Download Isovolumetric Relaxation?

1757
Is
or a
Preload-Independent Measure of
Isovolumetric Relaxation?
Shalendra K. Varma, MD, Robert M. Owen, BA,
Mark L. Smucker, MD, and Marc D. Feldman, MD
Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017
Several studies have been performed in patients with a variety of myocardial diseases that have
identified a prolongation of r. However, it is not clear whether prolongation of represents
abnormal myocardial physiology or the effect of excessive load associated with a particular
disease process. Accordingly, we evaluated the effect on r of an isolated decrease in preload
induced by inferior vena cava occlusion before the appearance of reflex changes in six patients
designated as normal by catheterization criteria. A computer-based digitization routine
identified cardiac contractions in all patients early after inferior vena cava occlusion where left
ventricular end-diastolic pressure decreased (18.3±6.3 to 9.3±5.8, p<0.05) while left ventric-
ular systolic pressure (113.3±13.8 to 111.8+14.0, p=NS) and heart rate (66.0±10.0 to
65.9±10.3, p=NS) did not change. After this alteration in preload, no change in from
baseline, as calculated by the logarithmic (TL), derivative (TD), or method of Mirsky (T1/2), was
noted: TLS 47.4±6.5 to 44.6±7.6; TD, 39.3±8.1 to 39.8±8.4; T112, 33.0±+ 4.0 to 31.8+4.6; all
p=NS. The baseline pressure extrapolated from isovolumetric relaxation did not change in these
preload beats compared with baseline (+4.26±6.20 to -0.80±4.87, p=NS). Subsequent beats
were identified where left ventricular systolic pressure showed a numeric decrease compared
with baseline (113.3±13.8 to 100.8±14.3,p=NS) despite no change in heart rate (66.0±10.0 to
66.8±10.5, p=NS). The extrapolated baseline pressure decreased in these subsequent beats
compared with baseline (+4.26±6.20 to -3.90±4.26, p<0.05) despite no change in r (TL,
47.4±6.5 to 41.6±8.4; TD, 39.3±8.1 to 40.8±11.1; TI,2, 33.0±4.0 to 31.7±4.2; all p=NS).
Visual display of the individual natural log of left ventricular pressure versus time values used
to calculate TL were consistent with exponential pressure decay as an appropriate model for
isovolumetric relaxation. This study demonstrates that r is a preload independent measure of
isovolumetric relaxation. (Circulation 1989;80:1757-1765)
T he relaxation of isolated papillary muscle is
dependent on the total load imposed on the
muscle. This concept was first demonstrated by Parmley and Sonnenblickt and more
recently expanded by Brutsaert et al.2 The muscle
preparations used in these studies included both
isometric and afterloaded isotonic contractions.
Because of the nonphysiologic sequence of relaxation during an afterloaded isotonic contraction
(isotonic before isometric relaxation), the load dependence of relaxation has been examined by "physiologically sequenced" relaxation. With this method
the load dependence of relaxation was reconfirmed
although at a temperature of 280 C.34 More recently,
From the Division of Cardiology, Department of Internal
Medicine, University of Virginia School of Medicine, Charlottesville, Virginia.
Address for correspondence: Marc D. Feldman, MD, Division
of Cardiology, Box 158, Department of Internal Medicine, School
of Medicine, University of Virginia, Charlottesville, VA 22908.
Received September 2, 1988; revision accepted July 27, 1989.
Gaasch et al demonstrated that variable preload,
with constant total load, did not produce a change
in isometric relaxation.5 Relaxation of isolated papillary muscle is, therefore, independent of preload
but dependent on total load.
Similar observations have been extended to the
intact animal heart. Karliner et al found that primary changes in afterload produced changes in the
time constant of isovolumetric left ventricular pressure (LVP) decline (X-), but volume infusion did not
produce such changes.6 Gaasch et al also found that
modest changes in left ventricular preload did not
influence i, but when volume loading was sufficient
to produce an increase in aortic pressure, r increased.7 Gaasch et al recently extended this observation to an isolated increase in left ventricular
preload, finding no associated change in r.5 In
contrast, Raft and Glantz found that volume loading
slowed r, and they concluded that this effect was a
reflection of both preload and afterload.8 However,
these conclusions were reached on the basis of
1758
Circulation Vol 80, No 6, December 1989
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multiple linear regression analysis and not pure
preload changes. Most data in the intact animal
heart favor r being independent of preload but
dependent on afterload.
The present study was designed to determine
whether r is a preload-independent measure of
isovolumetric relaxation in patients undergoing
cardiac catheterization. Several studies have been
performed in patients with a variety of myocardial
diseases and have identified a prolongation of
7.9-13 However, it is not clear whether prolongation of r represents abnormal myocardial physiology or the effect of excessive load associated with
a particular disease process. Accordingly, we evaluated the effect on r of an isolated decrease in
preload induced by inferior vena cava occlusion
before the appearance of reflex changes in six
patients without documentable cardiac disease by
catheterization criteria.
Methods
Study Group
Inferior vena cava occlusion with simultaneous
hemodynamic monitoring was performed at the
time of cardiac catheterization in eight patients.
One patient developed transient atrial fibrillation,
and a second had simultaneous falls in preload and
afterload. These two patients were excluded from
data analysis. Among the remaining six patients
there were five men and one woman with an age
range of 29-52 years. All medications were withheld for at least 18 hours prior to catheterization.
These patients all had atypical chest pain syndromes and normal physical examinations, electrocardiograms, right and left-heart pressures, cardiac
outputs, coronary arteriography, and biplane left
ventriculography. All patients gave written consent
to a protocol approved by the Human Investigation
Committee of the University of Virginia. There
were no complications as a result of this study.
Cardiac Catheterization and Angiography
Routine left-heart catheterization was performed
from the left groin and right-heart catheterization
from the right groin, leaving the latter for the
inferior vena cava balloon. Right-heart catheterization was performed with a 7F flow-directed, balloontipped catheter (Critikon, Tampa, Florida). Coronary angiography was performed by the Judkins
technique. Left ventriculography was performed
through a pigtail catheter with biplane cine recordings. Nonionic contrast (lopamidol, Squibb, New
Brunswick, New Jersey) was used to minimize the
myocardial depressant effects of contrast. Pressures were measured with thoroughly flushed disposable air reference transducers (Spectramed,
Oxnard, California). Recordings were inscribed by
means of a Honeywell Electronics-for-Medicine
VR-16 Recorder.
Inferior Vena Cava Occlusion Protocol
After completion of coronary angiography and
left ventriculography, the deflated 8F 40-mm occlusion balloon catheter (OBW 40/8/2/100, Mansfield
Scientific, Mansfield, Massachusetts) was introduced percutaneously into the right femoral vein,
positioned in the right atrium over an 0.035-in.
guidewire, and inflated. A 7F micromanometer pigtail catheter was subsequently introduced into the
left ventricle and balanced. Analog data from the
electrocardiogram (ECG), micromanometer LVP,
and on-line dP/dt were stored on a nine-channel
cassette FM recorder (MR-40, TEAC, Montebello,
California).
Thirty minutes passed between the last injection
of nonionic contrast and data collection. All patients
were instructed on breath-holding before the catheterization, and all data were collected at midexpiration. Analog recordings of ECG, LVP, and online dP/dt were continuously made throughout the
research portion of the catheterization. The 40-mm
balloon was pulled to the right atrial-inferior vena
cava junction. The occlusion was maintained until
left ventricular systolic pressure fell no lower than
80 mm Hg, at which point the balloon was readvanced into the right atrium. The baseline systolic
LVP for these six patients was 113 + 14 mm Hg, and
the nadir pressure in response to inferior vena cava
occlusion was 95 + 17 mm Hg. The goal of this study
was to obtain a decrease in preload and not afterload; therefore, the occlusions were often released
before obtaining a true maximal fall in pressure. Six
occlusions were performed in each patient, of which
only one was used for data analysis. The occlusions
not analyzed had either ectopy, inability of the
patient to hold his or her breath at midexpiration, or
no preload beats.
Data Analysis
The analog data recorded during the inferior vena
cava occlusion were played back to the computerbased digitization routine we developed. This routine
digitized each waveform and stored the data to be
analyzed. By handling the analog data in this manner, we eliminated the errors for off-line hand digitization of the analog signal traces. The sampling rate
for digitizing the analog signals was 1-msec intervals
(1 kHz), thus providing greater accuracy than the
5 -msec (200 Hz) digitization rates previously
reported.5 -8,10-11,14-16 The computer-based digitization hardware consisted of an LSI 11/23+ computer
with an on-board 12-bit analog-to-digital converter
(Andromeda Systems ADC1 1, Orange, California), a
video display, and our software.
X was calculated by three methods. The first used
a plot of ln(LVP) versus time, as derived by Weiss
et al (TL) 17 This approach assumed that LVP during
isovolumetric relaxation decays in a monoexponential manner to zero. The second method assumed a
variable asymptote to LVP decay, taking into
Varma et al Preload Independence of i
1759
TABLE 1. Mean Patient Data
HR (beats/min)
LVSP (mm Hg)
LVEDP (mm Hg), visual
LVEDP (mm Hg), computer derived
+dP/dt (mm Hg/sec)
-dP/dt (mm Hg/sec)
n
TL (msec)
R-TL
TD (msec)
R TD
T1J2 (msec)
PB (mm Hg)
Baseline
66.0±10.0
113.3±13.8
14+2
18.3±6.3
+1,576+129
-2,027+160
46.7±6.2
47.4±6.5
-0.996±0.004
39.3±8.1
-0.862±0.038
33.0±4.0
+4.26±6.20
Preload
65.9±10.3
111.8±14.0
8±2*
9.3+5.8*
+1,462±80*
-1,943± 196
54.2+5.5*
44.6±7.6
-0.99 ±0.005
39.8+±8.4
-0.861±+0.041
31.8+4.6
-0.80±4.87
Total load
66.8±10.5
100.8±14.3
3±3*t
6.3±6.4*t
+1,399+126*
-1,808+264*t
60.4±2.0*t
41.6±8.4
-0.996±0.005
40.8±+11.1
-0.857±0.042
31.7+4.2
-3.90+4.26*
*p<0.05 vs. control, tp<0.05 vs. preload.
HR, heart rate; LVSP, left ventricular systolic pressure; LVEDP, left ventricular end-diastolic pressure; n, number of points used to
calculate r; TL, r logarithmic; TD, 1 derivative; T112, r method of Mirsky; R, correlation coefficient; PB, pressure baseline.
Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017
account the effects of pleural and pericardial pressure. This method, developed by Raff and Glantz,
used a plot of negative dP/dt versus LVP (TD)8 and
allowed calculation of extrapolated, residual LVP,
assuming diastole to be infinite in duration (PB). The
preload dependence of PB was therefore also determined in this study. The third method computed the
time needed for LVP to fall to one half of its value
from peak negative dP/dt, using the method of
Mirsky (T1/2).18 T112 is similar to TL in that the latter
is the time it takes for pressure to fall from maximum negative dP/dt to 1 eth that pressure, and T1,2
uses one half instead of 1 eth. The use of T1/2
advocates not going through the exercise of the
exponential fit but simply determining r from the
pressure fall itself.
Statistical Analysis
Mean values and SDs were calculated at baseline, after preload reduction, and after total load
reduction. The three groups of data were compared by analysis of variance (ANOVA). Duncan's multiple-range test was used to directly
compare data at baseline versus preload reduction, baseline versus total load reduction, and
preload versus total load reduction. Ap value less
than 0.05 was considered significant.
Results
Hemodynamics
The mean hemodynamic data at baseline, after
reduction of only preload, and after a subsequent
reduction in total load (preload and afterload) with
inferior vena cava occlusion are shown in Table 1.
An example of hemodynamic data from a patient is
shown in Figure 1. The heart rate was not altered
after a reduction in preload or after a reduction in
total load (66.0+10.0 to 65.9+10.3 to 66.8+10.5
beats/min, respectively; p=NS). The systolic LVP
was not altered after a reduction in preload
(113.3± 13.8 to 111.8±14.0 mm Hg; p=NS). Although there was a numeric decrease in systolic LVP
in the total load beats from 113.3± 13.8 to 100.8± 14.3
mm Hg, statistical significance was not achieved.
The left ventricular end-diastolic pressure (LVEDP)
decreased after a reduction in preload and decreased
further with a reduction in total load (18.3±6.3 to
9.3 + 5.8 to 6.3 ± 6.4 mm Hg, respectively; p < 0.05).
Peak positive dP/dt decreased with a reduction in
preload (+1,576±129 to 1,462±80 mm Hg/sec;
p<0.05). With a reduction in total load, there was a
numeric decrease that did not achieve statistical
significance from preload (+ 1,462 ± 80 to 1, 399 + 126
mm Hg/sec, p=NS). Peak negative dP/dt was not
altered with a reduction in preload (-2,027±160 to
-1,943±196 mm Hg/sec;p=NS) but decreased with
a reduction in total load (-1,808±264 mm Hg/sec;
p<0.05 vs. baseline and preload).
Effect of Preload and Total Load Changes on r
TL, TD, and T1/2 are presented in Table 1 at
baseline, after a reduction of only preload, and after
a subsequent reduction in total load with inferior
vena cava occlusion. There were 46.7±6.2 points
used to calculate r at baseline. The number of
points increased in the preload and total load beats
(54.2±5 .5, 60.4±2.0, respectively; p<0.05). There
was no change in TL with a reduction in preload or
total load (47.4±6.5 to 44.6±7.6 to 41.6±8.4 msec;
respectively, p=NS). The correlation coefficient
(R) for TL was similar at baseline, after a reduction
in preload, and after a reduction in total load
(-0.996±0.004 to -0.995±0.005 to -0.996±0.005,
respectively; p= NS).
There was no change in TD from baseline with a
reduction of only preload and after a subsequent
reduction in total load (39.3±8.1 to 39.8±8.4 to
40.8± 11.1 msec, respectively;p=NS). R for TD was
similar at baseline, after a reduction in preload, and
after a reduction in total load (-0.862±0.038 to
1760
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-0.861±0.041 to -0.857±0.042, respectively,
p=NS), although it was less than R for TL. There
was no change in T1,, from baseline with a reduction
of only preload or after a subsequent reduction in
total load (33.0±4.0 to 31.8+4.6 to 31.7+4.2 msec,
respectively; p=NS).
Effect of Preload and Total Load Changes on PB
Determination of TD provided a calculation of the
extrapolated residual LVP (PB). At baseline PB was
+4.26±6.20 mm Hg. After a reduction in preload
with inferior vena cava occlusion, there was a
numeric decrease in PB that did not achieve statistical significance (-0.80±4.87 mm Hg; p==0.20 vs.
baseline). With a reduction in total load, PB did
decline to -3.9±4.26 (p<0.05 vs. baseline).
Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017
Linearity of lnP Versus Time
In Figure 2 the natural log of left ventricular
pressure versus time is depicted for each of the six
patients during inferior vena cava occlusion. The
open circles represent the baseline beat, the closed
circles a reduction in preload, and the closed triangles a reduction in total load. Each symbol is a lnP
versus time value digitized at a frequency of 1 kHz.
In all patients, there was a parallel downward shift
from baseline to preload to total load beats, consistent with no change in the slope of the ln(P) versus
time relation (or TL) despite a visibly evident
decrease in preload and total load. In addition, the
exponential nature of the pressure decline during
isovolumetric relaxation is visibly evident.
Bie,xponential Pressure Decay of Negative dP/dt
Versus Left Ventricular Pressure
In Figure 3 negative dP/dt versus LVP is depicted
for each of the six patients during inferior vena cava
occlusion. The open circles represent the baseline
beat, the closed circles a reduction in preload, and
the closed triangles a reduction in total load. Each
symbol is a negative dP/dt versus P value digitized
at a frequency of 1 kHz. The preload and total load
values separated from the baseline values only
during the first half of isovolumetric relaxation.
There was the appearance of biexponential pressure
decay, as previously described by Brower et al.19
Discussion
This study altered preload in six patients with
inferior vena cava occlusion before the appearance
of reflex increases in heart rate. After this alteration
in preload, no change was noted in r as calculated
by the logarithmic, derivative, or method of Mirsky. Although there was a decreasing trend for PB,
statistical significance was not achieved. Subsequent beats were also identified where systolic LVP
decreased although without reaching statistical significance. r calculated by the three methods above
still did not change, but PB decreased. Visual display of the individual ln of LVP versus time values
used to calculate r by the logarithmic method were
1761
consistent with exponential pressure decay as an
appropriate model for isovolumetric relaxation.
A strength of this study was the ability to alter
loading conditions in patients before the appearance
of reflex changes without the use of an intravenous
drug infusion. The technique used was transient
occlusion of the inferior vena cava, popularized in
the animal laboratory by Rankin and coworkers.20
However, traditional muscle mechanic studies in
patients have not taken advantage of this technique
but, rather, have used drug infusions to alter load.
For instance, Starling et al recently demonstrated
that r was a load-independent measure of isovolumetric relaxation.14 They altered load by infusing
methoxamine and nitroprusside while performing
atrial pacing to maintain a constant heart rate.
However, their study was weakened by the cardiovascular effects of these drugs. Methoxamine is a
relatively specific a,-adrenoceptor agonist. Human
myocardium contains a-adrenergic receptors in both
the atrium21 and the ventricle.22 Methoxamine infusion has both inotropic and chronotropic effects,
mediated by increased influx of calcium through
calcium channels. Scholz et al confirmed these
results, demonstrating an increased magnitude of
the slow inward calcium current and associated
inotropic effect.23 However, a decreased rate of
decay of the slow inward calcium current was also
noted by these same workers. Methoxamine can
also increase coronary resistance, override intrinsic
coronary regulatory influences, and produce ischemia in dogs with normal coronary arteries.24 The
variety of cardiovascular effects mentioned above
can have opposite effects on r and explain, in part,
the load independence of r demonstrated by Starling et al.14
A second strength of this study was accurate
calculation of r. Several hemodynamic studies performed in both the animal and cardiac catheterization laboratories determined r by reentering handtraced LVP recordings into a computer. Human
error could be introduced into the raw data before
computer calculation of r. We stored analog left
ventricular pressure signals on a tape recorder and,
with an analog-to-digital converter, reentered the
pressure signal into a computer for calculation of r.
Because no human error or bias was introduced
when converting the analog LVP signal to a digital
format, the data were digitized every 1 msec in the
current study, fivefold faster than previously
reported in the literature.5-8,10,11,14-16 r was calculated from a mean of 54+8 points for the logarithmic
and derivative methods.
In addition to its preload independence, r may be
independent of total load within a physiologic range.
There have been several clinical studies of hypertrophy and ischemia equating a prolongation of
myocardial relaxation (or r) with abnormal left
ventricular diastolic function.9-13These studies were
weakened by increased systolic LVP, LVEDP, or
both imposed on the myocardium when r was
1762
Circulation Vol 80, No 6, December 1989
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FIGURE 2. Plots of In of left ventricularpressure versus time for each ofsxpatients during inferior vena cava occlusion.
o, Baseline beat; *, reduction in preload; A, reduction in total load. (See text for discuission.)
prolonged. Our findings support the assumptions of
the above studies that alterations in r are independent of load changes. Although the goal of the
current investigation was to produce pure preload
beats, total number of load beats was identified as
well. No change in was noted with simultaneous
r
falls in systolic and diastolic LVP. To avoid a reflex
increase in heart rate, the total load beats produced
with inferior vena cava occlusion did not achieve a
significant change in left ventricular systolic pressure from baseline (113.3±13.8 to 100.8±14.3
mm Hg), although the trend was clear. However,
Varma et al Preload Independence of
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occlusion. o, Baseline beat; 0, reduction in preload; *, reduction in total load. (See text for discussion.)
cava
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Left Ventricular Pressure (mmHg)
Starling et al produced greater alterations in load
with drug infusions and confirmed the load independence of r in humans over a physiologic range in the
cardiac catheterization laboratory.'4 The present
investigation, in conjunction with the work of Starling et al, argues that given the physiologic constraints of hemodynamic studies performed in
patients, is a load-independent measure of isovolumetric relaxation.
r
To determine the preload dependence of r, the
current study decreased filling of the left ventricle,
while work by Gaasch et a15 and Karliner et a16 used
volume infusion. Occlusion of the inferior vena
cava to alter preload was the opposite of these
canine studies using volume infusion. In all of these
studies, was found to be independent of preload.
However, increasing preload enough to raise systolic LVP in the studies of Gaasch and Karliner did
r
1764
Circulation Vol 80, No 6, December 1989
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produce an increase in n. These studies imply that r
may be dependent on preload only to the extent that
changes in preload affect systolic loading. In the
present study and the work of Starling et al,14
decreases in load sufficient to decrease systolic
LVP did not change r. Thus, increasing as opposed
to decreasing load may change the rate of isovolumetric relaxation. For instance, when load is
increased, isovolumetric relaxation may be prolonged. Conversely, a decrease in load may have no
effect. However, in the study of Starling, an increase
in load did not prolong isovolumetric relaxation.
These data must temper the notions of the type of
systolic load (i.e., increasing load and prolonging r
versus decreasing load and not affecting j).
Unlike r, the baseline pressure (PB) extrapolated
from isovolumetric relaxation, which represents a
baseline to which pressure would fall if decay
continued infinitely, was found to be load dependent in the present study. PB may reflect a basal
level of diastolic myocardial tone, but its physiologic meaning has been unclear. Carroll et al, for
instance, attached important physiologic significance to PB and believed that exercise-induced
ischemic increases in PB represented an important
influence of slowed isovolumetric relaxation on
elevated pressures late in diastole.25 In contrast,
Thompson et al did not demonstrate pacing-induced
ischemic alterations in PB despite prolongation of
isovolumetric relaxation and elevation of LVEDP. 15
The present study demonstrated a downward trend
in PB with decreasing preload and a significant fall in
PB with a fall in both preload and afterload (Table 1).
Future studies in patients designed to examine
physiology with PB in the cardiac catheterization
laboratory will have to be tempered by the load
dependence demonstrated in this study.
In their original description Weiss et al believed r
was a reflection of the "active cardiac relaxation
system.'"17 Several investigators have since identified a prolongation in r in several disease states,
including myocardial ischemia, cardiac hypertrophy secondary to essential hypertension and valvular heart disease, hypertrophic cardiomyopathy,
and congestive cardiomyopathy. Grossman and
coworkers, in particular, have related this prolongation in isovolumetric relaxation in part to abnormal calcium handling.9-11 The present study supports using r as a reflection of calcium handling by
the myofilaments. As is visually evident in Figure 2,
the plot of the ln of LVP versus time was linear for
all baseline, preload, and total load beats. This
exponential decay of pressure was consistent with
mathematic models of calcium release from the
myofilaments. Potter et al, for instance, used a
numeric computer solution to display the exponential time course of calcium release from troponin
and calmodulin.26
There were several limitations to this study. The
absence of a change in r with a decrease in preload
may be due to opposite physiologic effects pro-
duced by the method chosen to alter load. Inferior
vena cava occlusion, by unloading the right ventricle, may change the radius of curvature of the
intraventricular septum. Resultant asynchronous
relaxation of the left ventricle would prolong T.27 A
simultaneous decrease in left ventricular preload,
however, would be expected to decrease r according to isolated cardiac muscle studies.2 These two
opposite effects might cancel one another and produce no change in r with alterations in preload, as
seen in this study. A second limitation of this study
was the inability of inferior vena cava occlusion to
produce a statistically significant decrease in systolic LVP before the appearance of a reflex increase
in heart rate. It is difficult, therefore, to reach firm
conclusions regarding the total load dependence of
r on the basis of this study. Third, although the
patients chosen to participate in this study were
normal by cardiac catheterization criteria, their
baseline LVEDPs were elevated. This finding was
an artifact of the computer digitization routine. The
computer software was written to locate LVEDP at
the peak of the R wave of the electrocardiogram.
Reanalysis of LVEDP "by hand" defined by the
atrial systolic deflection on the upstroke of LVP
gave a mean LVEDP of 14±2 mm Hg. Finally, our
results were not in conflict with the known load
dependence of relaxation in isolated papillary muscle. It is an intrinsic property of cardiac muscle that
the rate of relaxation is load dependent.1-4 Rather,
in the intact human heart, when isolated reductions
in preload are evaluated, - is found to be load
independent over a relatively narrow physiologic
range. Although we produced statistically significant reductions in preload, the magnitude of decrease
in LVEDP was only over an approximately 6-9
mm Hg range. Therefore, when isolated reductions
in preload are performed in patients, this method of
assessment of isovolumetric relaxation as a variable
of active muscle relaxation is not affected.
In conclusion, this study has demonstrated that r
is a preload-independent measure of isovolumetric
relaxation. This conclusion is strengthened by the
method used: altering load with inferior vena cava
occlusion before the onset of reflex changes and
recording pertinent analog signals on cassette tape
for later "on-line" computer digitization. Unlike r
the baseline pressure (PB) extrapolated from isovolumetric relaxation is load dependent. Because of
the frequency of computer digitization used, this
study lends support to exponential pressure decay
as an appropriate mathematic model for isovolumetric relaxation. Finally, this study supports the use
of i as a reflection of myocardial physiology because
of its load independence.
Acknowledgments
This study could not have been completed without the support of the cardiac catheterization staff
at the University of Virginia and the secretarial
expertise of Jerry Curtis.
Varma et al Preload Independence of r
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KEY WORDS *
* vena cava * occlusion
Is tau a preload-independent measure of isovolumetric relaxation?
S K Varma, R M Owen, M L Smucker and M D Feldman
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Circulation. 1989;80:1757-1765
doi: 10.1161/01.CIR.80.6.1757
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