Vol. 280, Issue 4, H1846-H1852, April 2001
Influence of timing and magnitude of arterial wave reflection
on left ventricular relaxation
Masafumi
Yano,
Michihiro
Kohno,
Shigeki
Kobayashi,
Masakazu
Obayashi,
Kohzaburo
Seki,
Tomoko
Ohkusa,
Toshiro
Miura,
Takashi
Fujii, and
Masunori
Matsuzaki
Second Department of Internal Medicine, Yamaguchi University
School of Medicine, Ube, Yamaguchi 755-8505, Japan
 |
ABSTRACT |
The influence of timing and magnitude of
arterial wave reflection (WR) on afterload-dependent relaxation was
evaluated in patients with a variety of heart diseases (group
1, age < 30 yr; group 2, age > 40 yr) and
in dogs. While both femoral arteries were compressed (FC), WR returned
just after the dicrotic notch (early diastole) in group 1 but before the dicrotic notch (late systole) in group 2. The
time constant of the left ventricular pressure decay (
) was
shortened during FC in group 1, whereas it was prolonged in
group 2. In dogs, a constriction of the thoracic aorta
induced a late systolic augmentation of WR with a prolongation of (cf. group 2), whereas constriction of the lower abdominal aorta induced an early diastolic augmentation of WR with a shortening of (cf. group 1). With aortic constriction, coronary
flow increased, and there was a close correlation between the peak
change in backward aortic pressure and that in coronary flow regardless
of the timing of WR. Thus the time at which WR returns during the
cardiac cycle may have an important effect on left ventricular
relaxation and coronary flow.
coronary flow; ventricular function; afterload
| |
INTRODUCTION |
IT IS WELL KNOWN
that left ventricular (LV) relaxation is influenced by afterload
(2, 5, 9, 20). Although the mechanism underlying this
afterload dependence remains to be elucidated, the systolic loading
sequence is considered to be an important factor (6, 8).
In particular, a late systolic pressure rise induces a slower
relaxation than early systolic pressure rise (6, 8, 12,
28). In a previous report (28), we demonstrated that a regional nonuniformity between the apical and basal regions is
produced by a late systolic pressure rise and that this contributes to
the slower LV relaxation. A rise in end-systolic pressure might also be
an important factor in this slower relaxation (12). Clinically, Murgo and Westerhof (16) divided human
arterial pressure waveforms into three different types (viz. those
peaking in early systole, in middle systole, or in late systole) and
examined the aortic impedance spectra associated with each type of
systolic loading sequence. They demonstrated that the occurrence of a
pressure rise in late systole was associated with an early return of an increased arterial wave reflection and was frequently observed in older
subjects (in whom arterial compliance is significantly decreased).
Taking all these findings together, we hypothesized that a given
increase in the arterial wave reflection might produce this different
systolic loading condition depending on the age of the subject and
that, in turn, this might have different effects on the
afterload-dependent relaxation. The goal of this study was to clarify
how the timing and magnitude of the arterial wave reflection influences
the systolic loading sequence and hence the afterload-dependent
relaxation. The investigations were conducted in patients with heart
disease and also in experimental animals (dogs).
| |
MATERIALS AND METHODS |
Patient classification and protocol.
The selection of the patients was based on a sequence of patients
prospectively selected only on the basis of age (
30 or 
40 yr) with
the following exclusion criteria: there were no atrial fibrillation,
aortic regurgitation, and arteriosclerosis obliterans. In 20 patients
who underwent cardiac catheterization for diagnosis and matched with
the above criteria, 4 patients were excluded because the multisensor
catheter could not be passed into the ascending aorta through the
brachial artery. In the remaining 16 patients, clinical study was
performed. Group 1 consisted of eight patients (age < 30 yr, average age 20 ± 5 yr): four patients with dilated
cardiomyopathy (DCM) and four patients with idiopathic ventricular
tachycardia (VT). Group 2 consisted of eight patients (age > 40 yr, average age 55 ± 9 yr): six patients with
coronary artery disease (CAD) without significant stenosis (>75%),
one patient with DCM, and one patient with nonobstructive hypertrophic cardiomyopathy (HCM). One patient with CAD had essential hypertension. All patients had a sinus rhythm, and none had arteriosclerosis obliterans or aortic regurgitation (as confirmed by color Doppler echocardiography). Vasodilators and other drugs influencing LV relaxation were discontinued 48 h before the study. During routine cardiac catheterization, a multisensor catheter (Millar) was introduced via the brachial artery to enable measurement of aortic and LV pressures and aortic flow velocity. Cardiac output was obtained by the
thermodilution method.
After control recordings had been made, both femoral arteries
were compressed manually for 20 s. During this compression, the
pulsation of the dorsal pedis artery disappeared.
Before the clinical study, informed consent was obtained from all
patients, and approval was given by the local ethics committee. This
investigation conforms with the principles outlined in the Declaration
of Helsinki.
Experimental model and instrumentation.
The investigation conforms with the Guide for the Care and Use of
Laboratory Animals, published by the National Institutes of Health
(NIH Publication No. 85-23, Revised 1996).
Instrumentation was performed as described previously (27,
28) in seven mongrel dogs weighing 10-15 kg. They were
anesthetized with morphine (5 mg sc) followed by the administration of
-chloralose (100 mg/kg iv). After endotracheal intubation, the
animals were ventilated with a Harvard respirator (respiration
rate = 30 breaths/min, tidal volume = 15 ml/kg). With
the dog on its right side, a left thoracotomy was performed at the
fifth intercostal space. The pericardium was excised and used to
support the heart in a pericardial cradle. The sinus node was crushed,
and the left atrial appendage was electronically paced (pacing rate set
at 100 beats/min). One electromagnetic flowmeter probe (model
FR-100T or MF-27, Nihon Koden) was placed around the proximal ascending
aorta for measuring aortic flow, and another was placed around the
circumflex coronary artery for measuring coronary flow. The frequency
response of this flow measuring system was 3 dB down at 30 Hz. At this
setting, the phase lag was linear with respect to frequency. After
stabilization, no zero shift in the flow signals was detected
throughout the experiment. The LV and ascending aortic pressures were
measured by means of high-fidelity 7-Fr micromanometer-tipped catheters (Millar) inserted via the left carotid artery femoral artery, respectively. The tip of the micromanometer for measuring
aortic pressure was placed just distal to the flow probe so as not to interfere with the aortic flow signal. Before insertion, the catheter was calibrated at 37°C using a mercury manometer. Any zero shift in
the pressure signal was checked by simultaneous recording using a
fluid-filled transducer for which the zero reference point was taken to
be at the level of the right atrium. The LV and aortic pressures were
each measured by way of a low-pass filter with a cutoff frequency of
100 Hz, and the aortic flow signal was measured by way of a low-pass
filter with a cutoff frequency of 25 Hz.
After control recordings had been made, either the thoracic aorta (just
below the origin of the left brachiocephalic artery) or the lower
abdominal aorta (just above the iliac bifurcation) was gently ligated
for 20 s. Each dog underwent one period of constriction at each of
the two aortic sites, the order being randomized. An interval of
5-10 min was allowed between the constrictions in a given dog.
The care of the animals and the protocols used were in accordance with
guidelines laid down by the Animal Ethics Committee of Yamaguchi
University School of Medicine.
Data analysis.
All data were recorded at end expiration on a multichannel recorder
(VR12, Electronics for Medicine), digitized at intervals of 2 ms via an
on-line analog-to-digital converter, and stored on a disk. To obtain
data for analysis, we used the average of 10 consecutive cardiac
cycles. Aortic compliance was calculated as the ratio of the time
constant of diastolic aortic pressure decay to total systemic
resistance (21). Aortic pressure and flow signals were
transformed to a Fourier series, and aortic input impedance was
computed as a function of frequency. Characteristic impedance
(Zc) was estimated by averaging impedance moduli
between 2 and 12 Hz (14). Input resistance
(Rin) was determined as the modulus of the
impedance at 0 Hz. The first harmonic of the impedance modulus
(Z1) was taken as an index of arterial wave
reflection. The reflection coefficient (RC) was computed from aortic
impedance spectra; thus RC = (Z1 
Zc)/(Z1 + Zc). To clarify changes in the timing of the
arterial wave reflection, we dissected the measured pressure and flow
waves into their incident (or forward) and reflected (or backward)
components by means of mathematical techniques (26).
End diastole was defined by the peak of the R wave in the
electrocardiogram. The timing of peak negative change in pressure over
time (dP/dt), obtained from the digital data derived from the dP/dt signal, was used to estimate end systole. The time
constant of the LV pressure decay () during the isovolumic
relaxation period was calculated as the negative inverse slope of the
natural log of the pressure versus time relationship, with the
assumption of a pressure asymptote of 0 mmHg and with the use of data
from peak negative dP/dt to 10 mmHg above end-diastolic
pressure (5, 25).
Statistics.
Data are presented in the form of means ± SD. An unpaired
t-test was used to compare hemodynamic data between
groups 1 and 2. A paired t-test was
used for the analysis of experimental data from the dog study. A
P value < 0.05 was accepted as statistically significant.
| |
RESULTS |
Hemodynamic data in patients.
As summarized in Table 1, arterial
compliance was significantly lower in group 2 (age: 55 ± 9 yr) than group 1 (age: 20 ± 5 yr), but there was
no intergroup difference in ejection fraction. As shown in Table
2, peak systolic pressure was higher in
group 2 than group 1, with associated increases
in pulse pressure, Z1, RC, and
Zc. There were no significant intergroup
differences in Rin, end-diastolic LV pressure,
peak positive dP/dt of LV pressure, or .
Figure 1 shows averaged input impedance
spectra for the two. In group 2, the fluctuations in the
impedance modulus were larger than in group 1, and the point
at which the phase curve passed through zero was shifted toward a
higher frequency. These data indicate that in group 2, the
magnitude of the arterial wave reflection was augmented in association
with an increase in pulse wave velocity.
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Fig. 1.
Averaged aortic input impedance spectra. Aortic pressure
and flow signals were transformed to a Fourier series, and aortic input
impedance was computed as a function of frequency. Note that in
group 2, the fluctuations in the impedance modulus were
larger than in group 1, and the point at which the phase
curve passed through zero was shifted toward a higher frequency. Data
are means ± SD.  , Group 1;
 , group 2.
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As shown in Table 3, during compression
of both femoral arteries, peak systolic pressure did not change
significantly in groups 1 or 2. However, as shown
in Fig. 2, such compression led to an
early diastolic augmentation of the measured aortic pressure and of the
calculated backward pressure in group 1 but a late systolic
augmentation of these pressures in group 2. During the compression of the femoral arteries, Rin and
wave reflection indexes (Z1 and RC) were
significantly increased in both groups (Table 3); however, aortic
Zc did not change significantly in either group.
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Fig. 2.
Measured aortic pressure (Pm) and calculated
backward pressure (Pb) waveforms before (solid lines) and
during (dotted lines) compression of both femoral arteries. As
indicated by the arrows, the backward pressure peaked in early diastole
in group 1 (G1) but in late systole in group 2 (G2). S, systolic phase; D, diastolic phase.
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In the baseline data, there were no significant intergroup differences
in during the isovolumic relaxation period. During the compression
of the femoral arteries, was shortened in group 1 but
prolonged in group 2. Figure 3
shows the relationship between aortic compliance at rest and during
constriction of the femoral arteries. The significant inverse linear
correlation between these two parameters indicates that as aortic
compliance decreased, became more prolonged. Thus individuals with
a decreased aortic compliance (especially group 2 patients)
showed an earlier return of the arterial wave reflection (in the late
systolic phase in group 2).
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Fig. 3.
Relationship between aortic compliance at rest and the
time constant of LV pressure decay () during compression of femoral
arteries. was expressed as a percentage of control. The significant
inverse linear correlation between these two parameters indicates that
as aortic compliance decreased, became more prolonged.
, Group 1; , group
2.
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Hemodynamic data in experimental dogs.
To try to clarify the above clinically obtained findings indicating
that a change in the timing of the arterial wave reflection leads to a
change in LV relaxation, we performed an experimental study in dogs in
which the timing of the arterial wave reflection was altered by aortic
constriction at one of two sites.
Table 4 summarizes the hemodynamic
changes seen during constriction of the thoracic or lower abdominal
aorta. Peak aortic pressure was increased to a similar extent by either
constriction, whereas LV end-diastolic pressure and LV peak (positive)
dP/dt were both unchanged. Although
Rin increased to a similar extent during the two
constrictions, Z1 and RF each increased to a
greater extent during constriction of the thoracic aorta. As shown in Fig. 4, during lower abdominal aortic
constriction, the backward pressure peaked just after the dicrotic
notch (during diastole) in association with a shortening of (see
Table 4). However, during thoracic aortic constriction, it peaked
before the dicrotic notch (during systole) in association with a
prolongation of .
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Fig. 4.
Representative changes in backward pressure and coronary
flow during the constriction of the lower abdominal (A) or
thoracic aorta (B) from a single dog. Whatever the timing of
the return in backward pressure, the peak change in coronary flow
closely corresponded with the peak in backward pressure. DN, timing of
dicrotic notch.
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Figure 4 shows representative changes in backward pressure and coronary
flow during constriction of the thoracic or lower abdominal aorta.
Whatever the timing of the return in backward pressure, the peak change
in coronary flow corresponded closely in timing with the peak change in
backward pressure. Indeed, as shown in Fig.
5, there was a good correlation between
the timing of these two peak changes during constriction of either the
lower abdominal or thoracic aorta. The good correlation between the peak change in coronary flow and that in backward pressure (Fig. 6) suggests a direct augmentative effect
of backward pressure (as perfusion pressure) on coronary flow.
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Fig. 5.
Correlation between the timing of peak change ( ) in
coronary flow and that in backward pressure during constriction of
either the lower abdominal () or thoracic aorta
() in dogs. Particularly, there was a good correlation
between the timing of these two peak changes with less overlap between
these two different types of constriction. Each datum point represents
the average of the values obtained by the same two procedures, and the
deviation from the averaged value in each procedure was <10% of the
averaged value.
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Fig. 6.
Correlation between the peak change in coronary flow and
that in backward pressure during constriction of either the lower
abdominal () or thoracic aorta () in
dogs. Each datum point represents the average of the values obtained by
the same two procedures, and the deviation from the averaged value in
each procedure was <10% of the averaged value.
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DISCUSSION |
Our major finding in this study is that the timing of the return
of the arterial wave reflection during the cardiac cycle could have an
important influence on LV relaxation and coronary flow. In younger
patients (<30 yr old) with compliant arteries, the arterial wave
reflection returned during early diastole, followed by an acceleration
in LV relaxation. In contrast, in older patients (>40 yr old) with
stiffer arteries, arterial wave reflection returned earlier, during
late systole, followed by a slower LV relaxation. Our experimental
study in dogs confirmed the close relationship between the timing of
the arterial wave reflection and the speed of LV relaxation and the
association between the return of the arterial wave reflection and the
peak change in coronary flow.
The shape of the aortic pressure waveform during ejection is
essentially determined by the interaction of LV ejection with aortic
impedance but is modified by wave reflection from peripheral arterial
sites (4, 11, 18, 19, 27). Aging substantially influences
this aortic pressure waveform (16, 17). The stiffer arterial tree present in older individuals transmits the pulse wave
with a higher velocity so that reflected waves return to the aortic
root during the ejection period itself, leading to a late systolic peak
in aortic pressure (13). In younger individuals, because
of the compliant arterial system, pulse wave velocity is not so high,
and the reflected wave returns to the aortic root during the diastolic
period, leading to an augmentation of aortic pressure during early
diastole (13). Kelly et al. (10) investigated the effects of LV ejection into a stiff vascular system on in vivo
systolic mechanics and energetics. They showed that the energetic cost
to the heart for maintaining adequate flow is increased, whereas the
contractile function and efficiency of normal hearts are not altered by
ejection into a stiff vascular system. As they mentioned, this suggests
a mechanism whereby vascular stiffening in humans may yield little
functional decrement at rest but limit reserve capacity under stress
condition. Therefore, in older subjects, a stiffening of the aorta may
limit exercise capacity.
The timing and magnitude of the reflection can be properly assessed by
dissecting the measured waves into their forward and backward
components (26). In the present study, we clearly
demonstrated that the peak change in backward pressure occurred before
the closure of the aortic valve in older patients but after its closure of in young patients. There is also a progressive change in the contour
of the ascending aortic flow wave with age (17). During late systole, the descending part of the wave is normally convex to the
right, but with aging this convexity gradually disappears, to be
replaced by a concavity to the right. This concavity corresponds in
time to the augmentation of the pressure wave in late in systole caused
by the early return of the wave reflection in older subjects (15,
23).
The LV relaxation rate decreases as the systolic pressure increases
(2, 5, 9, 20). The time course of systolic loading,
manifested by the LV pressure waveform, is also considered an important
regulator of relaxation (6, 8, 12, 28). However, there is
a discrepancy in the influence of the timing of pressure rise on LV
relaxation. Several investigators (6, 8, 12, 28) showed
that a late systolic pressure rise induces a slower relaxation than an
early systolic pressure rise. In contrast, other investigators
(7, 22) demonstrated that abruptly increasing afterload
during early systole resulted in a delay in the onset of relaxation and
a decreased rate of relaxation, whereas increasing afterload late in
systole resulted in an increase in the rate of relaxation. By changing
the timing of an abrupt occlusion of the aorta during systole in intact
dogs, Solomon et al. (22) elegantly determined the
transition point during systole when load ceases to sustain the
cross-bridges (termination of contraction) and starts opposing their
formation (beginning of relaxation). They reported that the onset of LV
relaxation during normal ejection occurs very early in systole, after
only ~16% of ejection is completed. At a molecular level, the
afterload dependence of relaxation has been ascribed to the mode of
recruitment of cross-bridges (3). An early increase in
systolic load increases the recruitment of cross-bridges and hence
increases the duration of systole possibly by slowing the rate of
relaxation. In the case of a late increase in systolic load, the
cross-bridges cannot maintain the increased load, resulting in
cross-bridge disruption and in an increase in the rate of relaxation
and a subsequent decrease in the duration of systole (29).
Because the rate of relaxation is also influenced by end-systolic
pressure (2, 12) and regional nonuniformity
(28), the influence of the timing of pressure rise on LV
relaxation seems to be complex in an intact ejecting heart depending on
these factors. In the present study, the afterload dependence of the ventricular relaxation might explain the longer seen after the pressure rise in late systole induced by an early return of the arterial wave reflection (during compression of the femoral arteries in
older patients and during constriction of the thoracic aorta in dogs).
Before we can draw any final conclusions, several questions remain to
be answered. First, because we arbitrarily divided the patients who
underwent diagnostic cardiac catheterization according to age rather
than by disease, there was a difference in their types of basal heart
disease (group 1: 4 DCM and 4 VT patients; group
2: 6 CAD, 1 DCM, and 1 HCM patient). Although there was no
significant difference in LV ejection fraction between the groups, we
cannot exclude the possibility that the intergroup difference in basal
heart disease may have influenced the interaction between arterial wave
reflection and LV relaxation. Second, it remains to be explained why
was shortened by an augmentation of the backward pressure during
early diastole in both the clinical and experimental studies. Possibly,
the active relaxation of the ventricle may have been enhanced due to an
increase in the coronary arterial perfusion of the myocardium.
As extensively investigated by O'Rourke's group (1),
aortic compliance influences the timing of arterial wave reflection. As
the aortic wall becomes stiffer with aging or as a result of atherosclerosis, the arterial wave reflection returns late in systole
rather than early in diastole, thus impairing LV relaxation. In
contrast, when the arterial wave reflection returns early in diastole,
LV relaxation is faster, and there is a greater coronary flow. Thus the
time at which the arterial wave reflection returns during the cardiac
cycle may have an important effect on LV relaxation and coronary flow.
| |
FOOTNOTES |
Address for reprint requests and other correspondence: M. Yano,
Second Dept. of Internal Medicine, Yamaguchi Univ. School of Medicine,
1-1-1 Minamikogushi, Ube, Yamaguchi 755-8505, Japan (E-mail:
yanoma{at}po.cc.yamaguchi-u.ac.jp).
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 17 July 2000; accepted in final form 2 November 2000.
| |
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Am J Physiol Heart Circ Physiol
261:
H691-H699,
1991[Abstract/Free Full Text].
Am J Physiol Heart Circ Physiol 280(4):H1846-H1852
0363-6135/01 $5.00
Copyright © 2001 the American Physiological Society
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ABSTRACT
INTRODUCTION
