Download Alteration of Systolic Time Intervals in Right Ventricular

Alteration of Systolic Time Intervals in Right
Ventricular Failure
By JOSEPH S. ALPERT, M. D., FRANK D. RICKMAN, M.D., JOHN P. HOWE, M.D.,
LEWIS DEXTER, M. D., AND JAMES E. DALEN, M.D.
SUMMARY
Systolic time intervals (STI) were measured in matched patients with and without right ventricular failure
(RVF). STI were calculated from brachial arterial pressure tracings obtained at cardiac catheterization in
four groups of patients: 1) controls, without RVF; 2) acute pulmonary embolism with and without acute
RVF; 3) mitral stenosis, with and without chronic RVF; 4) primary pulmonary hypertension, with chronic
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RVF.
In patients with pulmonary embolism without acute RVF, STI were normal. However, patients with
acute RVF due to pulmonary embolism had significantly shortened left ventricular ejection times (LVETc)
and significantly increased pre-ejection periods (PEPc) and increased PEPc/LVETc ratios (P < 0.05,
P < 0.001, P < 0.001 respectively).
Similar results were obtained in patients with chronic RVF. In patients with mitral stenosis without RVF,
STI were normal. However, in patients with chronic RVF due to mitral stenosis or primary pulmonary
hypertension, PEPc and PEPc/LVETc ratios were lengthened and LVETc was shortened (P < 0.003,
P < 0.005, and P < 0.001 respectively).
PEPc/LVETc ratios increased as stroke index decreased (r= -0.55). There was also an association
between PEPc/LVETc and right atrial mean pressure (r = 0.70). These data demonstrate that patients with
acute and chronic right ventricular failure have abnormal systolic time intervals possibly secondary
ventricular dysfunction.
to
left
Additional Indexing Words:
Systolic time intervals
Right ventricular failure
LEFT VENTRICULAR FAILURE is the commonest cause of right ventricular failure. The
right heart fails in this circumstance due to the increased pressure work transmitted to it across the
lung.
The impact of right ventricular failure on left ventricular function is not as clearly defined. Chronic
right ventricular failure (RVF) has been shown to
cause left ventricular dysfunction in animals.1 2
Similarly there is some evidence that acute right ventricular overload may cause mild left ventricular
dysfunction in dogs.3 4
In man, there is only minimal direct evidence that
right ventricular failure (RVF) may affect left ventricular function. Several autopsy studies have
Left ventricular function
demonstrated unexplained left ventricular hypertrophy in patients with chronic cor pulmonale.5 It has
long been suspected clinically that acute right ventricular failure, as in acute pulmonary embolism, may
precipitate left ventricular failure.6 This observation
has not been confirmed by objective measurements.
Weissler and his associates have demonstrated that
systolic time intervals (STI) are sensitive indicators of
the state of left ventricular (LV) function.7 8 The present work assesses STI in patients with acute or chronic
right ventricular failure to determine if right ventricular failure can alter left ventricular function as
measured by STI.
Materials
Patients
From the Cardiovascular Laboratory and the Department of
Medicine, Peter Bent Brigham Hospital and Harvard Medical
School, Boston, Massachusetts.
Supported in part by the U.S. Public Health Service, National
Institutes of Health Grants: 1-F02-HL52672-01, 2-RO1-HL1243904, 5-F03-HL52672.
Address for reprints: Joseph S. Alpert, M.D., Peter Bent Brigham
Hospital, 721 Huntington Avenue, Boston, Massachusetts 02115.
Received November 30, 1973; revision accepted for publication
April 15, 1974.
317
Circutlation, Volume 50, August 1974
STI were calculated in four groups of patients (table 1).
Group 1 (controls) consisted of ten patients who had been
catheterized and found to have no evidence of organic heart
disease.
Group 2 (pulmonary embolism with or without acute
right ventricular failure) consisted of 20 patients, age and
sex matched with Group 1, with angiographically proven
acute pulmonary embolism. These patients were free of
prior heart disease on the basis of history, physical examination, ECG, and chest X-ray. Ten of these patients had
massive pulmonary embolism with acute right ventricular
3018
ALPERT ET AL.
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failure as judged by a right atrial mean pressure greater than
7 mm Hg and a stroke index less than 40 ml/beat/M2. Six of
these patients were studied a second time when their right
ventricular failure had improved or resolved completely.
The other ten patients with acute pulmonary embolism had
no hemodynamic evidence of right ventricular (RV) failure
(table 1).
Group 3 (mitral stenosis with or without chronic right
ventricular failure) consisted of 20 patients with
catheterization-proven pure mitral stenosis. These patients
were free of other valvular defects nor did they have any
evidence of coronary artery disease. They were age and sex
matched with group 1. Ten of tnese patients had critical
mitral stenosis with moderate to severe pulmonary vascular
disease and chronic right ventricular failure as judged by a
right atrial mean pressure greater than 7 mm Hg. The other
ten patients with pure mitral stenosis were free of
hemodynamic evidence of right ventricular failure.
Group 4 (chronic right ventricular failure) consisted of
four patients with primary pulmonary hypertension and
right ventricular failure.
None of the patients except for those with mitral stenosis
were receiving digitalis preparations. Digoxin was given to
nine of the ten patients with right ventricular failure and
seven of the ten patients without right ventricular failure.
All medication was held for 24 hours before catheterization.
No patient was receiving d-blocking drugs or any
catecholamine or similar agents.
Methods
Three indirect measurements of left ventricular function
were obtained from ECG, brachial arterial, and left ventricular (LV) pressure tracings taken at the time of cardiac
catheterization. Brachial artery pressure was obtained using
fluid-filled Teflon catheters, 22 em long with an internal
diameter of 1.0 mm. Left ventricular pressures were obtained through standard fluid-filled USCI #8 medium-tip
Lehman catheters. All pressures were recorded using
Statham 23db pressure manometers and an Electronics for
Medicine recorder. The pre-ejection period (PEP) was
derived from simultaneous brachial arteriai pressure and
ECG tracings recorded at 50 mm/see paper speed. PEP was
defined as that interval from the onset of the QRS (lead II)
to the onset of the upstroke of the brachial arterial pressure
tracing. The left ventricular ejection (LVET) was derived
from the brachial arterial pressure tracing recorded at 50
mm/sec and was defined as that interval from the start of
the upstroke to the midpoint of the dicrotic notch. The
Q-LV interval (analogous to the Q-1 interval) was measured
in all patients with mitral stenosis from simultaneous left
ventricular (LV) pressure and ECG tracings recorded at 50
mm/sec paper speed. The Q-LV interval was defined as that
time from the onset of the QRS to the onset of the upstroke
of the left ventricular (LV) pressure tracing.
The reported value for each interval was the average of 35 separate determinations for patients in normal sinus
rhythm and ten determinations for patients in atrial fibrillation. Atrial fibrillation occurred only in patients with mitral
stenosis. Nine of the ten patients with right ventricular
failure and seven of ten patients without right ventricular
(RV) failure were in atrial fibrillation. All values for PEP and
LVET were corrected for heart rate.7 9
Systolic time intervals were measured in a group of ten
patients who had two cardiac catheterization studies within
the span of several days to determine the reproducibility of
the systolic time intervals as calculated in the present work.
Patients were studied between 8:30 and 11 AM in the
fasting state. The only premedication was diazepam 10 mg
intramuscularly, a dosage shown to have minimal
hemodynamic effects.'0 All patients had QRS intervals of
0.10 sec or less. Means, standard deviations, and student's t
tests for paired and nonpaired variables were calculated using standard formulae.
Results
I. PEP corrected (PEPc)
A) Controls - PEPc in the ten controls without
heart disease ranged from 0.16 to 0.20 seconds (mean
Table 1
Hemodynamic Profiles of the Four Groups of Patients
Age
(years)
1.
Normal controls
HR
(beats/min)
SI
(cc/min/M2)
16
87
18
43
53 21
96
14
112 *22
55
RA mean
PA mean
(mm Hg)
(mm
15
3
2
15
41
19
4
2
23
7
15
21
31
11
27
22
Hg)
BA diastolic
(mm Hg)
3
69
9
20
6
77
10
5
34
3
70
-
14
5
1
25
7
72
-
17
7
12
5
58* 10
72
17 7
10
3
71 * 11
72 * 16
-
-
n = 10
2.
Pulmonary embolism
A. Without acute RVF
n = 10
B. With acute RVF
n
10
3.
4.
Mitral stenosis
A. Without chronic RVF
n = 10
B. With chronic RVF
n = 10
Primary pulmonary
54* 19
56
12
78
56
9
92
33
8
95 * 15
-
-
m
20
hypertension with RVF
n = 4
Values are reported * standard deviation.
Abbreviations: RVF = right ventricular failure; HR = heart rate; SI = stroke index; RA mean
PA mean = pulmonary artery mean pressure; BA diastolic = brachial artery diastolic pressure.
=
right atrial mean pressure;
Circuilation, Volzume 50. August 1974
319
STI AND RV FAILURE
Figure
Figure 2
1
Systolic time intervals at repeat study in
cardiac diseases.
ten patients
with different
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PEPc in patients with and without acute right ventricular failure.
PE without RVF= patients with pulmonary embolism without
right ventricular failure; PE with RVE = patients with pulmonary
embolism with right ventricular failure; PE with RVF,
F U= patients with pulmonary embolism with right ventricular
± 0.01). The reproducibility of PEPc as herein
measured was assessed in a group of ten patients with
heart disease but without RV failure who had two
hemodynamic studies within a period of several days.
The average difference of this measurement in the
same patient studied twice was 0.01 ± 0.01 seconds
(fig. 1).
B) Patients with and without acute RVF secondary
to acute pulmonary embolism
In the patients with
acute pulmonary embolism without RVF, PEPc
ranged from 0.16 to 0.21 sec (mean 0.18 ± 0.02). This
is almost identical to the results in the control group
(fig. 2; table 2). However, in the ten patients with
acute RVF secondary to pulmonary embolism, PEPc
0.02
was significantly prolonged (mean 0.23
seconds). Six of these ten patients with RVF had a
repeat study an average of 20 days after the initial
study. PEPc values had decreased toward the normal
range in four of the six patients (fig. 2; table 2).
In
C) Patients with and without chronic RVF
ten patients with mitral stenosis without RVF, PEPc
was comparable to that of the normal controls. It
ranged from 0.17-0.20 (mean 0.18 0.01 sec) (fig. 3;
table 3). However, in patients with chronic RVF due
0.18
failure, follow-up catheterization values.
mitral stenosis, PEPe was significantly prolonged
(mean 0.21 ± 0.02). Similarly in the small group of
four patients with primary pulmonary hypertension
PEPc was prolonged to a mean of 0.23 + 0.03 seconds
(fig. 3; table 3).
to
-
II.
LVET corrected (LVETc)
LVETc in the ten controls without
A) Controls
heart disease ranged from 0.39 to 0.47 (mean
0.43 + 0.03) sec. In the ten patients who had repeat
hemodynamic studies within days of each other
LVETc did not change (fig. 1). LVETc averaged
0.42 0.02 seconds at the time of the first study and
0.42 0.03 sec at the second study. The average
difference between the paired measurements was
0.02 0.01 sec (fig. 1).
In
B) Patients with and without acute RVF
patients with acute pulmonary embolism without
RVF, LVETc was essentially the same as in the controls; it ranged from 0.38 to 0.46 (mean 0.42 0.03)
sec. However, in the patients with acute RVF seconable 2
Effect of Acute Right Ventricular Failure (RVF)
Controls
PEPe (sec)
LVETc (see)
PEPc/LVETc
0.18 = 0.01
0.43 - 0.03
0.42 - 0.03
on
Systolic Time Intervals
Pulmonary embolism Pulmonary embolism Pulmonary embolism
with RVF-follow-up
with RVF
without RVF
0.18
0.42
0.43
-
0.02
0.03
0.04
0.23
0.40
0.58
-
-
0.02
0.02
0.05
0.21
0.42
0.49
0.02
0.01
0.05
P
values
P < 0.001
P < 0.03
P < 0.001
Values are reported - 1 standard deviation.
P values reflect t test for parameters in the pulmonary embolism without RVF and the pulmonary embolism
with RVF groups.
C.irc flatiOn \' tlu;iic 30(). X.Xigtist 1974
ALPERT ET AL.
320
Table 3
Effect of Chronic Right Ventricular Failure (RVF) on Systolic Time Intervals
Controls
PEPc (see)
LVETc (sec)
PEPc/LVETc
Q-LV (sec)
ICT (sec)
0.18
0.43
0.42
=
0.01
0.03
0.03
Mitral stenosis
without RVF
Mitral stenosis
with RVF
0.18 0.01
0.43 0.03
0.43 0.04
0.04 i 0.01
0.11 +0.01
0.21
0.39
0.54
0.04
0.13
Primary pulmonary
hypertension
P
with RVF
0.03
0.02
0.05
0.23
0.36
0.61
0.02
0.03
0.06
0.01
0.01
Values
P < 0.005/P < 0.001
P < 0.005/P < 0.001
P < 0.001/P < 0.001
NS
P < 0.001
Values are reported - 1 standard deviation.
The first P value reflects t test for parameters in mitral stenosis without RVF and mitral stenosis with RVF
groups. The second P value reflects t test for parameters in primary pulmonary hypertension and control groups.
ICT = isovolumic contraction time.
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dary to pulmonary embolism, LVETc was
significantly reduced (mean 0.40 ± 0.02 sec). Of the
six patients having a follow-up study, LVETc increased in five while the mean increased to
0.42 + 0.01 sec (fig. 4; table 2).
C) Patients with and without chronic RVF - In
the patients with mitral stenosis without RVF, mean
LVETc was the same as in the control group
(0.43 ± 0.03 sec). In patients with RVF due to mitral
stenosis, however, LVETc was significantly shortened
(0.39 ± 0.03 sec). Similarly, in the small group of
patients with primary pulmonary hypertension
LVETc was shortened to a mean of 0.36 ± 0.02 sec
(fig. 5; table 3).
III. PEPc/LVETc Ratio
A) Controls - PEPc/LVETc ratios ranged from
0.38 to 0.46 (mean 0.42 ± 0.03) in the group of nor-
0 26
mal controls. In the ten patients studied twice
PEPc/LVETc ratios did not change, with a mean
difference of 0.02 ± 0.01 units between the first and
second studies (fig. 1).
B) Patients with and without acute RVF - In
patients with pulmonary embolism without RVF,
PEPc/LVETc ratios were the same as in the normal
controls, ranging from 0.40 to 0.51 (mean
0.43 ± 0.04). In patients with acute RVF secondary to
pulmonary embolism, however, PEPc/LVETc ratios
were significantly increased (mean 0.58 + 0.05). In
the six patients with acute RVF who underwent
follow-up study, PEPc/LVETc ratios decreased
toward normal (mean 0.49 ± 0.05) in all six (fig. 6,
table 2).
C) Patients with and without chronic RVF - In
the patients with mitral stenosis without RVF mean
PEPc/LVETc ratios were the same as in the normal
controls (mean 0.43 ± 0.04). In patients with mitral
stenosis and right ventricular failure, however,
PEPc/LVETc ratios were significantly increased
(mean 0.54 ± 0.06). Likewise, patients with primary
0.24
0.48.
022
00
0.46
PEPc
(seconds)L
0
"Q
0.44
020
_ .
_
*
0
*
0
0
LVETc 042
(seconds)
0.40
_~
0 18
*
0
*
*0
*
0
*
0
0 38
0.16
s
Controls
,
MSs RVF MScRVF
PPHT
Figure 3
PEPc in patients with and without chronic right ventricularfailure.
MS without RVF = patients with mitral stenosis without right ventricular failure; MS with RVF = patients with mitral stenosis with
right ventricularfailure; PPHT = patients with primary pulmonary
hypertension and right ventricular failure.
0.36
U.J4'
Controls
PE s RVF
PE E RVF
PE C RVF, F/U
Figure 4
LVETc in patients with and without acute right ventricularfailure.
as in figure 2)
(abbreviations
Circulation, Volume 50( AXtgutst 1974
321
STI AND RV FAILURE
0.46
0.44
LVETc
*
0.40
0.62
@
*
0
0.58
*
S.
*
@0*S
*0
0
*
*
0
l_*
0.42
(seconds)
@0
PEPc 054
LV ETc
0.50
@0
*
S
0.46
0
l_*
@00
*
00
*0@
*
1-
MS g RVF
*
0
0.42
Controls
Ill:
S~~~
S
0.36
0
*
0.38
0.34 _
l-
0 AA,
0
t) AR.
MSERVF
I
PPHT
0.38
"
I-
Controls
Figure 5
LVETc in patients with and without chronic right ventricular
failure. (abbreviations as in figure 3)
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pulmonary hypertension had significantly increased
(mean 0.61 + 0.05) PEPc/LVETc ratios (fig. 7, table
3).
IV. Q-LV and ICT
Q-LV intervals were calculated in the patients with
mitral stenosis. They were the only patients in whom
left heart catheterization had been performed. The
Q-LV interval was the same (0.04 + 0.01 seconds) in
patients with and without RVF due to mitral stenosis.
Q-LV intervals were subtracted from PEP intervals in
these patients to obtain an estimate of the true left
ventricular isometric contraction time (ICT). Mean
left ventricular ICT was significantly longer in
patients with RV failure than in those without it
(table 3).
V. Relation of Systolic Time Intervals (STI) to Stroke Index (SI)
and Right Atrial Mean Pressure (MRAP)
As noted in table 4, modest correlations were present between the various systolic time intervals (PEPc,
LVETc, and PEPc/LVETc) and the two hemodynamic measurements, stroke index, and right atrial
mean pressure. These associations were strongest in
patients with pulmonary embolism and weakest in
patients with mitral stenosis (table 4, figs. 8, 9).
Discussion
Systolic time intervals have been reported to be
sensitive indicators of left ventricular function.7 111
They are capable of detecting acute or chronic
changes in ventricular function caused by
pathological conditions or drugs.7
Usually these parameters are measured noninvasively; however, systolic time intervals measured
with catheters in the left ventricle and aorta have correlated very closely with externally derived inCirculation. XVolutue .50( A utgutst I1974
PE E RVF
PE s RVF
PEE RVF, F/U
Figure 6
PEPc/LVETc ratios in patients with and without acute right
ventricular failure. (abbreviations as in figure 2)
dices."' 12 The present work derives systolic time intervals from pressure tracings recorded from the
brachial artery and the left ventricle. These internally
derived indices are highly reproducible as seen in a
group of ten patients catheterized twice several days
apart (fig. 1). Moreover, the systolic time intervals as
derived in the present work correlated with stroke index in all patient groups except those with mitral
stenosis. Similar correlations have been noted
previously, employing externally derived systolic time
intervals.7 8, 13, 14 In the present work, STI were also
noted to correlate with right atrial mean pressure.
The pre-ejection period (PEP) is composed of two
separate events, the electromechanical delay and the
isometric contraction period of the left ventricle. The
electromechanical delay period can be estimated by
measuring the Q-LV interval. In those patients who
had left ventricular catheterization, the Q-LV interval
0
0 66
S
0.62
S
0
S
PEPc 058
LVETc
0
*
0.54
*~~~~
0.50
*~~~~~~~~
0.46
**
0 42
*
@004
*
0
&
q
U1 ioIA,
O.;
Controls
0*0
0
0-
II0
v
op
MS E RVF
MS s RVF
PPHT
Figure 7
PEPc/LVETc ratios in patients with and without chronic right
ventricular failure. (abbreviations
as
in figure
3)
ALPERT ET AL.
322
Table 4
Correlation Coefficients
Patients with mitral
stenosis
All patients
PEPc/SI
LVETc/S1
PEPc/LVETc/SI
PEPc/RA mean
r =
r=
r =
r =
r =
r =
LVETc/RA mean
PEPc/LVETc/RA mean
-0.48
0.45
- 0.55
0.62
- 0.47
r =
r=
r =
r =
r =
r =
0.70
Patients with pulmonary
embolism
-0.43
0.24
- 0.39
0.26
- 0.55
r
r
r
r
r
r
0.45
=
-0.64
= 0.37
= - 0.66
= 0.79
= - 0.59
= 0.84
Abbreviations: SI = stroke index; RA mean = right atrial mean pressure.
unaffected by the presence or absence of RV
failure. When the Q-LV interval was subtracted from
the PEP an estimation of the isovolumic contraction
time was obtained which was significantly prolonged
in the patients with RV failure as compared with
patients without RV failure.
PEP and LVET as reported here were corrected for
heart rate employing the regression equations of
Weissler.7' 8. 9 The uncorrected values for PEP and
LVET, however, showed the same significant
differences between the groups with and without RV
failure, as did the values corrected for heart rate.
The fact that the present internally derived values
for PEPc are longer than the externally derived indices is the result of two factors: first, aortic to brachial
arterial pulse delay and second, pressure wave delay
in the fluid-filled catheter system. Values for internal
LVETc are similar to those obtained externally since
pulse and catheter delay affect both measurement
was
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224
* NO RVF
oMSiRVF
ARVF
2
A A
A
* MS E RVF
1g16 _
RA
MEAN
PRESSURE
A
internally and externally derived values for PEP
and LVET have been made previously.1' Therefore,
we believe that STI as measured here reflect left ventricular function to the same degree as externally
derived indices.
Four possible mechanisms exist to explain the abnormal systolic time intervals in patients with acute
and chronic right ventricular failure. First, left ventricular preload is decreased secondary to a reduced
stroke output from the failing right ventricle. A
decrease in left ventricular preload can result per se in
abnormalities in various left ventricular function
parameters including systolic time intervals.`5 16
A second explanation for the findings presented is
suggested by Braunwald's finding17 that acute increases in peripheral resistance result in shortened left
ventricular ejection times. In the same manner, increased right ventricular afterload, such as that seen in
our patients with right ventricular failure, may cause
alterations in right ventricular systolic events. Given
the close interplay between right and left ventricular
systolic events, the measured changes in left heart
systolic time intervals may in part reflect alterations in
right ventricular systolic time intervals.
on
U
A
12zuI
A
(mmHg) 12
points of this parameter equally. Similar observations
U
_
*
8 _A
~
AA
~~
US
A
100
UA
A
AU
0
80
0
4
_
0
<>
OS
.
0
S
0
1111*
111
0.34
0.38
0.42
0.46
0.50
0.54
0.58
0.62
0.66
A
a
STROKE
INDEX 60
*
(cc / beat/M2)
0.70
PE Pc/ LVETc
Figure 8
40
00
0.
*f
U&
20
A
a
0
Correlation between right atrial mean pressure and PEPc/LVETc
ratio. No RVF = normals and patients with pulmonary embolism
without right ventricular failure; MS without RVF = patients with
mitral stenosis without right ventricular failure; RVF = patients
having pulmonary embolism and primary pulmonary hypertension
with right ventricular failure; MS with RVF = patients with mitral
stenosis with right ventricular failure.
NO RVF
MS g RVF
RVF
MSE RVF
A
1
v _.
u
0.34
0.38
1
0.46
0.42
0.50
0.54
0.58
0.62
1L
0.66 0.70
PEPc/ LVETc
Figure 9
Correlation between stroke index and PEPc/LVETc ratio.
(abbreviations
as
in
figure 8)
Circutlation, Volume 50, Augtust 1974
323
STI AND RV FAILURE
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Actual alteration of the contractile function of the
left ventricle is the third possible explanation for the
present observations. Kelly et al.2 observed reduced
left ventricular peak systolic pressure, peak systolic
wall stress, peak dp/dt, peak contractile element
velocity and myocardial concentration of
norepinephrine in dogs with chronic right ventricular
failure. Left ventricular force velocity curves were also
markedly abnormal. Salel et al."8 noted abnormal left
ventricular contractility indices in a mixed group of
patients most of whom had chronic right ventricular
overload. Moreover, Machida and Rapaport4 observed
altered left ventricular compliance and decreased left
ventricular contractility parameters in dogs whose
pulmonary circulation had been embolized with
barium sulfate.
A fourth possible explanation for abnormal systolic
time intervals in right ventricular failure is the socalled "reversed Bernheim phenomenon", or septal
encroachment on the left ventricular cavity. The septal "bulge" is said to result in an alteration in left ventricular geometry and hence contractile function.
Taylor et al.`9 found that left ventricular distensibility
was considerably reduced during right ventricular distension. Dogs with acute4 or chronic2 right ventricular
overload have been noted to have decreased left ventricular compliance as measured by pressure/volume
curves. Stool et al.20 quantitated canine left ventricular septal to lateral wall diameter changes caused
by septal bulging secondary to right ventricular
pressure overload. Increasing pulmonary arterial
pressure to a mean of 60 mm Hg resulted in a 23%
decrease in septal-lateral left ventricular wall
diameter as well as concomitant decreases in left ventricular end-diastolic volume and stroke volume. In a
single clinical observation, Harken2' noted a
decreased left ventricular cavity secondary to septal
bulging in a patient with mitral stenosis and severe
right ventricular failure.
It is concluded that left ventricular function, insofar
as it can be measured by systolic time intervals, is
altered in acute and chronic right ventricular failure.
Four possible mechanisms exist to explain the alteration in left ventricular function noted in patients with
right ventricular failure: decreased left ventricular
preload, alteration in right ventricular systolic time intervals, decreased left ventricular contractility, and
altered left ventricular geometry and compliance.
The present data do not suggest which mechanism is
actually responsible for the abnormal systolic time intervals noted in patients with right ventricular failure.
Circulation. X'olinw .50, AXugust 1974
References
1. HECHT HH, KUIDA H, TSAGARIS TJ: Brisket disease IV:
Impairment of left ventricular function in a form of cor
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Br Heart
Alteration of Systolic Time Intervals in Right Ventricular Failure
JOSEPH S. ALPERT, FRANK D. RICKMAN, JOHN P. HOWE, LEWIS DEXTER and
JAMES E. DALEN
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Circulation. 1974;50:317-323
doi: 10.1161/01.CIR.50.2.317
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