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Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Most noninvasive measures of diastolic
function are made during left ventricular (LV) filling and are
therefore subject to "pseudonormalization," because variation in
left atrial (LA) pressure may confound the estimation of relaxation
rate. Counterclockwise twist of the LV develops during ejection, but
untwisting occurs rapidly during isovolumic relaxation, before mitral
opening. We hypothesized that the rate of untwisting might reflect the
process of relaxation independent of LA pressure. Recoil rate (RR), the velocity of LV untwisting, was measured by tagged magnetic resonance imaging and regressed against the relaxation time constant (
), recorded by catheterization, in 10 dogs at baseline and after dobutamine, saline, esmolol, and methoxamine treatment. RR correlated closely (average r = 
0.86) with and was
unaffected by elevated LA pressure. Multiple regression showed that
, but not LA or aortic pressure, was an independent predictor of RR
(P < 0.0001, P = 0.99, and
P = 0.18, respectively). The rate of recoil of torsion, determined wholly noninvasively, provides an isovolumic phase, preload-independent assessment of LV relaxation. Use of this novel parameter should allow the detailed study of diastolic function in
states known to affect filling rates, such as aging, hypertension, and
congestive heart failure.
diastole; hemodynamics; magnetic resonance imaging; imaging
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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LEFT VENTRICULAR (LV) relaxation is difficult to assess by noninvasive means, because imaging methods cannot directly measure cavity pressure. Echocardiographic, Doppler, and radionuclide parameters of diastolic function are derived from rates of inflow of blood or outward movement of the myocardium. However, the process of relaxation occurs mostly during the diastolic isovolumic period of the cardiac cycle, before blood flow or wall motion begins. Indexes measured later in the cycle examine only the final stages of relaxation (33). Furthermore, these parameters are subject to "pseudonormalization," because variation in left atrial (LA) pressure profoundly affects filling dynamics and thus confounds attempts to indirectly estimate the relaxation rate (22, 31, 40, 41). New echocardiographic methods that are less sensitive to LA pressure (7, 16, 21, 39) or "adjust" for an estimated LA pressure (2, 3, 24, 37) are in clinical use, but novel noninvasive ways of directly assessing relaxation are needed.
LV torsion is the wringing motion, or twist, of the heart imparted by
contraction of its obliquely spiralling fibers. Counterclockwise torsion develops during ejection, but the clockwise recoil of torsion,
or untwisting, is a deformation that occurs largely during isovolumic
relaxation, before mitral valve opening (6, 10, 23, 29, 34,
46). This recoil is associated with the release of restoring
forces that had been accumulated during systole and is thought to
contribute to diastolic suction (17, 29, 34, 46). The
extent of torsion is correlated with cavity pressure (14),
and its recoil rate (RR) may thereby be related to the rate of pressure
fall. This deformation can be quantified using magnetic resonance
imaging (MRI) with tagging, a noninvasive method for marking and
tracking specific myocardial sites (5, 47). In this study,
we explored the relationship between the rate of untwisting (RR) and
the relaxation time constant () using various interventions to alter
in intact canine hearts. The influence of LA pressure on RR was
assessed. The strength of the relationship between and RR was
compared with that between and isovolumic relaxation time (IVRT), a
standard index of relaxation that is known to be highly sensitive to
preload. We suggest that RR may provide a new isovolumic phase measure
of relaxation that is preload independent and can be determined noninvasively.
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METHODS |
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Terminology. In this paper, the term "LV relaxation" refers to the time course of LV pressure decline, a process that depends on both deactivation of actin-myosin cross-bridges and the release of restoring forces due to chamber and myocardial deformation (45). The term "preload" refers to LA pressure, which constitutes the preload to ventricular filling.
Animal preparation. Ten adult mongrel dogs (9 males and 1 female, weighing 24 ± 3 kg) were anesthetized with intravenous pentobarbital sodium (25-35 mg/kg). After intubation, the dogs were mechanically ventilated (model 613, Harvard Apparatus). The left jugular vein was cannulated for fluid and drug administration, and the right jugular vein was cannulated for placement of a right atrial pacing lead. Each dog was instrumented with magnetic-compatible micromanometer-tipped catheters (Millar Instruments) to measure LA, LV, and aortic pressures as follows. A left thoracotomy was performed, and a small transverse incision (~3 cm) was made at the ventrolateral pericardium along the base of the heart for the placement of a LA catheter through the LA appendage with a purse-string suture. A LV catheter was placed through cannulation of the left internal carotid artery. An aortic catheter was inserted through cannulation of the left femoral artery. After surgical preparation, the animal was allowed to stabilize for 30 min. Throughout the experiments, body temperature was maintained by a heating pad, the chest was left open, and the electrocardiogram (lead II) was monitored and also used as a trigger for MRI. At the end of experiment, the animal was euthanized using intravenous KCl. If hemodynamic instability or arrhythmias precluding further MRI developed, the protocol was terminated without additional interventions. All procedures were approved by the institutional Animal Care and Use Committee.
Experimental protocol.
Interventions were planned with the main goal of recording
hemodynamic and MRI data (during steady-state conditions) over a wide
range of values of and with variations of LA and aortic pressures.
The conditions studied were as follows: 1) first baseline, 2) dobutamine infusion, 3) dobutamine infusion
plus volume loading, 4) second baseline (stopping dobutamine
infusion), 5) esmolol infusion, 6) third baseline
(stopping esmolol infusion), and 7) methoxamine infusion.
Dobutamine (Eli Lilly) was diluted (250 mg in 500 ml saline) and
infused to increase systolic LV pressure by at least 15%. Volume load
was performed by infusing saline at 10-12 ml/kg body wt (range,
200-300 ml) in each individual experiment. Esmolol (Ohmeda) was
diluted (2,500 mg in 500 ml saline) and infused to decrease systolic LV
pressure by at least 15%. Methoxamine (Burroughs-Wellcome) was diluted
(20 mg in 500 ml saline) and infused to increase systolic LV pressure
by at least 15%. Solutions were mixed immediately before infusion.
After stabilization of each condition, hemodynamic and MRI data were acquired.
Hemodynamic analysis.
All signals were amplified (Gould Instrument) and digitized at
sampling frequencies of 250 Hz for 5 s under each condition. was calculated by measuring LV pressure every 4 ms from the point of
the minimal instantaneous rate of change of LV pressure with respect to
time (dP/dt) until its upturn and fitting the curve to the
following equation: p(t) = p0e
t/
+ p
(20), where p is pressure,
p0 is pressure at minimal dP/dt, t is
time thereafter, p represents the pressure asymptote.
IVRT was measured from the LA, LV, and aortic pressures as the interval
from the crossover of the LV and aortic pressures to the crossover of
the LV and LA pressures.
MRI image acquisition.
Myocardial tagging was used in these experiments to measure torsion and
its rate of recoil. Tags are noninvasive markers that are imprinted on
the myocardium by selective radiofrequency saturation of planes
perpendicular to the imaging planes; they change the magnetization of
the protons in the tagged plane compared with the neighboring nontagged
regions, resulting in a difference in signal intensity. When placed at
end diastole and then imaged throughout the cardiac cycle, tags reveal
the deformation and displacement of the myocardium on which they are
placed (Fig. 1). Tags may be positioned
in a radial pattern (47), which is ideal for the
measurement of torsion, or in a grid pattern (5), which is
commonly used for calculation of a full strain field.
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MRI image analysis. The digital MRI data were processed using a special software package (Cardiology Image Processing System, Johns Hopkins University). The tag-endocardium intersection points on both basal and apical short-axis images were identified manually and digitized (8 points/slice).
Torsion at each tag-endocardium intersection point was calculated as an angle between the tag line of the apical slice and the projection of the basal tag line on the apical slice at end systole, as previously reported (Fig. 2) (9, 14). With the use of this method, clockwise rotation of the base and counterclockwise rotation of the apex are combined to yield a measure of the total base-to-apex deformation. Mean torsion was then calculated as the average of eight values for the eight tag-endocardial intersection points. Recoil, the directional reversal of systolic counterclockwise torsion during diastole, was expressed as the percentage of maximum systolic torsion: recoil = Tort/Tormax × 100, where Tort is torsion at time t and Tormax is the maximum systolic torsion. [Normalization to maximum torsion was performed as the primary analysis here because,
the gold standard for relaxation, is based on the time required for a
percentage of pressure fall (1/eth) rather than
an absolute pressure drop in mmHg. However, analyses were repeated
using the non-normalized torsion values.] RR was defined as the slope
of the linear regression of recoil versus time, which is similar to the
method used by DeAnda et al. (13), during the first 64 ms
after peak torsion (i.e., using data from five images).
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Statistical analysis. The overall effect of each intervention (dobutamine, volume, esmolol, and methoxamine) on hemodynamic and MRI parameters was assessed by paired t-tests. A value of P < 0.05 was considered statistically significant.
The relationships between and RR, and likewise between and
IVRT, were initially explored by simple linear regression analysis. In
each individual animal, correlations (r and
r2) were determined for both
relationships. To compare the significance of these two
relationships (-RR vs. -IVRT), paired t-tests were applied based on the derived r2 for each
relationship; to compare the consistency of the two relationships, the
test for correlated variances was applied to SD2
(38). Overall correlations of and RR, and of and
IVRT, were derived using linear regression analysis adjusting for
effects in individual dogs (20).
Finally, multiple regression analysis was performed to determine the
significance of the -RR and -IVRT relationships in the presence
of other hemodynamic variables and to test whether the other variables
were independent determinants of RR and IVRT using the Generalized
Estimating Equation (GEE) method for repeated-measures data
(25). The independent, or explanatory, variables in the GEE model included LA pressure, aortic pressure, LV systolic pressure, , and peak +dP/dt. The dependent variables were RR for
the -RR relationship and IVRT for the -IVRT relationship. The
correlations among the repeated observations for individual dogs were
modeled as exchangeable correlations. A value of P < 0.05 was considered statistically significant. These analyses were all
repeated for the non-normalized RR.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Effects of interventions. Ten dogs were instrumented and studied. All 10 dogs had hemodynamic and MRI measurements at first baseline, during dobutamine infusion, and after volume loading. Seven dogs had additional measurements at second baseline and during esmolol infusion, and four dogs had additional measurements made at third baseline and during methoxamine infusion.
The average effects of catecholamine stimulation, volume infusion,
-blockade, and increased afterload on the variables of interest are
detailed in Table 1. Of note, the
predominant effect of dobutamine was a reduction in (from 34 to 27 ms, P = 0.0007); there was a concomitant increase in RR
(from 0.69 to 0.81 %/ms, P = 0.02), and IVRT
shortened. The predominant effect of volume infusion was an increase in
LA pressure (from 9.0 to 14.6 mmHg, P = 0.0001); RR was
unchanged, whereas IVRT shortened significantly. Esmolol reduced aortic
pressure without having a significant effect on , RR, or IVRT.
Methoxamine greatly increased LA and aortic pressures and caused to
increase, but did not significantly change RR or IVRT.
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Correlation of and RR.
The correlations of RR with in each individual dog for which at
least five measurements were available (7 of 10 dogs) are detailed in
Table 2. For comparison purposes, the
correlations of IVRT with are also shown. The -RR correlations
are high in each individual animal studied, with an average
r of 0.86 (ranging from 0.77 to 0.93) and with similar
slopes. The -IVRT relationships have less consistent slopes and
lower r2 values. The correlation of RR with is significantly better (P = 0.026 based on
r2) and less variable (P < 0.001 based on SD2) than the correlation of IVRT with .
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is plotted in Fig.
3. When data from all 10 dogs were pooled
and adjusted for individual dog effects using an indicator variable,
r was 0.92 and r2 was 0.85, with
P < 0.0001. The relation between and IVRT was also
significant, with r = 0.81, r2 = 0.65, and P < 0.0001.
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Multiple regression of hemodynamic parameters against RR and
against IVRT.
Multiple regression using GEE was performed to assess the correlation
of individual hemodynamic parameters with RR and IVRT, accounting for
the potential confounding effect of other variables (Table
3). was the only independent
predictor of RR (P < 0.0001); there was no independent
relation between RR and LA pressure (P = 0.817), aortic
notch pressure (P = 0.287), LV peak systolic pressure
(P = 0.604), or peak +dP/dt
(P = 0.060). In contrast, IVRT was closely related to
LA pressure (P < 0.0001) and aortic pressure
(P = 0.015) as well as to (P < 0.0001).
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and absolute RR (P = 0.004, coefficient = 0.0273). There was a weak but significant
relation between LA pressure and absolute RR (P = 0.02, coefficient = 0.0001), probably due to the preload dependence of
absolute values of torsion (14). The nonnormalized RR at
baseline was 0.084 ± 0.038 (SD) °/ms.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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LV relaxation begins when myofiber tension starts to decline
during late ejection (8), proceeds rapidly as pressure
falls during isovolumic relaxation, and continues through the period of
early filling. Relaxation is best quantified by measuring the rate of
LV pressure decay, which can be expressed as a time constant (),
based either on a monexponential model with a zero (44) or
nonzero asymptote (30) or on a "logistic" model
(27). The greatest portion of the pressure decline occurs
during isovolumic relaxation. The process of LV filling, which begins
at the time of mitral valve opening, profoundly alters the rate of LV
pressure decline; pressure changes that occur after mitral valve
opening do not reliably reflect the process of relaxation itself
(15, 30).
Noninvasive methods can detect the extent and velocity of motion of the myocardium or blood. However, standard measurements provide little information about the isovolumic period (other than its duration), during which most of the relaxation process occurs (19), because deformations that are routinely studied (e.g., myocardial lengthening or thinning, cavity volume increase, and blood inflow) are dependent on changes in LV volume. These deformations do not begin until after the mitral valve opens, when most of the relaxation process has already been completed. Like invasive measurement of pressure, these noninvasive parameters tend to be strongly influenced by factors other than relaxation that contribute to the early diastolic atrioventricular pressure gradient [i.e., LA pressure, passive myocardial stiffness (4), and viscoelasticity (15)].
Torsion mechanics. Torsion and its diastolic recoil display a unique behavior that is, in part, volume independent and therefore can be observed during the isovolumic periods. With the use of implanted markers (6, 29, 46), MRI tagging (34), and guidewire rotation during angioplasty (23), it has been clearly shown that during isovolumic relaxation, when cavity volume is fixed, there is a rapid recoil of ~40% of the torsion that had accumulated during systole. In addition, volume independence has been shown in a completely isovolumic beating heart preparation, in which there is considerable torsion and recoil, despite the absence of thickening or circumferential or longitudinal shortening (26).
Therefore, in contradistinction to other noninvasive indexes of diastolic function, recoil of torsion is largely an isovolumic event, as is the gold standard for relaxation,. Recently, Dong et al.
(14) found that during conditions of fixed cavity volume in an isolated perfused heart model, the extent of torsion depended on
cavity pressure. We therefore hypothesized that the rate of recoil
might reflect the rate of pressure fall during isovolumic relaxation
and that its measurement might provide a more physiological and direct
noninvasive method for quantification of relaxation than has heretofore
been available.
In this study, RR was indeed found to correlate closely and
reproducibly with . This finding is consistent with prior studies of
torsion during diastole in humans. Moon et al. (29)
altered load and contractility in transplant recipients with radiopaque markers and reported a close relationship of early diastolic untwist with both peak dP/dt and LV end-systolic volume, both of
which are closely related to . Yun et al. (46) noted
that early diastolic rapid recoil was markedly diminished during
cardiac transplant rejection, which would be expected to slow
relaxation: the time to 50% of peak twist was prolonged by 40%. This
phenomenon was a sensitive predictor of rejection. Knudtson et al.
(23) found that, whereas recoil of the apex was 37%
complete by the end of isovolumic relaxation in nonischemic
human hearts, recoil during isovolumic relaxation was essentially
absent during acute ischemia induced by angioplasty balloon
inflation, a condition known to prolong . Studies in dogs
have been less consistent. Rademakers et al. (34) reported
that inotropic stimulation caused an increase in the extent of recoil
during isovolumic relaxation, whereas Gibbons Kroeker et al.
(18) reported a decrease, but was not measured in
those studies.
Mechanistic significance of recoil. In addition to providing a means to measure the rate of LV pressure fall, the untwisting deformation may itself contribute to the pressure decay. Relaxation is dependent on the rate of deactivation of cross-bridges within the sarcomere but is also associated with the release of restoring forces from the ventricular wall. These forces are stored when systolic contraction of the cavity to volumes below an "equilibrium volume" results in the stretch or compression of cellular and extracellular proteins such as titin (11) and collagen (29, 34, 46). The development of counterclockwise torsion during systole leads to transmural equilibration of fiber shortening (4) and allows a greater deformation of elements within the wall for any given ventricular volume (14). This is particularly true in the endocardium, where the counterclockwise torque is in the direction opposite to the alignment of fibers, and considerable deformation of the connective tissue matrix must occur (35, 43). This may permit more energy to be stored within the wall. The release of this repository of force during isovolumic relaxation creates ventricular suction, returning the stored energy to the circulation (45).
Preload independence. As expected, IVRT shortened significantly with volume loading and proved highly dependent on LA pressure in the multivariate analysis. In contrast, RR was unchanged with fluid loading (which increased LA pressure from 9 to 14.6 mmHg), and, in the multivariate analysis, there was no contribution of LA pressure toward RR. This demonstration of preload independence suggests that RR may not be subject to "pseudonormalization" in situations where LA pressure rises or to overestimation of diastolic abnormalities in situations where LA pressure is low, for example, during dehydration. The influence of other factors not directly related to relaxation, such as mitral inertance and atrial contractility, on RR could not be assessed by this study but is likely to be less for this isovolumic phase index than for indexes of diastolic function measured during filling.
Two new Doppler measurements have also been shown to reflect relaxation with only minimal preload dependence. Color M-mode Doppler detects the velocity of propagation of the filling wave between the mitral valve and LV apex during early filling (7, 39). This velocity is dependent on the presence of intraventricular gradients, which appear to be more closely related to the ventricular relaxation process than to the atrial driving force. Tissue Doppler echocardiography (16, 21) detects myocardial long-axis lengthening velocity during early (E wave) and late (A wave) diastole. The preload independence of this method could relate to a preferential effect of ventricular relaxation on base-to-apex dimension changes, whereas atrial driving force might affect lengthening in the circumferential direction. However, both of these new echocardiographic methods depend on measurements made after most of the relaxation process has already been completed, which reduces their sensitivity. More importantly, they are recorded after filling begins so some influence of load is therefore to be expected (1, 32, 42). A third type of Doppler method has been described, which can be measured during isovolumic relaxation; the rate of decay of a mitral regurgitation jet (12) or rate of acceleration of an aortic regurgitation jet (36) is interrogated. However, this measure requires the presence of a regurgitant jet that is large enough to produce a continuous signal, and this method is not load independent, because mitral regurgitation is determined by atrial as well as ventricular pressure and aortic regurgitation is closely related to aortic diastolic pressure. The current study utilized only MRI and hemodynamic variables and could not compare the utility of RR with these new echocardiographic parameters. However, we were able to compare RR with IVRT, an older index of relaxation that can be measured by echocardiography (28). IVRT was significantly affected by volume loading, and its correlation with was less consistent and more variable than that of RR,
probably due to its greater dependence on LA pressure.
Limitations.
Several limitations exist in the interpretation of these data. First,
as noted above, our study did not allow comparison of the relative
value of this new index of relaxation with newer echocardiographic
techniques. We also did not assess the effects of regional wall motion
abnormalities. Such studies will be important in defining the role that
this method will ultimately play. Second, correlation of RR with was high (0.86 for individual experiments, 0.92 for pooled data),
but the corresponding r2 values (0.75 and 0.84, respectively) indicate that there are components of the variation of RR
that are not entirely explained by . Note that the SD of RR is
higher than that of . Errors in defining the endocardial-tag
intersections (which was done by hand), limitations in image resolution
due to pixel size (which averaged 1.5 mm), and image times of several
minutes in the absence of respiratory gating may have contributed to
this variation. Automatic tag-tracking algorithms and improved speed
and pixel resolution in newer magnetic resonance systems will reduce
these problems in the future. Third, the heart rates in the dogs
studied were high due to anesthesia and the need for atrial pacing at a
constant rate (to assure accurate gating); this prevented us from
studying the rate dependence of RR. It also raises the question of
whether our results are generalizable to slower rates. We suspect that
rate is not an important confounder here because studies of human
transplant recipients (28, 45) at physiological rates yielded results consistent with ours. Fourth, RR was determined using a
linear regression of recoil versus time, whereas pressure is known to
decline in an exponential fashion starting at peak dP/dt
(44). We tested an exponential model as well and found similar correlations, but chose the more simple linear model because our temporal resolution was not adequate to define an appropriate starting point (i.e, peak dP/dt) for an exponential
relationship. Higher temporal resolution is now available using the
latest magnetic resonance scanners, and future studies might attempt
various exponential fits. The pioneering works in this field by Yun et
al. (46) and Moon et al. (29) also used
linear models. Finally, we used tagged MRI for these experiments. The
availability of this technique is currently limited, and specialized
software is required for analysis. However, cardiac magnetic resonance
is recognized as an excellent research tool and is growing in
popularity and accessibility for clinical care. Furthermore, there may
be potential for visualizing LV apical rotation and recoil using tissue
Doppler echocardiography, a widely available technology.
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ACKNOWLEDGEMENTS |
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We are grateful to Dr. Edward G. Lakatta for thoughtful critiques of these concepts and to Stephanie Bosley for superb technical operation of the MRI scanner and processing of the image data.
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FOOTNOTES |
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This study was supported by National Heart, Lung, and Blood Institute Grant RO1 HL-46223 (to E. P. Shapiro).
This paper was presented in part at the 70th Annual Scientific Sessions of the American Heart Association, Orlando, Florida, November 1997.
Address for reprint requests and other correspondence: E. P. Shapiro, Div. of Cardiology, Johns Hopkins Univ. School of Medicine, 4940 Eastern Ave., Baltimore, MD 21224 (E-mail: eshapiro{at}jhmi.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 7 December 2000; accepted in final form 18 July 2001.
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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) between the apical tag position
(point d) and the basal tag position (reflected onto the
apex as point e). Torsion therefore combines the opposite
rotations of base and apex into a single deformation. Arrows show the
direction of torsion and recoil.
