(Circulation. 1999;100:427-436.)
© 1999 American Heart Association, Inc.
Basic Science Reports |
Left Atrial Relaxation and Left Ventricular Systolic Function Determine Left Atrial Reservoir Function
From the Cardiovascular Research Institute and Department of Medicine, University of California, San Francisco, and the Istituto di Cardiologia dell'Università di Milano, CNR, Fondazione Monzino, IRCCS, via Parea 4, 20138 Milan, Italy (P.B.).
Correspondence to Stanton A. Glantz, PhD, Cardiology Division, University of California, San Francisco, CA 94143-0124. E-mail glantz{at}medicine.ucsf.edu
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Abstract |
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Background—Determinants of left atrial (LA) reservoir function and its influence on left ventricular (LV) function have not been quantified.
Methods and Results—In an open-pericardium, paced (70 and 90 bpm)
pig model of LV regional ischemia (left anterior descending
coronary constriction), with high-fidelity LV, LA, and RV
pressure recordings, we obtained the LA area with 2D automated
border detection echocardiography, LA pressure-area
loops, and Doppler transmitral flow. We calculated LV 
,
LA relaxation (a-x pressure difference divided by time, normalized by
a pressure), and stiffness (slope between x and v pressure points of v
loop). Determinants of total LA reservoir (maximum-minimum area,
cm2) were identified by multiple regression
analysis. Different mean rates of LA area increase identified 2
consecutive (early rapid and late slow) reservoir phases. During
ischemia, LV long-axis shortening (LAS, LV base
systolic descent) and LA reservoir area change decreased
(7.3±0.3 [SEM] versus 5.6±0.3 cm2,
P<0.001) and LA stiffness increased (1.6±0.3 versus
3.1±0.3 mm Hg/cm2, P=0.009). Early
reservoir area change depended on LA mean ejection rate (LA area at ECG
P wave minus minimum area divided by time; multiple regression
coefficient=0.9; P<0.001) and relaxation
(coefficient=4.9 cm2xms/s; P<0.001). Late
reservoir area change depended on LAS (coefficient=8 cm/s;
P<0.001). Total reservoir filling depended on LA
stiffness (coefficient=-0.31 cm4/mm Hg;
P=0.001) and cardiac output (coefficient=0.001
cm2xmin/L; P=0.002). The strongest
predictor of cardiac output was LA reservoir filling (coefficient=301
L/minxcm2; P<0.001). The v loop area was
determined by cardiac output, LV ejection time, , and early
transmitral flow.
Conclusions—Two (early and late) reservoir phases are determined by LA contraction and relaxation and LV base descent. Acute LV regional ischemia increases LA stiffness and impairs LA reservoir function by reducing LV base descent.
Key Words: hemodynamics • mechanics • atrium
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Introduction |
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Left atrial (LA) function includes 3 phases: reservoir (inflow during ventricular systole), conduit (passive emptying during ventricular relaxation and diastasis), and contraction (active emptying near ventricular end diastole). LA relaxation,1 stiffness,2 3 4 and contractility5 influence LA reservoir, conduit, and contraction function. Historically, LA function has been expressed by its booster pump contribution to cardiac output.5 6 7 8 9 10 LA reservoir function is influenced by LA relaxation,7 11 12 left ventricular (LV) contraction through the descent of the base during systole,12 13 LA chamber stiffness,2 3 4 8 and right ventricular (RV) systole through pulmonary venous (PV) inflow.14 15 The relative contributions of these factors have not been quantified.11 15
The influence of LA chamber stiffness,2 8 and thus LA reservoir function, on cardiac output has been inferred, but no in vivo data exist to support the hypothesis that the LA reservoir phase determines cardiac output.
This study quantifies the relationship between LA reservoir function, LV systolic function, and the transmitted RV systolic pressure pulse. We use a model of acute LV regional supply ischemia during right atrial pacing in open-pericardium pigs to measure the independent effects of acute changes of LV systolic function and heart rate on LA reservoir function (chamber dimension changes and stiffness). LA relaxation and systolic descent of the cardiac base are the main determinants of 2 (early and late) distinct LA reservoir phases, respectively. The systolic descent of the cardiac base has a stronger influence on the LA dimension changes during reservoir than the transmitted RV systolic pressure pulse. The LA reservoir function is the main determinant of cardiac output in this model of regional LV ischemia.
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Methods |
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With the approval of the University of California, San Francisco, Animal Research Committee, we studied 12 juvenile Yorkshire pigs (42.3±0.4 [SEM] kg) in an open-chest, open-pericardium model of LV regional supply ischemia at 2 heart rates. Methods have been described in detail previously.16
Surgical Preparation and Instrumentation
The pigs were anesthetized with 
-chloralose (100
mg/kg IV), then fentanyl (30 mg) and pancuronium (4 mg) as
needed, and were mechanically ventilated (room air and oxygen). Animals
were placed supine, and a pericardial cradle was created after a
midline sternotomy and partial rib excision for epicardial positioning
of the ultrasound transducers (Hewlett Packard Sonos 2500, 2.5/3.5 and
5.0 MHz). We placed 5F Millar micromanometer-tipped
catheters in the LV through the apical dimple, in the LA through the LA
appendage, and in the RV cavity. Pacing electrodes on the right atrial
appendage permitted pacing with 1:1 atrioventricular
conduction after administration of zatebradine (ULFS 49, 2 mg/kg). A
C-clamp constrictor was placed around the left anterior descending
coronary artery to reduce flow and regional myocardial
shortening, measured with 2 pairs of segment-length crystals
(Sonometrics) in the mid anterior wall (ischemic region) and
basal lateral wall (reference region). An occluder was placed around
the inferior vena cava. A single-lead ECG was recorded
to synchronize hemodynamic and
echocardiographic measurements. Data were digitized at
200 Hz with the respirator off at end expiration.
Echocardiographic and Doppler Recordings
We recorded biplane LV 4- and 2-chamber views with minimal
transducer contact on the apical dimple. In the 4-chamber view, the LA
area (including the appendage) was maximized by transducer rotation. A
50-Hz frame rate minimized the LA automated border detection (ABD)
pressure signal delay (Figure 1
).17 Diastolic
LV filling was recorded from Doppler transmitral annular flow.
Cardiac output was calculated from LV outflow tract area and velocities
in the apical 5-chamber view. A 5.0-MHz transducer on the
posterosuperior LA wall recorded PV flow with the pulsed
Doppler sample volume (3 mm3) in a left
lower PV, 5 mm proximal to a PV sinus. We used Doppler color
flow to screen for mitral and tricuspid regurgitation
(Niquist limit 60 cm/s). Echocardiographic and
Doppler recordings were stored in S-VHS tape and measured
offline (Tomtec Imaging Systems).
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Protocol
Regional LV ischemia was obtained by tightening the
constrictor for 
15 minutes to achieve a 20% decrease in
segment-length shortening of the anterior wall crystals. Tracings of LA
ABD areas, LV outflow velocities, LV 4- and 2-chamber views, and PV
flow velocities were obtained within a 5-minute interval, during
baseline and ischemia, each paced at 70 and 90 bpm.
Inferior vena cava occlusions were performed to define the
LV diastolic pressure-volume curve over a wide range of
end-diastolic volumes.
Measurements
Echocardiographic and Doppler measurements
were obtained by averaging 3 to 5 consecutive beats.
Hemodynamic data were averaged over 15 beats that
included these 3 to 5 beats.
We calculated LV end-diastolic pressure and the time
constant of isovolumic relaxation, .16 We measured LA
peak a (Pa), c, v, and x
(Px) trough pressures (Figure 2), their timings, and mean LA pressure.
LA relaxation was defined as the time during which the LA pressure
decreased after atrial contraction, between the peak a wave and the x
trough and quantified with [(Pa
-Px)/Pa]/(tx-ta).
Systolic RV-LA transpulmonary pressure gradient was RV
peak systolic pressure minus LA peak v pressure difference.
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Biplane LV (4- and 2-chamber) end-diastolic (at ECG R wave) and end-systolic (at minimum LV dimension) volumes (area-length method), ejection fraction, and long-axis systolic shortening were calculated. The midsystolic LV outflow tract area and biplane end-systolic mitral annulus area (at basal insertion of the leaflets) were calculated from their diameters, assuming circular orifices. Stroke volume was calculated as velocity-time integral times outflow area, and cardiac output as stroke volume times heart rate. LV ejection time was calculated as time to end minus time to start of LV outflow.
We measured maximum and minimum LA areas (cm2)
and the area occurring before atrial contraction (at ECG P wave)
(Figure 3). We calculated total reservoir
area change (maximum minus minimum area, cm2) as
an index of reservoir function,3 duration of the reservoir
phase, stroke area (area before atrial contraction minus minimum area,
cm2), fractional shortening (stroke area/area
before atrial contraction), and mean LA ejection rate [stroke
area/(time of minimum area minus time of area before atrial
contraction), cm2/s]. To synchronize digitized
LA pressure and area,17 we aligned the LA area point
before atrial contraction with the beginning of the LA a wave and the
end of the ECG P wave (Figure 3).
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LA pressure-area curves (Figure 4) have 2
loops. The "a" loop corresponds to LA work during active
contraction and relaxation5 6 8 9 10 18 and the "v"
loop to LA passive filling and emptying. We computed a and v loop areas
(mm Hg · cm2) and an index of LA chamber
stiffness as the slope connecting the x and v pressure points of the v
loop (Figure 4).
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Statistical Analysis
The effects of ischemia and heart rate (and their
interaction) were analyzed by 2-way repeated-measures general
linear model ANOVA. The tables report the least-squares means
and SEMs from the ANOVA. We compared the values of 2 different related
variables (eg, LA early and late mean filling rates) using a 3-way
repeated-measures ANOVA including a factor to distinguish the 2
variables. We report only the probability value related to this
factor and its interactions. ABD variables related to the LA
contraction phase were analyzed comparing only baseline paced
at 70 bpm with ischemia paced at 70 bpm using a paired
t test, because LA contraction often overlapped with the
preceding conduit phase at 90 bpm.
To test for a linear relationship between 2 variables across the
experimental conditions, we used a multiple regression including
effects-coded dummy variables for the different pigs. We used
stepwise multiple regression forcing dummy variables to account for
between-pig effects to identify the independent predictors of the LA
reservoir total area change, the mean rates of LA early and late area
changes, the LA v loop, cardiac output, and the PV early and late
systolic peak velocities and velocity-time integrals (Table 1). Computations were done with
SPSS 7.5, with P<0.05 considered significant. Results are
presented as mean±SEM.
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Results |
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Baseline
Atrioventricular conduction time was normal (Table 2
).
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Baseline LV16 and RV hemodynamics (Table 3), LV volumes, and systolic
function (Table 4) were typical for an
anesthetized open-chest pig. Mitral
regurgitation was absent or trace.
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LA peak a pressure was higher than peak c pressure and slightly higher
than peak v pressure, as reported in open-pericardium
pigs19 (Tables 3
and 5).
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Within 100 ms of the ECG R wave, the ABD tracing slope decreased. This
point correlated with the LA x pressure point (coefficient=0.32,
SEM=0.13, P=0.02) (Figure 3). The LA area increase to
the ABD slope change occurred during LA relaxation, the acceleration of
early systolic PV flow and LV ejection, and LV isovolumic
contraction (LA pressure c wave) (Table 2 and Figures 3 and 5). The area increase after the slope
change occurred during LA pressure increase, to maximum LA area and
peak v pressure, including the acceleration of PV late systolic
flow. We subdivided LA reservoir area increase into early (time of LA
area at slope change minus time of minimum area) and late (time of LA
maximum area minus time of LA area at slope change) phases (Table 2 and Figure 3).7 For each phase, we
measured the area change (early=area at slope change minus minimum
area; late=maximum area minus area at slope change,
cm2) and mean rate of area increase (early=early
area change/duration, cm2/s; late=late area
change/duration) (Table 7). The LA area changes during the early
and late reservoir phases were similar (Tables 5 and 7).
Because the early phase was shorter than the late phase, the mean rate
of LA area change was greater during the early reservoir phase (Tables 2, 5, and 7).
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LA stroke area correlated with mean rate of early reservoir area change
(r=0.7, P=0.02), and LA mean ejection rate
correlated with PV early systolic peak flow velocity
(r=0.8, P=0.02), indicating a relationship
between LA contraction and LA filling during relaxation. The direction
of both the LA a and v pressure-area loops was counterclockwise (Figure 4). The a and v loop areas were similar (Tables 5 and 8).
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Effects of LV Ischemia
The atrioventricular conduction time did not
change during LV ischemia (Table 2). Mitral
regurgitation never exceeded grade II and did not
influence LA reservoir function (Table 1).
RV and LV systolic pressures did not change with regional
ischemia. LV relaxation slowed, and end-diastolic
pressure increased16 (Table 3).
Echocardiography showed severe hypokinesis of mid
to apical interventricular septum and apical anterior wall.
End-diastolic and end-systolic LV volumes
increased, and ejection fraction and long-axis shortening decreased
(Table 4). Ischemia reduced early diastolic
LV inflow and cardiac output.16
All LA pressure values increased during LV ischemia (Table 3), with a pressure increasing more than v pressure (Table 5). The LA relaxation index did not change.
LA minimum area increased during LV ischemia. Total LA
reservoir area change, both early and late area changes, and mean rates
of area change decreased (Tables 5 and 7). A marked
decrease in slope of LA late reservoir and change occurred during
ischemia (Figure 3). The mean rate of late area change
was related to LV long-axis shortening (coefficient=6.7 cm/s, SEM=1.2,
P<0.001). Greater systolic descent of the LV base
was associated with increased rate of LA area increase. LV
ischemia prolonged LA late reservoir phase duration by delaying
both the beginning and end of LV ejection, each positively related to
late reservoir duration (coefficient=0.9, SEM=0.3, P=0.004,
and coefficient=0.6, SEM=0.2, P=0.002, respectively) (Table 2). LV ischemia decreased PV flow late systolic
peak velocity (Table 6), which
paralleled its effects on the ABD pattern during the LA reservoir
phase.
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Mean rate of LA early reservoir area change increased with LA stroke area (coefficient=0.05 s-1, SEM=0.02, P=0.03), fractional shortening (coefficient=0.6 cm2/s, SEM=0.1, P=0.003), and mean ejection rate (coefficient=0.72, SEM=0.2, P=0.001). During ischemia, as during baseline, LA contraction and relaxation indexes were positively correlated.
The areas of the LA pressure-area a and v loops did not change during
ischemia. The LA stiffness index increased (Table 8) and
was displaced upward and to the left (Figure 4).
Effect of Increased Heart Rate
The atrioventricular conduction time did not
change with increasing heart rate from 70 to 90 bpm (Table 3).
LV end-diastolic pressure and decreased (Table 2). End-diastolic LV volume decreased, resulting in
a lower ejection fraction (Table 4). Long-axis shortening and
cardiac output did not change (Table 6). All LA pressure values
decreased. Both LA late reservoir phase and total reservoir phase
shortened (Table 2). Increasing heart rate did not affect total
LA area change (Table 7), PV flow (Table 6), LA loops, or stiffness index (Table 8).
Correspondence Between Dimensional and Doppler Velocity
Analysis of LA Reservoir Filling
During baseline paced at 70 bpm, mean rate of early reservoir area
change correlated with PV early systolic velocity-time integral
(r=0.6, P=0.05). During
ischemia, the mean rate of early area change correlated with
early systolic peak velocity and velocity-time integral
(r=0.8, P=0.02 for both). By use of
pooled data in a multiple regression analysis, late reservoir
LA area change was significantly related to both late PV peak flow
velocity (coefficient=7.6 cm · s, SEM=2.8, P=0.01)
and velocity-time integral (coefficient=2.2 cm, SEM=0.9,
P=0.03).
Independent Predictors of LA Reservoir Function
LA Relaxation and LV Systole
LA x pressure timing depended on LA reservoir slope change
(coefficient=0.3, SEM=0.1, P=0.02) and PV early
systolic peak velocity (coefficient=0.4, SEM=0.1,
P=0.02) timings. LA mean ejection rate and relaxation index
were independent predictors of mean rate of LA early reservoir (Table 1). Thus, the rate of LA reservoir dimension increase was
proportional to both LA contraction and LA pressure change during
relaxation. In contrast, during the late reservoir phase, the mean rate
of LA area change depended only on LV long-axis shortening (ie, the
systolic descent of the cardiac base).
LA Stiffness and Cardiac Function
Total LA reservoir area change depended on LA stiffness index and
cardiac output (Table 1). Thus, increased LA chamber stiffness
or decreased cardiac output predicted a decrease in LA reservoir
function. LA reservoir phase duration depended on LV ejection time
(coefficient=0.4, SEM=0.1, P=0.009), consistent with
a relation between LV systolic and LA reservoir function.
Multiple regression analysis confirmed that LA total area
change per se was a determinant of cardiac output2
(Table 1).
LA Pressure-Dimension Analysis
LA v loop area determinants were related to both LV
systolic (cardiac output and LV ejection time) and
diastolic (LV and early diastolic flow)
function (Table 1). The ascending limb of the v loop reflects LA
reservoir, and the descending limb the LV filling.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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We sought to identify the determinants of LA reservoir function and test Suga's hypothesis2 that LA reservoir function is a determinant of cardiac output. The reservoir phase is the diastolic phase of the LA. It has been suggested, but not demonstrated, that LA filling is determined initially by LA myocardial fiber relaxation7 11 12 and later by the combined influence of LA chamber stiffness,2 3 4 8 20 descent of the cardiac base,12 13 and the RV systolic pressure pulse transmitted through the pulmonary circulation.14 We show that there are 2 LA reservoir phases: an early phase (Figure 3
) related to relaxation from the
preceding LA contraction and a late phase related to LV longitudinal
fiber systolic shortening (the descent of the cardiac base) and
LA chamber stiffness. These findings indicate that LA contraction and
LV systolic function determine, sequentially, the 2 reservoir
phases. LA reservoir function is an independent determinant of cardiac
output.
Toma et al7 used LA x pressure trough timing to
identify an early reservoir phase during LA relaxation but did not
consider similarities with the biphasic nature of systolic PV
flow.12 We show a consistent decrease of the rate
of LA area increase (Figure 3) during the reservoir phase that
reflects a transition between the early and late LA reservoir phases
and depends on different factors.
Determinants of LA Early Reservoir Function
The early reservoir phase includes 50% of LA filling and
coincides with LA relaxation (LA pressure fall to the x trough) and
early systolic PV flow acceleration (Figures 2, 3, 5, and 6). The
mean rate of early area change depends on LA relaxation, a conclusion
similar to that reached in Doppler studies12 based on
indirect evidence21 showing a constant temporal relation
between LA contraction and the early PV flow wave.
Consistent with a previous angiographic study in
humans7 and the suggestion that LA relaxation depends on
the previous LA contraction (as in the LV), we identify LA mean
ejection rate as a determinant of the mean rate of early LA reservoir
filling and of PV peak early systolic velocity. In contrast,
despite the temporal coincidence (Table 2 and Figure 5),
we do not find a relation between LA early reservoir filling and LV
isovolumic contraction (the LA peak c wave) or LV ejection indexes.
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Both extent and rate of LA early reservoir area change were reduced by LV ischemia. The explanation for this finding is that LV ischemia increases LV end-diastolic pressure, which causes an afterload-dependent9 decrease of LA mean ejection rate. Because LA early reservoir filling is positively related to the LA mean ejection rate, both are decreased by LV ischemia.
Determinants of LA Late Reservoir Function
The late reservoir phase is characterized by a slower rate of LA
area increase than the early phase (Figure 3). During this
phase, LA area increases in parallel with LA pressure as PV flow
distends the relaxed LA chamber. Atrial and ventricular
diastolic functions are similar: early diastole
is regulated by relaxation, and during late diastole (LA
late reservoir phase), both LV and LA chamber characteristics are
described by a (passive) pressure-dimension curve20
(Figure 4). In addition, the LA expands secondary to
systolic descent of the cardiac base (Table 1), thus
drawing in PV blood like a piston during late systole, as previously
suggested.12 13 In contrast to previous suggestions that
the LA inflow pattern is determined either by the transmitted RV
systolic pressure pulse alone14 or in combination
with left heart mechanics,15 we show that the descent of
the cardiac base is the only determinant of LA late reservoir area
change.
Role of LV Ischemia
Acute regional LV ischemia reduces LV longitudinal fiber
shortening and extent and rate of LA late area change (decreasing total
LA reservoir filling by 23%), establishing a direct cause-and-effect
influence of LV systole on late LA reservoir filling. The upward and
leftward displacement of the LA v loop slope indicates that LA chamber
stiffness is also increased during LV ischemia (Figure 4). Previous authors have shown that LV ischemia
influences LA contraction through the Frank-Starling
mechanism.6 LV ischemia directly affects LA
reservoir function, and as a consequence, the dynamics of the cardiac
base directly influences LA chamber stiffness.
Pressure-Area v Loop
The LA v loop area has been proposed as an index of LA reservoir
work10 18 or work done on the LA by PV
inflow.10 In contrast, our v loop area is related to both
LV systolic work (LV ejection time and cardiac output) and
relaxation (LV and early diastolic inflow) but not to LA
reservoir function or RV energy delivered through systolic PV
flow.5 6 8 9 10 18 19 This finding is expected because the
v loop represents LA pressure-area changes that occur not only
during the late reservoir phase (the v loop ascending limb) but also
during the LA early conduit phase (Table 1 and Figures 3 and 4).
We described a counterclockwise v loop pattern (Figure 4) and
speculate that it is a result of elastic energy stored by the LA during
the reservoir phase.18 This energy comes from stretching
by systolic descent of the cardiac base and PV flow and is
returned during early LV diastole (during the LA conduit
phase) to facilitate LV filling. The discrepancy with previously
described clockwise v loops probably is a result of methodological
differences. We demonstrate that LV relaxation and early inflow are
independent predictors of the v loop area. Early transmitral flow is
greater in dogs22 than in pigs, suggesting a faster early
diastolic LA pressure decrease, a steeper
pressure-dimension slope during early conduit, and consequently a
clockwise v loop in dogs.5 8 Species-specific differences
in relative LA appendage volume compared with its main chamber may
affect LA compliance and thus may influence the v loop
pattern.4 20 Previous angiographic studies lacked the
higher time resolution of ultrasonic crystals or ABD, and 1-dimensional
LA measurements with ultrasonic crystals6 9 may not
adequately represent LA phasic geometric changes because of
chamber asymmetry.
Effects of LA Reservoir Function on Cardiac Output
Our multiple regression analysis pointed to LA total
reservoir area change as the strongest predictor of cardiac output,
together with v loop area (and thus LV systolic and
diastolic functions). Suga2 theorized that LA
chamber stiffness during the reservoir phase may have influenced
cardiac performance. A direct relation between LA compliance
(using an LA pressure-dimension curve) and LA reservoir function (using
PV flow) has been demonstrated in dogs4 and in
humans20 when LA compliance was reduced by LA appendectomy
or appendage clamping, respectively. An indirect relation has been
shown between cardiac output and LA reservoir function in
humans23 and dogs24 through the LA
Frank-Starling mechanism, which links increased LA
end-diastolic volume (at the ECG P wave) and augmented
emptying.4 24 Consistent with our results,
Doppler PV systolic flow correlated with cardiac output
both in patients with normal LV systolic function during acute
pharmacological intervention25 and in patients with
congestive heart failure.26
Limitations of the Study
The young age of the pigs may limit the applicability of our
findings to understanding the effects of LV ischemia in older
humans. However, porcine transmitral and PV flow patterns are more
similar to those of adult, middle-aged humans27 than those
of dogs22 or young humans.27 Our
open-pericardium model differs from the clinical setting with intact
pericardium. However, the increase in LV end-diastolic
volume with ischemia was clinically negligible, and an intact
pericardium would have strengthened our findings by increasing
ventriculoatrial interaction.
Conclusions
Our findings confirm and extend Suga's hypothesis of a direct
relation between LA reservoir function and cardiac performance,
broadening the analysis to an in vivo animal model with
physiologically complete LA function. We
identify 2 (early and late) reservoir phases that are sequentially
determined by LA contraction and relaxation and LV systolic
function and point to a strong relation between LV systolic and
LA reservoir function. The descent of the cardiac base determines LA
reservoir function by influencing LA stiffness, whereas LA reservoir
function independently predicts LV performance.
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Acknowledgments |
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This study was supported by NHLBI grant HL-25869 and Fondazione I. Monzino, IRCCS, Milan, Italy. We thank Jim Stoughton for assistance with the experiments.
Received December 17, 1998; revision received March 25, 1999; accepted March 26, 1999.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Couttenye M, Clerck ND, Goethals M, Brutsaert D. Relaxation properties of mammalian atrial muscle. Circ Res. 1981;48:352–356.
2.
Suga H. Importance of atrial compliance in cardiac
performance. Circ Res. 1974;35:39–43.
3. Hoit BD, Walsh RA. Regional atrial distensibility. Am J Physiol. 1992;31:H1356–H1360.
4.
Hoit BD, Shao Y, Tsai L-M, Patel R, Gabel M, Walsh RA.
Altered left atrial compliance after atrial appendectomy: influence on
left atrial and ventricular filling. Circ Res. 1993;72:167–175.
5.
Hoit BD, Shao Y, Gabel M, Walsh RA. In vivo assessment
of left atrial contractile performance in normal and
pathological conditions using a time-varying elastance model.
Circulation. 1994;89:1829–1838.
6.
Matsuda Y, Toma Y, Ogawa H, Matsuzaki M, Katayama K,
Fujii T, Yoshino F, Moritani K, Kumada T, Kusukawa R. Importance of
left atrial function in patients with myocardial infarction.
Circulation. 1983;67:566–571.
7. Toma Y, Matsuda Y, Moritani K, Ogawa H, Matsuzaki M, Kusukawa R. Left atrial filling in normal human subjects: relation between left atrial contraction and left atrial early filling. Cardiovasc Res. 1987;21:255–259.[Medline] [Order article via Infotrieve]
8.
Kihara Y, Sasayama S, Miyazaki S, Onodera T, Susawa T,
Nakamura Y, Fujiwara H, Kawai C. Role of the left atrium in adaptation
of the heart to chronic mitral regurgitation in
conscious dogs. Circ Res. 1988;62:543–553.
9. Sanada H, Shimizu M, Shimizu K, Kita Y, Sugihara N, Takeda R. Left atrial afterload mismatch in hypertrophic cardiomyopathy. Am J Cardiol. 1991;68:1049–1054.[Medline] [Order article via Infotrieve]
10. Hoit BD, Shao Y, Gabel M, Walsh RA. Left atrial mechanical and biochemical adaptation to pacing induced heart failure. Cardiovasc Res. 1995;29:469–474.[Medline] [Order article via Infotrieve]
11. Rajagopalan B, Friend JA, Stallard T, Lee J. Blood flow in pulmonary veins, I: studies in dog and man. Cardiovasc Res. 1979;13:667–676.[Medline] [Order article via Infotrieve]
12. Castello R, Pearson AC, Lenzen P, Labovitz AJ. Evaluation of pulmonary venous flow by transesophageal echocardiography in subjects with a normal heart: comparison with transthoracic echocardiography. J Am Coll Cardiol. 1991;18:65–71.[Abstract]
13. Fujii K, Ozari M, Yamagishi T, Ishine K, Furutani Y, Nagano H, Yamamoto K, Saiki A, Matsuzaki M. Effect of left ventricular contractile performance on passive left atrial filling: clinical study using radionuclide angiography. Clin Cardiol. 1994;17:258–262.[Medline] [Order article via Infotrieve]
14. Wiener F, Morkin E, Skalak R, Fishman A. Wave propagation in the pulmonary circulation. Circ Res. 1966;277:834–850.
15. Appleton CP. Hemodynamic determinants of Doppler pulmonary venous flow velocity components: new insights from studies in lightly sedated normal dogs. J Am Coll Cardiol. 1997;30:1562–1574.[Abstract]
16.
Solomon S, Barbier P, Glantz SA. Changes in porcine
transmitral flow velocity pattern and its diastolic
determinants during partial coronary occlusion. J Am
Coll Cardiol. 1999;33:854–866.
17. Keren A, Deanda A, Komeda M, Tye T, Handen C, Daughters G, Ingels N, Miller C, Popp R, Nikolic S. Pitfalls in creation of left atrial pressure-area relationship with automated border detection. J Am Soc Echocardiogr. 1995;8:669–678.[Medline] [Order article via Infotrieve]
18. Grant C, Bummell LL, Greene DG. The reservoir function of the left atrium during ventricular systole: an angiocardiographic study of atrial stroke volume and work. Am J Med. 1964;37:36–43.[Medline] [Order article via Infotrieve]
19.
Leistad E, Christensen G, Ilebekk A. Effects of atrial
fibrillation on left and right atrial dimensions, pressures, and
compliances. Am J Physiol. 1993;264:H1093–H1097.
20. Tabata T, Oki T, Yamada H, Iuchi A, Ito S, Hori T, Kitagawa T, Kato I, Kitahata H, Oshita S. Role of left atrial appendage in left atrial reservoir function as evaluated by left atrial appendage clamping during cardiac surgery. Am J Cardiol. 1998;81:327–332.[Medline] [Order article via Infotrieve]
21. Tsakiris AG, Padiyar R, Gordon DA, Lipton L. Left atrial size and geometry in the intact dog. Am J Physiol. 1977;232:H167–H172.
22. Appleton CP, Gonzalez MS, Basnight MA. Relationship of left atrial pressure and pulmonary venous flow velocities: importance of baseline mitral and pulmonary venous flow velocity patterns studied in lightly sedated dogs. J Am Soc Echocardiogr. 1994;7:264–275.[Medline] [Order article via Infotrieve]
23. Furukawa K, Kitamura H, Nishida K, Yamada C, Niki S, Sugihara H, Katsume H, Tsuji H, Kunishige H, Ijichi H. Simultaneous changes of left ventricular and left atrial size and function in normal subjects during exercise. Jpn Heart J. 1984;25:487–497.[Medline] [Order article via Infotrieve]
24.
Nishikawa Y, Roberts JP, Tan P, Klopfenstein CE,
Klopfenstein HS. Effect of dynamic exercise on left atrial function in
conscious dogs. J Physiol. 1994;481:457–468.
25.
Nishimura R, Abel M, Hatle L, Tajik AJ. Relation of
pulmonary vein to mitral flow velocities by
transesophageal Doppler
echocardiography: effect of different loading
conditions. Circulation. 1990;81:1488–1497.
26. Masuyama T, Lee J-M, Nagano R, Nariyama K, Yamamoto K, Naito J, Mano T, Kondo H, Hori M, Kamada T. Doppler echocardiographic pulmonary venous flow-velocity pattern for assessment of the hemodynamic profile in acute congestive heart failure. Am Heart J. 1995;129:107–113.[Medline] [Order article via Infotrieve]
27.
Gentile F, Mantero A, Lippolis A, Ornaghi M, Azzolini
M, Barbier P, Beretta L, Casazza F, Corno R, Faletra F, Giagnoni E,
Gualtierotti C, Lombroso S, Mattioli R, Morabito A, Pepi M, Todd S,
Pezzano A. Pulmonary venous flow velocity patterns in 143
normal subjects aged 20 to 80 years old: an echo 2D colour Doppler
cooperative study. Eur Heart J. 1997;18:148–164.We evaluated the determinants of left atrial (LA)
reservoir filling and its role in left ventricular (LV)
function in an open-pericardium pig model of LV regional
ischemia. Acute LV ischemia decreased LA reservoir
function by reducing LV long-axis shortening and increasing LA
stiffness. The main determinant of total LA reservoir filling was LA
stiffness. Two LA reservoir phases, early and late, were identified,
which were sequentially determined by LA mean ejection rate and LA
relaxation and by LV long-axis shortening (descent of the cardiac
base). LA reservoir filling was the strongest predictor of cardiac
output.
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