for a given time period. Area was used for these
analyses because compared with the burst amplitude, it more
appropriately reflects the changes in SNA associated with the wide
variations in arterial BP that can occur during
ventricular pacing. Arterial BP was directly
recorded with a 5F catheter inserted into the right femoral artery.
CVP was continuously recorded with a catheter placed in the right
atrium via the right femoral vein. Heart rate (HR) was derived from
continuous ECG recording of at least 2 leads (typically leads
II and V1).
Statistics
All data sets were tested for normality with a
Kolmogorov-Smirnov test. Group comparisons of RV, LV, and BV pacing
were performed with a 1-way ANOVA with a repeated measure design. When
main effect differences were obtained, post hoc comparisons were
performed with a Tukey’s multiple range test to distinguish individual
differences between pacing conditions. A rank sum test was used for
post hoc comparisons in which normality failed. A linear regression was
used to assess the relation of QRS duration to the difference between
LV and BV pacing for each variable. For all analyses,
significance was set at an 
level of 0.05.
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Results |
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Patient Characteristics
All patients were men with a mean age of 66±8 years. The mean ejection fraction was 0.28±0.07, with coronary artery disease present in all patients except 1. Baseline ECG revealed a wide spectrum of intraventricular conduction delay with a mean QRS duration of 123±31 ms. Six of 13 patients had a QRS duration of >120 ms, and 4 of these 6 patients had left bundle-branch block. A summary of patient characteristics and the ECG measurements is provided in the Table
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Hemodynamic Changes During RV, LV, and BV
Pacing
Figure 1 illustrates a sample
tracing of arterial BP, CVP, and the integrated neurogram
for SNA during each pacing mode. Arterial BPs were slightly
higher during both LV and BV pacing compared with RV pacing. The
average hemodynamic data for all patients (n=13) during
each pacing mode are summarized in Figure 2. Both LV (151±7/85±3 mm Hg) and
BV (151±6/85±3 mm Hg) pacing resulted in arterial
BPs that were greater (P<0.05) than during RV pacing
(146±7/82±3 mm Hg). There were no differences in CVP among all
pacing modes (P=0.27).
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Sympathetic Activity During RV, LV, and BV Pacing
The normal pulse synchrony of SNA bursts was maintained under all
conditions (Figure 1
).The average data during each pacing mode
are summarized in Figure 3. The
sympathetic neural responses were a mirror image of the
arterial BP responses. SNA was significantly less
(P<0.02) during both LV (606±35 U) and BV (582±41 U)
pacing compared with RV pacing (685±32 U) (P<0.02).
However, BV pacing was not significantly less than LV pacing
(P=0.56).
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Correlation Between QRS Duration and
Hemodynamic/Sympathetic Neural Responses
The patient population demonstrated a wide range of QRS durations
(from 94 to 188 ms). Although the mean data for the patient group as a
whole did not differ between LV and BV pacing, on inspection of
individual data, there appeared to be some possible differences between
LV and BV pacing when patients with a narrow QRS were compared with
those with a wide QRS. Therefore, each hemodynamic
variable and SNA were correlated against QRS duration to determine
whether differences between LV and BV pacing may exist in some
patients. Figure 4 illustrates the linear
regression analysis between QRS duration and the difference
between LV and BV pacing for mean BP (top) and SNA (bottom). Similar
results were obtained for systolic and diastolic
BPs. For each variable, there was a trend toward narrow QRS
durations with a lower mean BP and higher SNA during LV pacing compared
with during BV pacing; however, the correlation coefficient values
(range 0.42 to 0.49) were not statistically significant
(P=0.08 to 0.14).
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Discussion |
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The main findings of the present study are that (1) BV pacing results in improved hemodynamics and a decrease in sympathetic activity compared with RV pacing in patients with LV dysfunction regardless of the QRS duration and (2) the same benefits can be achieved with LV pacing alone. To the best of our knowledge, this is the first study to show that acute BV or LV pacing results in a decrease in sympathetic activity compared with RV pacing in patients with depressed ejection fraction. Increased sympathetic activity has been shown to be a negative prognostic factor in patients with congestive heart failure; therefore, if our present findings persist with long-term pacing, BV or LV pacing should be considered in patients with a depressed ejection fraction and an indication for chronic pacing.
Dual Chamber Pacing as a Treatment of Congestive Heart
Failure
The usefulness of physiological dual chamber
pacing with a short AV delay in patients with congestive heart failure
was tested more than a decade ago. Brecker et al9
demonstrated that in selected patients with shortened
diastolic filling times, AV synchronous pacing with a short
AV delay improved cardiac output and exercise duration. Pacing in these
patients was associated with an increase in diastolic
filling time and a reduction in presystolic mitral or tricuspid
regurgitation, or both. Similarly, Nishimura et
al10 showed that DDD pacing could significantly improve
cardiac performance in patients with a long PR interval and
evidence of AV dyssynchrony in the left heart. These results, however,
were soon challenged by other studies that showed no improvement or
even a decrease in cardiac performance with DDD pacing. Innes
et al1 tested the effect of AV synchronous pacing with an
AV delay of 60 and 100 ms in 12 patients with stable heart failure.
Pacing increased diastolic filling time but reduced the
stroke volume and cardiac index. Linde et al2 studied the
long-term effect of AV synchronous pacing in 10 patients with NYHA
class III or IV heart failure. Despite optimization of the AV delay
with Doppler echocardiographic measurements,
consistent improvement in stroke volume and cardiac output was
observed in only 1 patient. The interest in conventional short AV delay
DDD pacing in patients with heart failure waned as the result of a
double-blinded randomized study that showed no immediate improvement in
hemodynamics and no long-term change in ejection
fraction or NYHA functional class.11 With failure of
conventional DDD pacing to show consistent improvement in
hemodynamics in these patients, the interest has
shifted to BV pacing.
Effect of BV Pacing Versus RV Pacing on Hemodynamics
The mechanisms via which BV pacing is thought to improve
cardiac function include the following: (1) a decrease in mitral
regurgitation, (2) an increase in filling time, (3)
optimization of left-sided mechanical AV delay, and (4) normalization
of ventricular electrical activation. In patients with mild
to moderate congestive heart failure, BV pacing has been shown to
acutely improve global systolic ventricular
function, presumably by improving coordination of segmental
ventricular contraction.12 In patients with
intraventricular conduction delay, it is suggested
that BV pacing restores the normal activation pattern, resulting in a
decrease in mitral regurgitation and an improvement in
effective preload.13 Although some studies have considered
the effect of BV pacing in patients with depressed ejection fraction,
comparison between BV pacing and RV pacing has been assessed in only a
few studies.5 6 12 14 Cazeau et al5 compared
the hemodynamic effects of BV pacing with those of RV
pacing in 8 patients with widened QRS and end-stage heart failure.
Regardless of the AV delay, BV pacing was superior to RV pacing,
resulting in a higher cardiac output and a decrease in
pulmonary capillary wedge pressure and mean V-wave amplitude.
Leclercq et al6 assessed the acute
hemodynamic effects of BV pacing in 18 patients with
severe congestive heart failure and major
intraventricular conduction delay (QRS 170±37 ms).
With AAI pacing used as a reference, this acute
hemodynamic study demonstrated that BV DDD pacing
significantly improved cardiac index compared with intrinsic conduction
and single-site RV DDD pacing.
Our findings are consistent with those of these previous studies. Compared with RV pacing, BV pacing resulted in a significantly higher arterial BP with no significant change in CVP. This improvement was seen regardless of the presence or absence of intraventricular conduction delay. Thus, BV pacing was consistently superior to RV pacing.
Effect on Hemodynamics of BV Pacing Versus LV
Pacing
With the superiority of BV pacing compared with RV pacing, the
question emerged of whether the same hemodynamic
improvement can be observed with LV pacing alone. Few studies have
addressed this question by comparing the effect of LV pacing alone with
that of BV pacing or baseline sinus rhythm in patients with severe
heart failure.8 12 14 15 Blanc et al8
compared the acute hemodynamic changes associated with
(1) RV apex or RV outflow tract pacing, (2) LV pacing, or (3) RV apex
and LV pacing combined. Twenty-three patients with NYHA class III or
IV, pulmonary capillary wedge pressure of >15 mm Hg, and
either first-degree AV block or bundle-branch block (or both) were
enrolled. Pacing from different ventricular sites was
performed in either VDD mode (AVI 100 ms) or VVI mode in patients with
atrial fibrillation. BV pacing resulted in higher systolic BP,
lower pulmonary capillary wedge pressure, and lower V-wave
amplitude than either baseline or RV pacing. Interestingly, the results
with LV pacing alone were similar to those obtained with BV pacing.
Kass et al15 measured aortic and LV pressures in 18
patients with heart failure during VDD pacing at varying sites and AV
delays. LV and BV pacing enhanced systolic BPs in patients with
LV dysfunction and intraventricular conduction
delay. In addition, the authors demonstrated that these changes were
primarily the result of a direct improvement in LV systolic
function with minimal changes in diastolic filling
pressures or relaxation. Recently, Auricchio et al14
showed that BV and LV pacing increased maximum LV pressure and pulse
pressure more than RV pacing in patients with congestive heart failure
and wide surface QRS. Furthermore, these changes were more significant
with LV pacing than with BV pacing.
Our results are similar to those of these previous studies. In patients with depressed ejection fraction and intraventricular conduction delay, LV pacing resulted in hemodynamic changes similar to those obtained with BV pacing. In addition, we found that patients without intraventricular conduction delay are also likely to benefit from LV pacing alone. We do not find this surprising because the beneficial effects of LV-based pacing are not limited to normalization of ventricular electrical activation but also include an increase in filling time, optimization of left-side mechanical atrioventricular delay, and a decrease in mitral regurgitation. However, our findings suggest that the beneficial effect of LV pacing alone tended to decrease as the QRS duration decreased, suggesting that patients with a wider QRS duration are more likely to benefit equally from LV and BV pacing, whereas those with a narrow QRS duration may benefit more from BV pacing.
Sympathetic Activity in Congestive Heart Failure
Sympathetic activity is increased in patients with congestive
heart failure. This is evidenced by elevated levels of circulating
norepinephrine levels16 17 18 and increases in
adrenergic nerve outflow, as measured with
microneurography.19 The cause of this increase is thought
to be in part secondary to abnormal baroreflex control of adrenergic
outflow from the central nervous system. Patients with heart failure
have been shown to have a blunted HR response and a reflex increase in
forearm vascular resistance during tilt-table
testing.20 21 Although the increase in sympathetic
activity may play a compensatory role early during the disease process,
chronic adrenergic activation is recognized as a contributor to the
vicious cycle that promotes progression of the disease through multiple
effects, including increased afterload, exertion of a direct toxic
effect on the failing myocardium, increased myocardial
oxygen demand, and triggered ventricular
arrhythmias. Indeed, elevated plasma norepinephrine
levels have been shown to correlate with cardiac mortality rates and
are a better prognostic predictor than ejection
fraction.22 It is not clear, however, whether this is a
cause of death or simply a marker of the underlying cardiac
disease.
The adverse effect of adrenergic stimulation prompted the use of ß-blocker therapy in patients with congestive heart failure. In the present study, we sought to compare the effects of single-site and multisite pacing on sympathetic outflow in patients with LV dysfunction. A reduction in sympathetic activity with a given pacing mode would provide an additional method of interrupting the deleterious cycle that is facilitated by increased sympathetic activity in patients with heart failure.
Effect of Pacing on Sympathetic Activity
Saxon et al23 recently showed a decrease in
serum norepinephrine levels after 12 weeks of BV pacing in
patients with congestive heart failure and conduction delay. This
decrease was noted only in 21 patients with baseline
norepinephrine levels of >800 pg/mL. The authors explained
these findings with the positive inotropic effect of BV pacing in these
patients. To our knowledge, this is the only study that assessed the
effect of chronic BV pacing on serum catecholamine levels
in patients with congestive heart failure.
The purpose of the present study was to compare BV pacing with single-site pacing in patients with LV dysfunction. We did not, therefore, compare BV pacing with sinus rhythm. Our results indicate for the first time that acute BV and LV pacing reduces sympathetic activity compared with RV pacing in patients with LV dysfunction regardless of the QRS duration. Although not statistically significant, a comparison of the differences between BV and LV pacing and the QRS duration revealed a correlation with r=0.42. This correlation suggests that the narrower the QRS, the greater is the benefit of BV pacing relative to LV pacing. On the other hand, the wider the QRS, the smaller is the difference and the more likely patients are to benefit equally from LV and BV pacing. Nevertheless, these data suggest that there may be a modest advantage to BV pacing compared with LV pacing alone, particularly in patients with narrow QRS durations.
We believe the changes in SNA are the result of the changes in arterial BP. The decrease in SNA during LV and BV pacing compared with RV pacing occurred in the setting of an increase in arterial BP, suggesting an arterial baroreflex–mediated sympathoexcitation. Another possible mechanism for the decrease in sympathetic activity is a direct effect of pacing on the cardiopulmonary baroreceptors resulting in increased cardioinhibition and thus a decrease in peripheral sympathetic activity. We believe this is very unlikely because RA filling pressures were similar in all three pacing modes.
Clinical Implications
If the hemodynamic and autonomic changes
noted with acute pacing prove to be present with chronic pacing,
then LV-based pacing should be offered to patients with LV dysfunction
and an indication for chronic pacing. In addition to the
hemodynamic improvement, the decrease in sympathetic
activity may have an impact on mortality rate in these patients. As
previously discussed, elevated levels of serum
norepinephrine levels have been shown to correlate with
mortality rates in patients with congestive heart failure. Therefore, a
decrease in sympathetic activity, which has been shown to correlate
with serum norepinephrine levels, may result in improved
survival rates. This hypothesis must be tested in prospective studies
that assess the long-term benefits of LV-based pacing.
Study Limitations
This study has limitations. First, pacing was performed at
a rate slightly faster than sinus rhythm, and therefore our findings
may not be present during an atrium-sensed/ventricle-paced mode. We
think this is unlikely, and we believe our method is a better one
because it allowed a direct comparison between single-site and
multisite pacing while avoiding the spontaneous variations in HR
commonly seen during DDD or VDD pacing. Second, our results were
obtained with an AV interval of 100 ms and may not be present
with a shorter or longer AV delay. The duration of the AV interval
during pacing has been shown to be an important variable that
modulates the hemodynamic outcome. We chose an AV
interval of 100 ms to avoid competition with intrinsic conduction, and
we cannot exclude the possibility that a different PR interval may have
yielded different results. Finally, it should be emphasized that the
current findings are the result of acute pacing, and the same
conclusions may not be true with chronic pacing. This study, however,
provides the basis for an evaluation of the chronic effect of multisite
pacing on sympathetic activity in patients with congestive heart
failure.
Received September 8, 1999; revision received March 7, 2000; accepted March 27, 2000.
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B. Pieske Reverse remodeling in heart failure - fact or fiction? Eur. Heart J. Suppl., August 1, 2004; 6(suppl_D): D66 - D78. [Abstract] [Full Text] [PDF]
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C. Stellbrink, O.-A. Breithardt, A. Franke, S. Sack, P. Bakker, A. Auricchio, T. Pochet, R. Salo, A. Kramer, and J. Spinelli Impact of cardiac resynchronization therapy using hemodynamically optimized pacing on left ventricular remodeling in patients with congestive heart failure and ventricular conduction disturbances J. Am. Coll. Cardiol., December 1, 2001; 38(7): 1957 - 1965. [Abstract] [Full Text] [PDF]
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